The DOI matches its Crossref record; 129 of the 129 references it cites were found in a registry or an index; 51 of the 139 sources its claims cite were checked for support.
Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review
Open accessAbstract
Dementia is one of the major causes of disability in later life, and ischemic heart disease is a leading cause of morbidity and mortality. Apolipoprotein E (apoE) plays a pivotal role in lipoprotein metabolism in the brain and in the periphery, and is implicated in both dementia and ischemic heart disease. Peripherally, liver-derived apoE is the main source of plasma apoE. Approximately half of plasma apoE is associated with triglyceride-rich lipoproteins, where apoE serves as the main ligand for the low density lipoprotein (LDL) receptor and the LDL receptor Related Protein (LRP). In the brain, apoE is produced mainly by astrocytes. Astrocyte-derived apoE is pivotal for cerebral cholesterol metabolism and clearance of β-amyloid, a major pathological hallmark of Alzheimer disease. Plasma levels of apoE and other lipids and lipoproteins are under strong genetic influence by the APOE polymorphism, and the ε4 allele is a strong genetic risk factor for Alzheimer disease. The characteristics of the APOE polymorphism thus suggest the qualitative importance of apoE, whereas studies of familial absolute apoE deficiency suggest a quantitative importance of plasma apoE levels in lipid metabolism. Whether plasma levels of apoE are associated with increased risk of dementia and ischemic heart disease, and whether these associations are independent of the APOE polymorphism and of lipids and lipoproteins has only recently been established. The aim of this review is to summarize and discuss the current epidemiological and biological evidence for an association of plasma levels of apoE with risk of dementia and ischemic heart disease.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review summarizes evidence that plasma apolipoprotein E (apoE) levels and APOE genotype are linked to dementia and ischemic heart disease, with low apoE associated with future dementia and high apoE with ischemic heart disease. It argues for the qualitative importance of the APOE polymorphism and an emerging quantitative importance of plasma apoE, though associations differ by disease and are partly mediated by lipids and triglyceride-rich lipoproteins.
Key findings
- Plasma apoE levels are strongly influenced by APOE genotype, with stepwise decreases from ε22 to ε32 to ε42 to ε33 to ε43 to ε44; the APOE polymorphism accounts for roughly 15–25% of variability in plasma apoE. In the Copenhagen General Population Study and Copenhagen City Heart Study, genotype frequencies were 0.7%, 12.4%, 2.9%, 55.8%, 25.4%, and 2.9% for ε22, ε32, ε42, ε33, ε43, and ε44, respectively.
- The ε4 allele is a major genetic risk factor for late-onset Alzheimer disease: one copy is associated with a two- to three-times increased risk, and two copies with roughly an eight- to ten-times increased risk; ε2 is associated with decreased risk. Low plasma apoE levels were epidemiologically associated with increased risk of future dementia in the general population, independent of APOE genotype.
- For ischemic heart disease, high plasma apoE was associated with increased risk in men but not women in a prospective general population cohort of ~91,000 participants; the association was not attenuated by adjustment for APOE genotype but was attenuated after adjustment for triglycerides. In a population-based study of 546 elderly individuals, high plasma apoE was associated with increased cardiovascular mortality in both genders, independently of APOE genotype and plasma triglycerides, LDL cholesterol, and HDL cholesterol.
- Mechanistically, liver-derived apoE is the main source of plasma apoE, and approximately half of plasma apoE is associated with triglyceride-rich lipoproteins, where it serves as the main ligand for the LDL receptor and LRP. In the brain, astrocyte-derived apoE is pivotal for cerebral cholesterol metabolism and amyloid-β clearance, and both decreased apoE levels and APOE genotype may contribute to dementia via impaired amyloid-β clearance.
Methods
- Narrative review summarizing epidemiological and biological evidence on plasma apoE levels, APOE genotype, and risk of dementia and ischemic heart disease.
- Draws on population studies including the Copenhagen General Population Study and Copenhagen City Heart Study, the ApoEurope project, the Rotterdam Study, and a prospective general population cohort of ~91,000 participants, as well as animal and in vitro studies.
- No new primary data collection or meta-analysis is reported; the paper synthesizes prior findings and presents combined CGPS/CCHS data in figures.
Limitations
- Stated: word and reference limits required prioritization of the literature; human studies of plasma or cerebrospinal fluid apoE in Alzheimer disease are conflicting, possibly reflecting different disease stages; immunoassay results may be biased by isoform-dependent epitope masking and lipid complexation; animal model results differ and complicate translation to humans.
- Stated: whether blood apoE levels reflect cerebral apoE levels has been debated, although cerebrospinal fluid apoE shows a genotype-dependent pattern similar to plasma.
- Evident from the text: this is a narrative rather than systematic review, so literature selection and synthesis may be selective; observational associations cannot establish causality; and the contrasting directions of apoE associations with dementia versus ischemic heart disease indicate different disease mechanisms that remain incompletely understood.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
30 No full text of the sources · 19 Own interpretation · 16 Partly supported · 15 Supported · 10 Not checked yet · 9 Supported so far · 7 Sources not found · 1 Mixed support · 1 Not supported · 1 No basis given · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“The importance of high C-reactive protein levels has been investigated by some studies, however Rasmussen et al. showed that adjustment for C-reactive protein did not have any impact on the risk between plasma levels of apoE and ischemic heart disease [44,116,121,122].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 10. Plasma levels of apolipoprotein E and risk of ischemic heart disease
What the sources say
- Disputedcites [44] Mooijaart, 2006, ApoE plasma levels and risk of cardiovascular mortality in old age, PLoS Med. sourceExperimental — accuracy not yet measured
The Results section (page unavailable) reports that cardiovascular mortality risk associated with high apoE depended on CRP level: it was highest at low CRP levels and absent at high levels. The paper studies cardiovascular mortality, not ischemic heart disease, and does not report the claimed finding about adjustment for CRP. (LLM, conf=0.82)
Checked by a reasoning model — may be wrong.
- Not checked — no full text of the sourcecites [116] Rasmussen, 2016, Plasma levels of apolipoprotein E and risk of ischemic heart disease in the general population, Atherosclerosis source
- Disputedcites [121] Corsetti, 2012, Apolipoprotein E predicts incident cardiovascular disease risk in women but not in men with concurrently high levels of high-density lipoprotein cholesterol and C-reactive protein, Metabolism sourceExperimental — accuracy not yet measured
The Discussion (section 4; page not given) says apoE-associated risk was absent in women with high HDL-C and low CRP, while the Results (section 3.3; page not given) report risk in the high-CRP subgroup. That is contrary to the claim that CRP had no impact on the association. The paper also does not report a Rasmussen analysis of CRP adjustment. (LLM, conf=0.76)
Checked by a reasoning model — may be wrong.
- Partly supportedcites [122] Corsetti, 2012, Apolipoprotein A-II influences apolipoprotein E-linked cardiovascular disease risk in women with high levels of HDL cholesterol and C-reactive protein, PLoS One sourceExperimental — accuracy not yet measured
The Study Populations section (page unavailable) reports that apoE predicted cardiovascular disease risk in women with high CRP. The Statistical Analyses section lists CRP among potential adjustment variables, but neither passage says CRP adjustment left the apoE risk association unchanged. The cited paper also does not establish the claim about Rasmussen et al. or specifically ischemic heart disease. (LLM, conf=0.82)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Hypertriglyceridemic patients have higher plasma levels of apoE compared with normal control subjects; this could probably be explained by the finding, that increased levels of apoE stimulate VLDL triglyceride production in the liver and impairs lipoprotein lipase-mediated lipolysis, thus leading to hypertriglyceridemia [56,65].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked — no full text of the sourcecites [56] Rifai, 1987, A simple immunotechnique for the determination of serum concentration of apolipoprotein E, Clin. Chim. Acta source
- Supportedcites [65] Huang, 1998, Overexpression and accumulation of apolipoprotein E as a cause of hypertriglyceridemia, J. Biol. Chem. source
The Results section reports that plasma apoE levels were 2.5–4 times higher in 27 patients with hypertriglyceridemia than in six normal controls. This directly supports the attributed comparison; the supplied passage does not give a page number. (LLM, conf=0.95)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Recent in vitro studies have found that apoE4 expressed in neurons -but not in astrocytes - reduces the mitochondrial function [41].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Supportedcites [41] Chen, 2011, Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer disease, J. Biol. Chem. source
The Discussion states that full-length apoE4 induced mitochondrial dysfunction in cultured cortical neurons and N2A cells, but not in astrocytes. The results section also reports reduced mitochondrial respiratory-complex levels in apoE4-expressing neurons, with no comparable reduction in astrocytes. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The ε4 allele increased brain amyloid burden in a dose-dependent manner in normal elderly individuals and in mild cognitive impairment patients [93,94].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Partly supportedcites [93] Reiman, 2009, Fibrillar amyloid-beta burden in cognitively normal people at 3 levels of genetic risk for Alzheimer's disease, Proc. Natl. Acad. Sci. U. S. A. sourceExperimental — accuracy not yet measured
The Results report that fibrillar amyloid-β burden increased with APOE ε4 gene dose among 28 cognitively normal participants. The paper includes only one participant with mild cognitive impairment, whose burden was high; it does not establish a dose-dependent relationship in MCI patients. (LLM, conf=0.90)
- Partly supportedcites [94] Villemagne, 2011, Longitudinal assessment of Abeta and cognition in aging and Alzheimer disease, Ann. Neurol. sourceExperimental — accuracy not yet measured
The PiB Baseline Results report higher amyloid burden in ε4 carriers than noncarriers in both healthy controls and MCI patients. The Follow-up PiB Studies report a dose-dependent relationship only when clinical groups were combined, with no significant differences when each group was examined separately. The copy therefore does not support a dose-dependent finding in each of the two populations named. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Conversely, expression of apoE3 results in a dose-dependent decrease in amyloid burden [95].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Supportedcites [95] DeMattos, 2004, ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivo, Neuron source
The passage labeled Abstract explicitly says that increased apoE3 expression in the brain produces a dose-dependent decrease in Aβ levels and deposition. It identifies the supporting observations as unpublished data; the citing sentence accurately paraphrases the reported relationship. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“One copy of the ε4 allele is associated with a two to three times increased risk for Alzheimer disease, and two copies of the ε4 allele is associated with roughly an eight to ten times increased risk [23,100].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 7. Genetic variation in APOE and risk of dementia
What the sources say
- Not checked — no full text of the sourcecites [23] Rasmussen, 2015, Plasma levels of apolipoprotein E and risk of dementia in the general population, Ann. Neurol. source
- Partly supportedcites [100] Verghese, 2011, Apolipoprotein E in Alzheimer's disease and other neurological disorders, Lancet Neurol. sourceExperimental — accuracy not yet measured
The *APOE* and Alzheimer’s disease section says that two copies of ε4 increase late-onset Alzheimer’s disease risk approximately 12-fold. It supports the increased-risk association, but not the cited estimate of roughly eight to ten times. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“However, levels of apoE in human cerebrospinal fluid do display genotype-dependent pattern similar to the pattern in plasma, further murine interstitial fluid was observed to have genotype-dependent apoE levels similar to the pattern in cerebrospinal fluid [105,112,113].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 8. Plasma levels of apolipoprotein E and risk of dementia
What the sources say
- Not checked — no full text of the sourcecites [105] Cruchaga, 2012, Cerebrospinal fluid APOE levels: an endophenotype for genetic studies for Alzheimer's disease, Hum. Mol. Genet. source
- Supportedcites [112] Ulrich, 2013, In vivo measurement of apolipoprotein E from the brain interstitial fluid using microdialysis, Mol. Neurodegener. source
The Results and discussion report isoform-dependent apoE levels in the hippocampal interstitial fluid of apoE knock-in mice, with apoE2 highest and apoE4 lowest. The authors explicitly state that these differences are similar to those seen in cerebrospinal fluid. (LLM, conf=0.94)
- Could not verifycites [113] Deane, 2008, apoE isoform-specific disruption of amyloid beta peptide clearance from mouse brain, J. Clin. Investig. sourceExperimental — accuracy not yet measured
The Results (page unavailable) describe clearance of apoE isoforms experimentally microinfused into mouse brain interstitial fluid, including their appearance in CSF. They do not report genotype-dependent apoE levels in murine interstitial fluid or compare those levels with a genotype-dependent CSF pattern. I searched for endogenous apoE concentrations and genotype comparisons in both compartments. (LLM, conf=0.76)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“In a population-based study of 546 elderly individuals, prospectively followed for specific causes of death for 5 years, high plasma levels of apoE were associated with increased cardiovascular mortality in both genders, independently of APOE genotype and plasma levels of triglycerides, LDL cholesterol and HDL cholesterol [44].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 10. Plasma levels of apolipoprotein E and risk of ischemic heart disease
What the sources say
- Supportedcites [44] Mooijaart, 2006, ApoE plasma levels and risk of cardiovascular mortality in old age, PLoS Med. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A limited blood brain barrier permeability to circulating lipidpoor apoE2, apoE3, and apoE4 supports that apoE in blood and brain are regulated independently [72,107,108].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 8. Plasma levels of apolipoprotein E and risk of dementia
What the sources say
- Partly supportedcites [72] Linton, 1991, Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation, J. Clin. Investig. sourceExperimental — accuracy not yet measured
The Results (page not provided) report that serum apoE phenotypes changed after liver transplantation while CSF phenotypes did not, implying that most CSF apoE is produced locally. This supports largely separate blood and brain apoE pools, but the paper does not test blood-brain barrier permeability specifically for circulating lipid-poor apoE2, apoE3, and apoE4. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [107] Martel, 1997, Isoform-specific effects of apolipoproteins E2, E3, and E4 on cerebral capillary sequestration and blood-brain barrier transport of circulating Alzheimer's amyloid beta, J. Neurochem. source
- Not checked — no full text of the sourcecites [108] Wahrle, 2003, Differential metabolism of ApoE isoforms in plasma and CSF, Exp. Neurol. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Both the level of apoE and apoE isoform plays a role: lack of murine Apoe protein as well as targeted replacement of murine Apoe with human apoE4, leads to blood-brain barrier breakdown by activating a proinflammatory cyclophilin A-nuclear factor kB-matrix metalloproteinase-9 pathway in pericytes [87].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Supportedcites [87] Bell, 2012, Apolipoprotein E controls cerebrovascular integrity via cyclophilin A, Nature source
The Abstract states that lack of murine Apoe and expression of human APOE4 cause BBB breakdown through the CypA–NF-κB–MMP9 pathway in pericytes. It also identifies targeted-replacement APOE4 mice among the models studied. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
- It may state two separate claims as one. 47
- Probably not a substantial claim. 18
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“At the level of an individual the effect of the APOE polymorphism on plasma lipid levels is moderate, however since the APOE polymorphism is common, it contributes substantially to the total phenotypic variability in plasma lipid levels in the general population [21,24,58].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked — no full text of the sourcecites [21] Smit, 1988, Apolipoprotein E polymorphism in The Netherlands and its effect on plasma lipid and apolipoprotein levels, Hum. Genet. source
- Not checked — no full text of the sourcecites [24] Davignon, 1988, Apolipoprotein E polymorphism and atherosclerosis, Arteriosclerosis source
- Disputedcites [58] Haddy, 2002, The importance of plasma apolipoprotein E concentration in addition to its common polymorphism on inter-individual variation in lipid levels: results from Apo Europe, Eur. J. Hum. Genet. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 1 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“The characteristics of the APOE polymorphism thus suggest a qualitative importance of apoE, whereas studies of familial absolute apoE deficiency suggest a quantitative importance of plasma apoE levels in lipid metabolism [26,27].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 1. Introduction
What the sources say
- Supportedcites [26] Schaefer, 1986, Familial apolipoprotein E deficiency, J. Clin. Investig. source
The Introduction describes apoE isoforms with different amino acid sequences and associations with lipid disorders, supporting the qualitative contrast. The Lipoprotein analysis and discussion report trace plasma apoE in homozygotes with marked lipid abnormalities, and conclude that apoE is essential for normal catabolism of triglyceride-rich lipoprotein remnants. This supports the suggested importance of apoE quantity in lipid metabolism. (LLM, conf=0.90)
- Supportedcites [27] Mak, 2014, Effects of the absence of apolipoprotein e on lipoproteins, neurocognitive function, and retinal function, JAMA Neurol. source
The paper’s introductory discussion of APOE variants describes lower receptor-binding activity for apoE2 than apoE3, supporting a qualitative difference between isoforms. Its Results and Discussion report that a patient with no detectable apoE in plasma had severe lipoprotein abnormalities, supporting the suggested importance of apoE availability in lipid metabolism. The copy provides no page numbers for these passages. (LLM, conf=0.87)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“ApoE4 exhibits a near-normal and slightly changed affinity to the LDL receptor, whereas apoE4 has a slightly more compact structure compared with apoE3 [33].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 3. Protein structure of apolipoprotein E
What the sources say
- Partly supportedcites [33] Mahley, 2009, Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS, J. Lipid Res. sourceExperimental — accuracy not yet measured
The section on apoE2 and LDL-receptor binding says that apoE3 and apoE4 both bind avidly to LDL receptors, supporting the near-normal binding characterization, but it does not establish a slight difference in their affinity. The apoE4 section explicitly says apoE4 has a more compact conformation than apoE3. Page numbers are unavailable in our copy. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In the brain, apoE is mainly produced by astrocytes, although microglia and neurons can synthesize apoE under various physiological and pathological conditions [66,67].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Not checked — no full text of the sourcecites [66] Huang, 2004, Apolipoprotein E: diversity of cellular origins, structural and biophysical properties, and effects in Alzheimer's disease, J. Mol. Neurosci. source
- Supportedcites [67] Kim, 2009, The role of apolipoprotein E in Alzheimer's disease, Neuron source
The Physiological Function of ApoE section says astrocytes are the main brain cells expressing apoE, microglia express it to a lesser extent, and neurons can produce it under certain conditions. This supports the citing sentence’s account of the cellular sources of apoE. (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Despite near-normal receptor affinity of apoE4 the amino acid change leads to differences in distribution in lipoprotein classes: apoE3 shows preference for high density lipoprotein (HDL) particles, whereas apoE4 shows preference for very low density lipoprotein (VLDL) particles [38].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 3. Protein structure of apolipoprotein E
What the sources say
- Supportedcites [38] Gregg, 1986, Abnormal in vivo metabolism of apolipoprotein E4 in humans, J. Clin. Investig. source
The Results (p. 2) report that HDL contained the largest amount of labeled apoE3, whereas apoE4 was present primarily on VLDL. The Discussion (p. 4) likewise describes a higher percentage of apoE4 on VLDL and less on HDL than apoE3. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Lipid-free apoE consists of two domains connected by a “hinge region”: the amino-terminal domain (amino acids 1 to 191) contains the receptor-binding function and the carboxyl-terminal domain (~amino acids 225 to 299) contains the lipid-binding function [28,33].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 3. Protein structure of apolipoprotein E
What the sources say
- Not checked — no full text of the sourcecites [28] Weisgraber, 1994, Apolipoprotein E: structure-function relationships, Adv. Protein Chem. source
- Supportedcites [33] Mahley, 2009, Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS, J. Lipid Res. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Additional common variation includes promoter SNPs located in the 5 0 region of the APOE gene: À491A>T (rs449647), À427T>C (rs769446), and À219G>T (rs405509) [31,32].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 2. Gene structure of APOE
What the sources say
- Partly supportedcites [31] Artiga, 1998, Allelic polymorphisms in the transcriptional regulatory region of apolipoprotein E gene, FEBS Lett. sourceExperimental — accuracy not yet measured
The Results and discussion identifies promoter polymorphisms at −491 A/T, −427 T/C, and −219 T/G, and reports measuring their frequencies in 215 individuals. The paper does not give the three rs identifiers, so our copy cannot verify the claimed mappings; G/T at −219 describes the same allele pair in reverse order. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [32] Frikke-Schmidt, 2004, Gender- and age-specific contributions of additional DNA sequence variation in the 5' regulatory region of the APOE gene to prediction of measures of lipid metabolism, Hum. Genet. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Interestingly, insufficient levels of apoE also lead to hypertriglyceridemia, because less apoE protein is present to serve as ligands for the LDL receptor and LRP, clinically illustrated by familial apoE deficiency [9,26,27].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked yetcites [9] Mahley, 2001, Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal lipoprotein metabolism
- Partly supportedcites [26] Schaefer, 1986, Familial apolipoprotein E deficiency, J. Clin. Investig. sourceExperimental — accuracy not yet measured
The Lipoprotein analysis section reports increased VLDL and IDL triglycerides in homozygotes with familial apoE deficiency. The paper also suggests that apoE is essential for receptor-mediated clearance of triglyceride-rich remnants, but the passages do not identify both the LDL receptor and LRP as the receptors responsible. Its finding is specific to homozygous deficiency; heterozygotes generally had normal plasma lipids. (LLM, conf=0.85)
- Supportedcites [27] Mak, 2014, Effects of the absence of apolipoprotein e on lipoproteins, neurocognitive function, and retinal function, JAMA Neurol. source
The Results report no detectable apoE and elevated triglycerides (534 mg/dL) in the patient. The Discussion explains that apoE enables remnant uptake through the LDL receptor and LDLR-related protein, and that VLDL and remnant accumulation reflects the absence of this ligand. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In the brain, apoE is mainly produced by astrocytes, although microglia and neurons can synthesize apoE under various physiological and pathological conditions [66,67].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Not checked — no full text of the sourcecites [66] Huang, 2004, Apolipoprotein E: diversity of cellular origins, structural and biophysical properties, and effects in Alzheimer's disease, J. Mol. Neurosci. source
- Supportedcites [67] Kim, 2009, The role of apolipoprotein E in Alzheimer's disease, Neuron source
The “Physiological Function of ApoE” section says astrocytes are the main brain cells expressing apoE, microglia express it to a lesser extent, and neurons can produce it under certain conditions. The neuroinflammation section also describes increased apoE production in response to Aβ. No page numbers are provided in our copy. (LLM, conf=0.91)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“ApoE is the major cholesterol carrier in the central nervous system: in the brain, lipids are transported on lipoproteins that resemble HDL particles, but while apolipoprotein A1 (apoA1) is the primary apolipoprotein and apoE is present in lower levels in HDL in the circulation, in contrast apoE is the primary apolipoprotein on these HDL-like particles found in the brain [67,73,75].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Supportedcites [67] Kim, 2009, The role of apolipoprotein E in Alzheimer's disease, Neuron source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [73] Hirsch-Reinshagen, 2009, Why lipids are important for Alzheimer disease?, Mol. Cell Biochem. source
- Supportedcites [75] Mahley, 2016, Central nervous system lipoproteins: ApoE and regulation of cholesterol metabolism, Arterioscler. Thromb. Vasc. Biol. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In men, the levels of apoE leveled off after the age of 45 years, whereas they continued to increase in women [58].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 4. Plasma levels of apolipoprotein E and APOE genotype, age and gender
What the sources say
- Supportedcites [58] Haddy, 2002, The importance of plasma apolipoprotein E concentration in addition to its common polymorphism on inter-individual variation in lipid levels: results from Apo Europe, Eur. J. Hum. Genet. source
The Results section states that apoE concentrations leveled off after age 45 in men but continued to rise with age in women. The Discussion reiterates this sex-specific pattern beyond age 45. (LLM, conf=0.95)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Type III hyperlipoproteinemia is characterized by elevations of both plasma cholesterol and triglycerides due to an increase in chylomicron remnants, VLDL and IDL [9,26,52].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked yetcites [9] Mahley, 2001, Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal lipoprotein metabolism
- Supportedcites [26] Schaefer, 1986, Familial apolipoprotein E deficiency, J. Clin. Investig. source
The Introduction states that type III hyperlipoproteinemia involves elevated plasma cholesterol and triglycerides due to increased chylomicron remnants, VLDL, and IDL. The passage matches the attributed claim; no page number is supplied in our copy. (LLM, conf=0.95)
- Not checked — no full text of the sourcecites [52] Brewer, 1983, NIH conference. Type III hyperlipoproteinemia: diagnosis, molecular defects, pathology, and treatment, Ann. Intern Med. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Pericyte inflammation leads to neuronal uptake of neurotoxic proteins from the blood, and microvascular and cerebral blood flow reductions, which altogether subsequently lead to impaired clearance of amyloid-b [86,87].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Partly supportedcites [86] Zlokovic, 2011, Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders, Nat. Rev. Neurosci. sourceExperimental — accuracy not yet measured
In “Blood–brain barrier breakdown” (page not provided), the review links pericyte deficiency to BBB leakage and microvascular degeneration, and describes blood-derived molecules entering the brain and suppressing capillary flow. In “Alzheimer’s disease” (page not provided), it links BBB dysfunction to impaired amyloid-β clearance. It does not identify pericyte inflammation as the initiating cause or say that neurons take up the leaked proteins; nor does it establish the claimed sequence in which all these effects lead to impaired clearance. (LLM, conf=0.88)
- Partly supportedcites [87] Bell, 2012, Apolipoprotein E controls cerebrovascular integrity via cyclophilin A, Nature sourceExperimental — accuracy not yet measured
The paper reports that activation of a proinflammatory pathway in pericytes of APOE4-expressing and Apoe-deficient mice leads to neuronal uptake of blood-derived neurotoxic proteins and reductions in microvasculature and cerebral blood flow (opening summary, page unavailable). It does not say that these changes subsequently impair amyloid-β clearance; clearance appears in the titles of works in its References, not as a finding establishing that sequence. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Whereas there is convincing evidence to suggest that the APOE polymorphism is involved in development of Alzheimer disease, cerebral amyloid angiopathy as well as traumatic brain injury, the role of APOE has not been quite as clear for other subtypes of dementia or for other neurological diseases [100].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 7. Genetic variation in APOE and risk of dementia
What the sources say
- Partly supportedcites [100] Verghese, 2011, Apolipoprotein E in Alzheimer's disease and other neurological disorders, Lancet Neurol. sourceExperimental — accuracy not yet measured
The Summary and Introduction support a strong association of APOE genotype with Alzheimer disease and cerebral amyloid angiopathy risk, and say associations with other neurological diseases are less clear. For traumatic brain injury, however, the Summary and Table 1 link APOE to outcome after injury, not to the development of the injury. (LLM, conf=0.90)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Finally, studies of familial apoE deficiency describe persons examined in their 40s without neurological defects, although the peripheral lipid metabolism was affected [27,97].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Supportedcites [27] Mak, 2014, Effects of the absence of apolipoprotein e on lipoproteins, neurocognitive function, and retinal function, JAMA Neurol. source
The Methods (Participants; page not available) describe a 40-year-old man with apoE deficiency and no signs or symptoms of neurological deficit. The Results report essentially normal neurological testing, while the Abstract (Results) documents marked lipoprotein abnormalities. This paper supplies one of the cases described collectively by the citing sentence. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [97] Lohse, 1992, Familial apolipoprotein E deficiency and type III hyperlipoproteinemia due to a premature stop codon in the apolipoprotein E gene, J. Lipid Res. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The APOE polymorphism affects risk of Alzheimer disease in a dose-dependent manner; the ε4 allele is associated with an increased risk and the ε2 allele is associated with a decreased risk [100].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 7. Genetic variation in APOE and risk of dementia
What the sources say
- Supportedcites [100] Verghese, 2011, Apolipoprotein E in Alzheimer's disease and other neurological disorders, Lancet Neurol. source
The Summary states that APOE ε2, ε3, and ε4 dose-dependently alter the likelihood of Alzheimer’s disease, with ε4 increasing risk and ε2 decreasing it. The APOE and Alzheimer’s disease section also gives higher risk for two ε4 copies than for one. (LLM, conf=0.95)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Additionally, induction of murine Apoe expression improves amyloid-b clearance and cognition; this finding also underlines the importance of the level of apoE [89].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Supportedcites [89] Cramer, 2012, ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models, Science source
In the study’s results (page not provided), bexarotene increased apoE expression in AD mouse models and enhanced Aβ clearance; the clearance effect was absent in apoE-null mice. The paper also reports improved cognition and memory after bexarotene treatment. It does not separately establish that apoE induction alone caused the cognitive improvement. (LLM, conf=0.89)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Previously, in vitro studies have shown that the apoA-II and apoE heterodimeric complex on HDL cholesterol modulates the receptor affinity for the LDL receptor, and that the LDL receptor affinity is dependent on available apoE, an affinity probably dependent on apoE isoform [124,125].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 10. Plasma levels of apolipoprotein E and risk of ischemic heart disease
What the sources say
- Partly supportedcites [124] Weisgraber, 1978, Apoprotein (E–A-II) complex of human plasma lipoproteins. I. Characterization of this mixed disulfide and its identification in a high density lipoprotein subfraction, J. Biol. Chem. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [125] Innerarity, 1978, Apoprotein (E–A-II) complex of human plasma lipoproteins. II. Receptor binding activity of a high density lipoprotein subfraction modulated by the apo(E–A-II) complex, J. Biol. Chem. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
In the paper
“In the Copenhagen General Population Study (CGPS) and the Copenhagen City Heart Study (CCHS), the APOE genotype frequencies were 0.7%, 12.4%, 2.9%, 55.8%, 25.4%, and 2.9% for ε22, ε32, ε42, ε33, ε43, and ε44, respectively [23].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 2. Gene structure of APOE
What the sources say
- Not checked — no full text of the sourcecites [23] Rasmussen, 2015, Plasma levels of apolipoprotein E and risk of dementia in the general population, Ann. Neurol. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The mature apoE protein consists of 299 amino acids and an 18amino acid signal peptide is removed post-translationally [17,28].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 3. Protein structure of apolipoprotein E
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The low density lipoprotein (LDL) receptor binding region is situated in helix four between amino acids 136 and 150 [17,28].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 3. Protein structure of apolipoprotein E
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Plasma levels of apoE and other lipids and lipoproteins are under strong genetic influence by the APOE polymorphism defining the three apoE isoforms, and the ε4 allele is a strong genetic risk factor for Alzheimer disease [18e25].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 1. Introduction
What the sources say
- Not matchedcites [18e25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“Approximately half of plasma apoE is associated with triglyceriderich lipoproteins, and apoE serves as the main ligand for the LDL receptor and LDL receptor Related Protein (LRP) [9,60,61].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked yetcites [9] Mahley, 2001, Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal lipoprotein metabolism
- Not checked — no full text of the sourcecites [60] Bersot, 1976, Interaction of swine lipoproteins with the low density lipoprotein receptor in human fibroblasts, J. Biol. Chem. source
- Not checked yetcites [61] Havel, 2001, Introduction: structure and metabolism of plasma lipoproteins
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The two genotypes combine into six common APOE genotypes, ε22, ε32, ε42, ε33, ε43 and ε44, corresponding to six plasma apoE phenotypes: apoE22, apoE32, apoE42, apoE33, apoE43 and apoE44 [14].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 2. Gene structure of APOE
What the sources say
- Not checked — no full text of the sourcecites [14] Zannis, 1982, Proposed nomenclature of apoE isoproteins, apoE genotypes, and phenotypes, J. Lipid Res. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“The APOE gene is located on chromosome 19 and consists of four exons [28].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 2. Gene structure of APOE
What the sources say
- Not checked — no full text of the sourcecites [28] Weisgraber, 1994, Apolipoprotein E: structure-function relationships, Adv. Protein Chem. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Human apoE has three isoforms: apoE2, apoE3, and apoE4.Genetically, these isoforms correspond to three common alleles, ε2, ε3, and ε4, defined by two exonic single nucleotide polymorphisms (SNPs; rs429358/ε4, rs7412/ε2) in APOE [13,29].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 2. Gene structure of APOE
What the sources say
- Not checked — no full text of the sourcecites [13] Zannis, 1981, Human apolipoprotein E isoprotein subclasses are genetically determined, Am. J. Hum. Genet.
- Not checked — no full text of the sourcecites [29] Zannis, 1981, Human very low density lipoprotein apolipoprotein E isoprotein polymorphism is explained by genetic variation and posttranslational modification, Biochemistry source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Apolipoprotein E (apoE) plays a pivotal role in lipoprotein metabolism in the brain and in the periphery, and is implicated both in dementia and ischemic heart disease.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 1. Introduction
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“Boerwinkle and Utermann found that 1% of the inter-individual variation in plasma apoE levels was attributable to variation of age and sex in a sample of 563 blood-bank donors [20].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 4. Plasma levels of apolipoprotein E and APOE genotype, age and gender
What the sources say
- Not checked — no full text of the sourcecites [20] Boerwinkle, 1988, Simultaneous effects of the apolipoprotein E polymorphism on apolipoprotein E, apolipoprotein B, and cholesterol metabolism, Am. J. Hum. Genet.
plaincorrelationaln = 563- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Further, the mentioned three common promoter SNPs as well as rare variation in APOE affect plasma levels of apoE [23,51e53].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 4. Plasma levels of apolipoprotein E and APOE genotype, age and gender
What the sources say
- Not matchedcites [23,51e53]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Utermann et al. studied the association between levels of apoE in serum and the common APOE genotypes, and found that genotypes with the ε2 allele had highest and those with the ε4 allele had lowest average levels [20,43].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 4. Plasma levels of apolipoprotein E and APOE genotype, age and gender
What the sources say
- Not checked — no full text of the sourcecites [20] Boerwinkle, 1988, Simultaneous effects of the apolipoprotein E polymorphism on apolipoprotein E, apolipoprotein B, and cholesterol metabolism, Am. J. Hum. Genet.
- Not checked — no full text of the sourcecites [43] Utermann, 1985, Apolipoprotein E mutants, hyperlipidemia and arteriosclerosis, Adv. Exp. Med. Biol. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Subsequently, it has been shown repeatedly that plasma levels of apoE are under strong genetic influence by the three common APOE alleles, ε2, ε3, and ε4 with stepwise decreases from ε22 to ε32 to ε42 to ε33 to ε43 to ε44 genotype [23,44e50].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 4. Plasma levels of apolipoprotein E and APOE genotype, age and gender
What the sources say
- Not matchedcites [23,44e50]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“The ε2 allele is associated with lower levels of plasma cholesterol and LDL cholesterol and higher levels of triglycerides compared with the ε3 allele, whereas the ε4 allele is associated with higher levels of total cholesterol, LDL cholesterol and triglycerides [18,19].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked — no full text of the sourcecites [18] Bennet, 2007, Association of apolipoprotein E genotypes with lipid levels and coronary risk, JAMA source
- Not checked yetcites [19] Sing, 1985, Role of the apolipoprotein E polymorphism in determining normal plasma lipid and lipoprotein variation, Am. J. Hum. Genet.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Plasma levels of apoE vary only slightly between the fasting and non-fasting state [64].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked — no full text of the sourcecites [64] Annuzzi, 1989, Concentrations of apolipoproteins B, C-I, C-II, C-III, E and lipids in serum and serum lipoproteins of normal subjects during alimentary lipaemia, Scand. J. Clin. Lab. Investig. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“VLDL and IDL are cleared mainly by apoE interaction with the LDL receptor and LRP, whereas LDL is cleared via the LDL receptor by interaction with apoB100 [61].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked yetcites [61] Havel, 2001, Introduction: structure and metabolism of plasma lipoproteins
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“ABCA1 regulates apoE levels and lipidation of apoE in the brain; in mice, deficiency of ABCA1 leads to loss of apoE with residual apoE being poorly lipidated; in contrast, overexpression of ABCA1 promotes apoE lipidation and reduces formation of amyloid plaques [73].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Not checked — no full text of the sourcecites [73] Hirsch-Reinshagen, 2009, Why lipids are important for Alzheimer disease?, Mol. Cell Biochem. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, increased content of apoE in apoB containing lipoproteins have the potential to increase the deposition in the arterial wall, resulting in increased atherosclerosis.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“It is estimated that less than one in 20 individuals with the ε22 genotype will have overt type III hyperlipoproteinemia [24].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked — no full text of the sourcecites [24] Davignon, 1988, Apolipoprotein E polymorphism and atherosclerosis, Arteriosclerosis source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In the general population, a loss-of-function mutation in ABCA1 has been shown to be associated with low levels of apoE and increased risk of Alzheimer disease [79].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Not checked — no full text of the sourcecites [79] Nordestgaard, 2015, Loss-of-function mutation in ABCA1 and risk of Alzheimer's disease and cerebrovascular disease, Alzheimers Dement. source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The pattern of associations between the six common APOE genotypes and plasma lipid levels is similar across populations, although the magnitude of the associations differs between populations and subgroups within populations; thus both context-dependent and invariant associations could be suggested [9,24,30].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked yetcites [9] Mahley, 2001, Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal lipoprotein metabolism
- Not checked — no full text of the sourcecites [24] Davignon, 1988, Apolipoprotein E polymorphism and atherosclerosis, Arteriosclerosis source
- Not checked — no full text of the sourcecites [30] Frikke-Schmidt, 2000, Context-dependent and invariant associations between APOE genotype and levels of lipoproteins and risk of ischemic heart disease: a review, Scand. J. Clin. Lab. Investig. Suppl.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“APOE ε22 homozygotes have the propensity to develop type III hyperlipoproteinemia, which can be triggered by secondary factors such as age, diabetes, hypothyroidism and obesity [9,52].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked yetcites [9] Mahley, 2001, Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal lipoprotein metabolism
- Not checked — no full text of the sourcecites [52] Brewer, 1983, NIH conference. Type III hyperlipoproteinemia: diagnosis, molecular defects, pathology, and treatment, Ann. Intern Med. source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Pericytes are important for the maintenance of the bloodebrain barrier [96].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Not checked — no full text of the sourcecites [96] Armulik, 2010, Pericytes regulate the blood-brain barrier, Nature source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“ApoE is involved in amyloid precursor protein processing and amyloid-b production and the deposition of amyloid-b [80e82].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Not matchedcites [80e82]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“The brain is the most cholesterol-rich organ in the body, containing ~25% of total body cholesterol [73].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
What the sources say
- Not checked — no full text of the sourcecites [73] Hirsch-Reinshagen, 2009, Why lipids are important for Alzheimer disease?, Mol. Cell Biochem. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Triglyceride-rich lipoproteins are causally associated with risk of ischemic heart disease and apoE plays a central role in their plasma clearance via receptor mediated uptake by the liver [9,59].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 5. Apolipoprotein E and lipid metabolism in the periphery
What the sources say
- Not checked yetcites [9] Mahley, 2001, Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal lipoprotein metabolism
- Not checked — no full text of the sourcecites [59] Nordestgaard, 2014, Triglycerides and cardiovascular disease, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Further, deficiency of apoE in the preclinical state may affect neuronal regeneration and plasticity through decreased cholesterol and phospholipid cell supply.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 8. Plasma levels of apolipoprotein E and risk of dementia
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Previously, some human studies of plasma or serum levels of apoE have found decreased levels in Alzheimer disease patients compared with control individuals, whereas other studies have reported that there was no differences [48e50, 103,104].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 8. Plasma levels of apolipoprotein E and risk of dementia
What the sources say
- Not matchedcites [48e50, 103,104]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Whether lack of murine Apoe is beneficial or detrimental for Alzheimer disease seems to be influenced by the mouse model studied, and this complicates the interpretation of results from experimental animal models to the human situation.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In several meta-analyses, ε4 has been associated with a moderately increased risk of ischemic heart disease, whereas ε2 has been associated with reduced risk [18,117e120].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 9. Genetic variation in APOE and risk of ischemic heart disease
What the sources say
- Not matchedcites [18,117e120]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, experimental and epidemiological data suggest that both decreased apoE levels and APOE genotype are involved in dementia, possibly via impaired amyloid-b clearance from the brain.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 6. Apolipoprotein E and lipid metabolism in the brain
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Although the more frequent ε32 genotype is associated with a decreased risk of ischemic heart disease, rare ε22 homozygotes have the propensity to develop type III hyperlipoproteinemia with an increased risk of atherosclerosis and premature cardiovascular disease [9].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 9. Genetic variation in APOE and risk of ischemic heart disease
What the sources say
- Not checked yetcites [9] Mahley, 2001, Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal lipoprotein metabolism
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The characteristics of the APOE polymorphism suggest a qualitative importance of apoE both for risk of dementia and for risk of ischemic heart disease.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 11. Conclusions
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In contrast, the general population cohort of ~91,000 individuals covers ages from 20 to 100þ years, and shows strong associations between all major lipids, lipoproteins and apolipoproteins and risk of ischemic heart disease [116].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 10. Plasma levels of apolipoprotein E and risk of ischemic heart disease
What the sources say
- Not checked — no full text of the sourcecites [116] Rasmussen, 2016, Plasma levels of apolipoprotein E and risk of ischemic heart disease in the general population, Atherosclerosis source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The effects are, however, more subtle than for dementia, and are possibly mediated by triglyceride-rich lipoproteins in accordance with the role of apoE in lipid metabolism.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 11. Conclusions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both ε22 homozygozity and the ε4 allele are associated with ischemic heart disease, although the receptor affinity of these isoforms is very different.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 11. Conclusions
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Interestingly, low levels of apoE are associated with future risk of dementia, whereas high levels of apoE are associated with future risk of ischemic heart disease, indicating different mechanisms of disease.”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 11. Conclusions
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Taken together, high plasma levels of apoE seems to be associated with increased risk of ischemic heart disease, an association possibly mediated by triglyceride-rich lipoproteins [116].”
§ Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review > 10. Plasma levels of apolipoprotein E and risk of ischemic heart disease
What the sources say
- Not checked — no full text of the sourcecites [116] Rasmussen, 2016, Plasma levels of apolipoprotein E and risk of ischemic heart disease in the general population, Atherosclerosis source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Whether plasma levels of apoE are associated with increased risk of dementia and ischemic heart disease, and whether these associations are independent of the APOE polymorphism and of lipids and lipoproteins, has only recently been established.
“Whether plasma levels of apoE are associated with increased risk of dementia and ischemic heart disease, and whether these associations are independent of the APOE polymorphism and of lipids and lipoproteins has only recently been established.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The ɛ4 allele has detrimental effects on production, deposition, and clearance of amyloid-β, in phosphorylation of tau, in neurotoxicity, mitochondrial dysfunction, and in blood–brain barrier permeability.57,59,60”
From Plasma levels of apolipoprotein E, APOE genotype, and all-cause and cause-specific mortality in 105 949 individuals from a white general population cohort (2019) · cites this paper as [60]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Both mass-spectrometry-based and immunoassay-based approaches have shown that plasma ApoE isoform quantification can discriminate ε4 carriers from non-carriers with high accuracy [16–18].”
From Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era (2026) · cites this paper as [18]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“apoE is a central apolipoprotein in cerebral cholesterol metabolism and is involved in brain amyloid metabolism, blood brain barrier integrity, and transport of various lipid species to neuronal cells [15][16][17][18][19].”
From APOE and vascular disease: Sequencing and genotyping in general population cohorts (2023) · cites this paper as [19]
The cited source says what the claim attributes to it.
In the citing paper
“Whereas brain apoE plays a major role in brain amyloid metabolism, in blood‐brain barrier integrity, and in supplying cholesterol and phospholipids to neuronal cells, 12 , 13 , 14 , 16 , 30 , 31”
From APOE and dementia – resequencing and genotyping in 105,597 individuals (2020) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“However, plasma levels of apoE vary only slightly between the fasting and non-fasting state.60,79”
From Plasma levels of apolipoprotein E, APOE genotype, and all-cause and cause-specific mortality in 105 949 individuals from a white general population cohort (2019) · cites this paper as [60]
The cited source says what the claim attributes to it.
In the citing paper
“Earlier association studies of plasma ApoE level with AD have reported inconsistent findings [26–31]”
From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [30]
The cited source says what the claim attributes to it.
In the citing paper
“consistent with previous reports indicating reduced plasma ApoE concentrations in ε4 carriers [17, 18]”
From Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era (2026) · cites this paper as [18]
Citations
Cites
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
European Guidelines on cardiovascular disease prevention in clinical practice (version 2012)
Authors/Task Force Members:, Perk, J., De Backer, G., Gohlke, H., Graham, I., Reiner, Ž., Verschuren, M., Albus, C., Benlian, P., Boysen, G., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs092 · Cited by 8,490
The metabolic and molecular bases of inherited disease
Chen, Y.-T. (2001) · Medical Entomology and Zoology · Cited by 6,928
The global prevalence of dementia: a systematic review and metaanalysis.
Prince, M., Bryce, R., Albanese, E., Wimo, A., Ribeiro, W., & Ferri, C. P. (2013) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2012.11.007 · Cited by 4,941
Jack, C. R., Knopman, D. S., Jagust, W. J., Petersen, R. C., Weiner, M. W., Aisen, P. S., Shaw, L. M., Vemuri, P., Wiste, H. J., Weigand, S. D., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(12)70291-0 · Cited by 4,396
Meta-Analysis of 74,046 Individuals Identifies 11 New Susceptibility Loci for Alzheimer’s Disease
(EADI), E. A. D. I., Lambert, J.-C., (GERAD), G. A. E. R. I. A. D., Alzheimer's Disease Genetic Consortium (ADGC), (CHARGE), C. F. H. A. A. R. I. G. E., Ibrahim-Verbaas, C. A., Harold, D., Naj, A. C., Sims, R., Bellenguez, C., et al. (2013) · Nature Genetics · doi:10.1038/ng.2802 · Cited by 4,336
European guidelines on cardiovascular disease prevention in clinical practice: executive summary
Graham, I., Atar, D., Borch‐Johnsen, K., Boysen, G., Burell, G. K., Cífková, R., Dallongeville, J., Backer, G. D., Ebrahim, S. B. J., Gjelsvik, B., et al. (2007) · European Heart Journal · doi:10.1093/eurheartj/ehm316 · Cited by 3,865
Neurovascular pathways to neurodegeneration in Alzheimer’s disease and other disorders
Zlokovic, B. V. (2011) · Nature Reviews Neuroscience · doi:10.1038/nrn3114 · Cited by 2,969
Pericytes regulate the blood–brain barrier
Armulik, A., Genové, G., Mäe, M., Nisancioglu, M. H., Wallgard, E., Niaudet, C., He, L., Norlin, J., Lindblom, P., Strittmatter, K., et al. (2010) · Nature · doi:10.1038/nature09522 · Cited by 2,843
Potential for primary prevention of Alzheimer's disease: an analysis of population-based data
Norton, S., Matthews, F. E., Barnes, D. E., Yaffe, K., & Brayne, C. (2014) · The Lancet Neurology · doi:10.1016/s1474-4422(14)70136-x · Cited by 2,466
Cited by
Sorted by citations
A Quarter Century of APOE and Alzheimer’s Disease: Progress to Date and the Path Forward
Belloy, M. E., Napolioni, V., & Greicius, M. D. (2019) · Neuron · doi:10.1016/j.neuron.2019.01.056 · Cited by 570
APOE2: protective mechanism and therapeutic implications for Alzheimer’s disease
Li, Z., Shue, F., Zhao, N., Shinohara, M., & Bu, G. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00413-4 · Cited by 306
Beyond the CNS: The many peripheral roles of APOE
Martínez-Martínez, A. B., Torres-Perez, E., Devanney, N., Del Moral, R., Johnson, L. A., & Arbones-Mainar, J. M. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.104809 · Cited by 149
Byrne, C. D., & Targher, G. (2021) · Diabetes Obesity and Metabolism · doi:10.1111/dom.14484 · Cited by 125
ApoE and Neurodegenerative Diseases in Aging
Yin, Y., & Wang, Z. (2018) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-1117-8_5 · Cited by 111
Duong, M. T., Nasrallah, I. M., Wolk, D. A., Chang, C. C. Y., & Chang, T. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.647990 · Cited by 110
Integrative analysis of the plasma proteome and polygenic risk of cardiometabolic diseases
Ritchie, S. C., Lambert, S. A., Arnold, M., Teo, S. M., Lim, S. I., Šćepanović, P., Marten, J., Zahid, S., Chaffin, M. D., Liu, Y., et al. (2021) · Nature Metabolism · doi:10.1038/s42255-021-00478-5 · Cited by 96
Rasmussen, K. L., Tybjærg-Hansen, A., Nordestgaard, B. G., & Frikke-Schmidt, R. (2019) · European Heart Journal · doi:10.1093/eurheartj/ehz402 · Cited by 86
Self-citationKorologou-Linden, R., Bhatta, L., Brumpton, B. M., Howe, L. D., Millard, L. A. C., Kolaric, K., Ben-Shlomo, Y., Williams, D. M., Smith, G. D., Anderson, E. L., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-32183-6 · Cited by 71
Zhu, Z., Lin, Y., Li, X., Driver, J. A., & Liang, L. (2019) · Human Genetics · doi:10.1007/s00439-019-01988-9 · Cited by 69
APOE and dementia – resequencing and genotyping in 105,597 individuals
Rasmussen, K. L., Tybjærg‐Hansen, A., Nordestgaard, B. G., & Frikke‐Schmidt, R. (2020) · Alzheimer's & Dementia · doi:10.1002/alz.12165 · Cited by 64
Self-citationRole of estrogen in women's Alzheimer's disease risk as modified by APOE
Valencia‐Olvera, A. C., Weng, J. M., Christensen, A., LaDu, M. J., & Pike, C. J. (2022) · Journal of Neuroendocrinology · doi:10.1111/jne.13209 · Cited by 75
Rasmussen, K. L., Nordestgaard, B. G., Frikke‐Schmidt, R., & Nielsen, S. F. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.07.223 · Cited by 57
Self-citationZhou, Z., Zhang, S., Ding, S., Abudupataer, M., Zhang, Z., Zhu, X., Zhang, W., Zou, Y., Yang, X., Ge, J., et al. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/1209307 · Cited by 52
γ-Oryzanol Improves Cognitive Function and Modulates Hippocampal Proteome in Mice
Rungratanawanich, W., Cenini, G., Mastinu, A., Sylvester, M., Wilkening, A., Abate, G., Bonini, S. A., Aria, F., Marziano, M., Maccarinelli, G., et al. (2019) · Nutrients · doi:10.3390/nu11040753 · Cited by 52
Zhen, J., Huang, X., Halm‐Lutterodt, N. V., Dong, S., Ma, W., Xiao, R., & Yuan, L. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00248 · Cited by 50
Yuan, Y. L., Long, P., Liu, K., Xiao, Y., He, S., Li, J., Mo, T., Liu, Y., Yu, Y., Wang, H., et al. (2019) · Redox Biology · doi:10.1016/j.redox.2019.101404 · Cited by 48
Bridging systemic metabolic dysfunction and Alzheimer’s disease: the liver interface
Song, D., Yang, L., Yang, L.-L., Luo, Y., & Yao, X. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00849-6 · Cited by 53
Wang, W., Xu, L., Yao, X., Cheng, X., & Zhu, Y. (2018) · Medicine · doi:10.1097/md.0000000000012805 · Cited by 45
Interrelationship between Alzheimer’s disease and cardiac dysfunction: the brain–heart continuum?
Yang, M., Li, C., Zhang, Y., & Ren, J. T. (2019) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmz115 · Cited by 48
Kinetics of plasma apolipoprotein E isoforms by LC-MS/MS: a pilot study
Blanchard, V., Ramin-Mangata, S., Billon-Crossouard, S., Aguesse, A., Durand, M., Chemello, K., Nativel, B., Flet, L., Chétiveaux, M., Jacobi, D., et al. (2018) · Journal of Lipid Research · doi:10.1194/jlr.p083576 · Cited by 43
Frick, E. A., Emilsson, V., Jónmundsson, Þ., Steindorsdottir, A. E., Johnson, E. C. B., Puerta, R., Dammer, E. B., Shantaraman, A., Cano, A. C., Boada, M., et al. (2024) · Nature Aging · doi:10.1038/s43587-024-00693-1 · Cited by 47
Apolipoprotein E Genotype e2: Neuroprotection and Its Limits
Kim, H., Devanand, D. P., Carlson, S., & Goldberg, T. E. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.919712 · Cited by 42
Aslam, M. M., Fan, K.-H., Lawrence, E., Bedison, M. A., Snitz, B. E., DeKosky, S. T., Lopez, O. L., Feingold, E., & Kamboh, M. I. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02170-4 · Cited by 39
Wang, L., Sang, B., & Zheng, Z. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.985109 · Cited by 33
Cholesterol and Dementia: A Long and Complicated Relationship
McFarlane, O., & Kędziora–Kornatowska, K. (2019) · Current Aging Science · doi:10.2174/1874609812666190917155400 · Cited by 33
Lifestyle Affects Amyloid Burden and Cognition Differently in Men and Women
Bachmann, D., Roman, Z. J., Buchmann, A., Zuber, I., Studer, S. T., Saake, A., Rauen, K., Gruber, E., Nitsch, R. M., Höck, C., et al. (2022) · Annals of Neurology · doi:10.1002/ana.26417 · Cited by 31
Huguenard, C. J. C., Cseresznye, A., Evans, J. E., Oberlin, S., Langlois, H., Ferguson, S., Darcey, T. S., Nkiliza, A., Dretsch, M. N., MULLAN, M. J., et al. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00012 · Cited by 28
Plant-based dietary patterns and the risk of dementia: a population-based study
de Crom, T. O. E., Steur, M., Ikram, M. K., Ikram, M. A., & Voortman, T. (2023) · Age and Ageing · doi:10.1093/ageing/afad178 · Cited by 26
Global genetic diversity of human apolipoproteins and effects on cardiovascular disease risk
Zhou, Y., Mägi, R., Milani, L. A., & Lauschke, V. M. (2018) · Journal of Lipid Research · doi:10.1194/jlr.p086710 · Cited by 28
Apolipoprotein E deficiency induces a progressive increase in tissue iron contents with age in mice
Ma, J., Qian, C., Bao, Y., Liu, M., Ma, H., Shen, M., Li, W., Wang, J., Bao, Y.-X., Liu, Y., et al. (2021) · Redox Biology · doi:10.1016/j.redox.2021.101865 · Cited by 27
Lu, Q., Yu, A., Pu, J., Chen, D., Zhong, Y., Bai, D., & Yang, L. (2024) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2024.1375973 · Cited by 27
Orsi, F. A., Lijfering, W. M., van der Laarse, A., Ruhaak, L. R., Rosendaal, F. R., Cannegieter, S. C., & Cobbaert, C. M. (2019) · Clinical Epidemiology · doi:10.2147/clep.s196266 · Cited by 24
APOE – a genetic marker of comorbidity in subjects with morbid obesity
Farup, P. G., Rootwelt, H., & Hestad, K. A. (2020) · BMC Medical Genetics · doi:10.1186/s12881-020-01082-2 · Cited by 25
Magnesium treatment on methylation changes of transmembrane serine protease 2 (TMPRSS2)
Fan, L., Zhu, X., Zheng, Y., Zhang, W., Seidner, D. L., Ness, R. M., Murff, H. J., Yu, C., Huang, X., Shrubsole, M. J., et al. (2021) · Nutrition · doi:10.1016/j.nut.2021.111340 · Cited by 23
APOE and vascular disease: Sequencing and genotyping in general population cohorts
Rasmussen, K. L., Luo, J., Nordestgaard, B. G., Tybjærg-Hansen, A., & Frikke-Schmidt, R. (2023) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2023.117218 · Cited by 22
Self-citationApolipoprotein E Interferes with IAPP Aggregation and Protects Pericytes from IAPP-Induced Toxicity
Gharibyan, A. L., Islam, T., Pettersson, N., Surano, S., Lundgren, J., Johansson, G., Genot, M., Schultz, N., Wennström, M., & Olofsson, A. (2020) · Biomolecules · doi:10.3390/biom10010134 · Cited by 22
Yeh, K.-H., Wan, H., Teng, M., Chou, H., Hsu, L., & Ko, Y. (2022) · Genes · doi:10.3390/genes13081366 · Cited by 22
Apolipoprotein E is required for brain iron homeostasis in mice
Ma, J., Guo, Q., Shen, M., Li, W., Zhong, Q.-X., & Qian, Z. (2023) · Redox Biology · doi:10.1016/j.redox.2023.102779 · Cited by 22
Apolipoprotein and LRP1-Based Peptides as New Therapeutic Tools in Atherosclerosis
Amaro, A. B., Curco, A. S., Garcı́a, E., Julve, J., Rives, J., Benı́tez, S., & Llorente‐Cortés, V. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10163571 · Cited by 23
Liver Health and Dementia in an Italian Older Population: Findings From the Salus in Apulia Study
Lampignano, L., Donghia, R., Griseta, C., Lagravinese, G., Sciarra, S., Zupo, R., Castellana, F., Bortone, I., Guerra, V., Tirelli, S., et al. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.748888 · Cited by 21
Apolipoprotein E Facilitates Amyloid-β Oligomer-Induced Tau Phosphorylation
Hou, T.-T., Han, Y.-D., Cong, L., Liu, C.-C., Liang, X.-Y., Xue, F.-Z., & Du, Y.-F. (2020) · Journal of Alzheimer’s Disease · doi:10.3233/jad-190711 · Cited by 20
Lipids, lipoproteins, and apolipoproteins: Associations with cognition and dementia
Rasmussen, I. J., Luo, J. M., & Frikke‐Schmidt, R. (2024) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2024.118614 · Cited by 21
Establishment of a lipid metabolism disorder model in ApoEb mutant zebrafish
Hu, Y.-X., You, H.-M., Zhu, R.-F., Liang, Y., Li, F., Qin, Y., Zhao, X., Liang, C., & Jing, Q. (2022) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2022.10.008 · Cited by 18
Gene Expression Profiling as a Novel Diagnostic Tool for Neurodegenerative Disorders
Martínez-Iglesias, O. A., Naidoo, V., Carril, J. C., Seoane, S., Cacabelos, N., & Cacabelos, R. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24065746 · Cited by 18
Porzio, A. D., Barrella, V., Gatto, C., Cigliano, L., Spagnuolo, M. S., Crescenzo, R., Romano, I., Mauriello, G., Iossa, S., & Mazzoli, A. (2023) · Journal of Functional Foods · doi:10.1016/j.jff.2023.105805 · Cited by 19
Endogenous Human Proteins Interfering with Amyloid Formation
Gharibyan, A. L., Jayaweera, S. W., Lehmann, M., Anan, I., & Olofsson, A. (2022) · Biomolecules · doi:10.3390/biom12030446 · Cited by 17
Genetic and environmental risk factors for dementia in African adults: A systematic review
Donkor, D. M., Marfo, E., Bockarie, A. S., Tettevi, E. J., Antwi, M. H., Dogah, J., Osei, G. N., & Simpong, D. L. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70220 · Cited by 15
Distribution of APOE gene variations in the Jordanian population: Association with longevity
Khabour, O. F., & Abdelhalim, E. S. (2018) · Journal of King Saud University - Science · doi:10.1016/j.jksus.2018.08.004 · Cited by 14
Association of APOE genotype with lipid profiles and type 2 diabetes mellitus in a Korean population
Seo, J. Y., Youn, B. J., Cheong, H. S., & Shin, H. D. (2021) · Genes & Genomics · doi:10.1007/s13258-021-01095-y · Cited by 14
Genetic underpinnings of cerebral edema in acute brain injury: an opportunity for pathway discovery
Kirsch, E. P., Szejko, N., & Falcone, G. J. (2020) · Neuroscience Letters · doi:10.1016/j.neulet.2020.135046 · Cited by 13
Liu, S., Weng, R., Gu, X., Li, L., & Zhong, Z. (2021) · Journal of Clinical Laboratory Analysis · doi:10.1002/jcla.24061 · Cited by 13
Begcevic Brkovic, I., Zöhrer, B., Scholz, M., Reinicke, M., Dittrich, J., Kamalsada, S., Baber, R., Beutner, F., Teren, A., Engel, C., et al. (2022) · Nutrients · doi:10.3390/nu14122474 · Cited by 13
Kang, S., Lee, J., Ali, D. N., Choi, S. H., Nesbitt, J. J., Min, H.-K. P., Trushina, E. V., & Choi, D. (2024) · Scientific Reports · doi:10.1038/s41598-024-75202-w · Cited by 16
Fernández‐Vega, B., García, M., Olivares, L., Álvarez, L., González‐Fernández, A., Artime, E., Cueto, A. F., Cobo, T., Coca‐Prados, M., Vega, J. A., et al. (2019) · Acta Ophthalmologica · doi:10.1111/aos.14280 · Cited by 12
Alcohol Drinking, Apolipoprotein Polymorphisms and the Risk of Cardiovascular Diseases
Ceci, F. M., Ceccanti, M., Petrella, C., Vitali, M., Messina, M. P., Chaldakov, G. N., Greco, A., Ralli, M., Lucarelli, M., Angeloni, A., et al. (2021) · Current Neurovascular Research · doi:10.2174/1567202618666210406123503 · Cited by 11
APOE Gene Associated with Cholesterol-Related Traits in the Hispanic Population
Lozano, S., Padilla, V., Avila, M. L., Gil, M., Maestre, G. E., Wang, K., & Xu, C. D. (2021) · Genes · doi:10.3390/genes12111768 · Cited by 12
Alcohol Drinking, Apolipoprotein Polymorphisms and the Risk of Cardiovascular Diseases
Ceci, F. M. (2021) · Current Neurovascular Research · doi:10.2174/18755739mte1emjeg3 · Cited by 12
Giannisis, A., Al-Grety, A., Carlsson, H., Howell, J. C., Hu, W. T., Kultima, K., & Nielsen, H. M. (2023) · Alzheimer's Research & Therapy · doi:10.1186/s13195-023-01262-1 · Cited by 11
Bonaterra‐Pastra, A., Benítez, S., Pancorbo, O., Rodríguez‐Luna, D., Vert, C., Rovira, À., Freijo, M. D. M., Tur, S., Martínez-Zabaleta, M., Portela, P. C., et al. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1134399 · Cited by 11
Genetic Variants Associated With Alzheimer Disease in the 22 Arab Countries
Al-Thani, H. F., Ahmad, M. N., Younes, S. N., & Zayed, H. (2021) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000447 · Cited by 11
Li, M., Kwok, M.-K., & Schooling, C. M. (2021) · Nutrients · doi:10.3390/nu13072215 · Cited by 10
Genetic analysis of hsCRP in American Indians: The Strong Heart Family Study
Best, L. G., Balakrishnan, P., Cole, S. A., Haack, K., Kocarnik, J., Pankratz, N., Anderson, M. Z., Franceschini, N., Howard, B. V., Lee, E. T., et al. (2019) · PLoS ONE · doi:10.1371/journal.pone.0223574 · Cited by 9
Lipid-bound ApoE3 self-assemble into elliptical disc-shaped particles
Larsen, A. H., Johansen, N. T., Gajhede, M., Arleth, L., & Midtgaard, S. R. (2020) · Biochimica et Biophysica Acta (BBA) - Biomembranes · doi:10.1016/j.bbamem.2020.183495 · Cited by 8
Features of Lipid Metabolism in Humanized ApoE Knockin Rat Models
Wu, Y., Johnson, G., Zhao, F., Wu, Y., Zhao, G., Brown, A. J., You, S., Zou, M., & Song, P. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22158262 · Cited by 10
Assessing Genetic Overlap and Causality Between Blood Plasma Proteins and Alzheimer’s Disease
Handy, Á., Initiative, O. B. O. T. A. D. N., Lord, J., Green, R., Xu, J., Aarsland, D., Velayudhan, L., Hye, A., Dobson, R., & Proitsi, P. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210462 · Cited by 9
Ittisoponpisan, S., & David, A. (2018) · Journal of the Endocrine Society · doi:10.1210/js.2018-00077 · Cited by 8
Rodríguez, A., Calero, O., Veiga, S., Menacho-Román, M., Arribas, I., Cano, L., García-Ribas, G., & Calero, M. (2025) · Alzheimer's Research & Therapy · doi:10.1186/s13195-025-01811-w · Cited by 8
Wadop, Y. N., Bernal, R., Njamnshi, W. Y., Satizábal, C. L., Beiser, A., Ruiz, A., NJAMNSHI, A. K., Vasan, R. S., Seshadri, S. S., Himali, J. J., et al. (2025) · Journal of Neurology · doi:10.1007/s00415-025-13412-6 · Cited by 10
Nazarian, A., Loika, Y., He, L., Culminskaya, I. V., & Kulminski, A. M. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12540 · Cited by 8
Nkiliza, A., Huguenard, C. J. C., Aldrich, G. J., Ferguson, S., Cseresznye, A., Darcey, T. S., Evans, J. E., Dretsch, M. N., MULLAN, M. J., Crawford, F., et al. (2023) · Neurotrauma Reports · doi:10.1089/neur.2023.0045 · Cited by 8
Human serum proteomics reveals a molecular signature after one night of sleep deprivation
Bjørkum, A. A., Griebel, L., & Birkeland, E. (2024) · SLEEP Advances · doi:10.1093/sleepadvances/zpae042 · Cited by 6
Etuzé, T., Triniac, H., Zheng, Z., Vivien, D., & Dubois, F. (2025) · Neurobiology of Disease · doi:10.1016/j.nbd.2025.106896 · Cited by 8
Nakamura, T., Kawarabayashi, T., Ueda, T., Shimomura, S., Hoshino, M., Itoh, K., Ihara, K., Nakaji, S., Takatama, M., Ikeda, Y., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-220996 · Cited by 8
Apolipoproteins in circulation: At the interface of thrombosis and stroke initiation
Etuzé, T., Vivien, D., & Dubois, F. (2025) · Progress in Lipid Research · doi:10.1016/j.plipres.2025.101343 · Cited by 6
Ding, X., Zhang, H., Zhao, X., Yin, N., Han, S., Jin, X., Li, T., Xing, L., Qi, Z., Zhu, Y., et al. (2025) · MedComm · doi:10.1002/mco2.70392 · Cited by 5
Marron, M. M., Moore, S. C., Wendell, S. G., Boudreau, R. M., Miljkovic, I., Sekikawa, A. M., & Newman, A. B. (2021) · GeroScience · doi:10.1007/s11357-021-00382-6 · Cited by 5
Fukase, T., Dohi, T., Chikata, Y., Takahashi, N., Endo, H., Doi, S., Nishiyama, H., Kato, Y., Okai, I., Iwata, H., et al. (2021) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2021.08.021 · Cited by 5
Hypertriglyceridemia and Alzheimer Disease: Opening the Mind to New Therapeutic Opportunities
Watts, G. F., & Mamo, J. C. L. (2020) · Clinical Chemistry · doi:10.1093/clinchem/hvaa294 · Cited by 5
Sabherwal, S., Föcking, M., English, J. A., Fitzsimons, S., Hryniewiecka, M., Wynne, K. J., Scaife, C., Healy, C., Cannon, M. D., Belton, O., et al. (2019) · Schizophrenia Research · doi:10.1016/j.schres.2019.05.002 · Cited by 5
Maus, A. D., Figdore, D. J., Milosevic, D., Algeciras‐Schimnich, A., & Bornhorst, J. A. (2022) · Clinical Proteomics · doi:10.1186/s12014-022-09379-5 · Cited by 4
Kang, S., Lee, J., Choi, S., Nesbitt, J. J., Min, P. H., Trushina, E., & Choi, D.-S. (2023) · Research Square · doi:10.21203/rs.3.rs-3627637/v1 · Cited by 2
Geng, C.-F., Gao, P.-Y., & Tang, Y. (2025) · Archives of gerontology and geriatrics (Print) · doi:10.1016/j.archger.2025.105845 · Cited by 3
Nakajima, R., Sekiya, M., Furuta, Y., Miyamoto, T., Sato, M., Fukuda, K., Hattori, K., Suehara, Y., Sakata‐Yanagimoto, M., Chiba, S., et al. (2022) · Endocrinology Diabetes and Metabolism Case Reports · doi:10.1530/edm-22-0368 · Cited by 3
Abramova, O. V., Soloveva, K., Zorkina, Y., Gryadunov, D. A., Ikonnikova, A. Y., Fedoseeva, E., Emelyanova, M., Ochneva, A., Andriushchenko, N., Ka, P., et al. (2022) · Genes · doi:10.3390/genes13112174 · Cited by 3
Velilla, T. A., Estruch, E. B., Garrido, J. R., Jiménez, M. R., Sánchez, G. M. V., & Rico, I. V. (2021) · Clínica e Investigación en Arteriosclerosis · doi:10.1016/j.arteri.2021.01.001 · Cited by 2
Li, X.-L., Wang, Q., Jia, G.-D., Yin, H.-J., Wang, Y., Hu, C., Wang, X.-Q., & Yang, Y. (2022) · Age and Ageing · doi:10.1093/ageing/afac119 · Cited by 2
Characterization of APOE Christchurch carriers in 455,306 UK Biobank participantsPreprint
He, K., Khramtsova, E. A., Cabrera‐Socorro, A., Zhang, Y., Li, S., Sarver, B. A. J., Smets, B., Li, Q. S., Muynck, L. D., Parrado, A., et al. (2022) · medRxiv · doi:10.1101/2022.12.05.22283048 · Cited by 2
Sarkar, C., Chen, Y., Nguyen, D. P., Weldemariam, M. M., Morel, Y., Mehrabani-Tabari, A. A., Gorny, N., Pettyjohn-Robin, O., Hegdekar, N., Thapa, S., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.10.675421 · Cited by 2
Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era
Coraglia, F., Cecchetti, G., Rugarli, G., Spinelli, E. G., Ghirelli, A., Pisano, S., Canu, E., Filippi, M., & Agosta, F. (2026) · Alzheimer's Research & Therapy · doi:10.1186/s13195-026-02089-2 · Cited by 1
Kato, J., Okonogi, H., Kanzaki, G., Katsumata, H., Nakada, Y., Sagasaki, M., Komine, K., Ito, K., Saito, T., Matsunaga, A., et al. (2024) · BMC Nephrology · doi:10.1186/s12882-024-03612-z · Cited by 1
Li, Y., Wu, Q., Li, Z., Xiao, Y., & Wei, L. (2025) · International Journal of COPD · doi:10.2147/copd.s512096 · Cited by 1
Zhu, Y., Zhu, H., Zhou, J., Wu, J., Hu, X., Li, C., Cai, H., & Lu, Z. (2025) · Biomedicines · doi:10.3390/biomedicines13092114 · Cited by 1
Rasmussen, K. L., Luo, J., Nielsen, S. P., Nordestgaard, B. G., Tybjærg‐Hansen, A., & Frikke‐Schmidt, R. (2026) · ACR Open Rheumatology · doi:10.1002/acr2.70124 · Cited by 1
Self-citationDlouhá, D., Pompach, P., Horackova, J., Hubacek, J. A., & Blaha, V. (2026) · PROTEOMICS - CLINICAL APPLICATIONS · doi:10.1002/prca.70043 · Cited by 1
Endothelial MerTK impairment promotes cardiac dysfunction in the condition of high fat diet
Huang, H., Liu, S., Yao, J., Bai, X., Jin, Z., Xue, B., Shi, H., & Ding, Z. (2026) · Redox Biology · doi:10.1016/j.redox.2026.104184 · Cited by 1
Klafki, H., Derad, C., Hohberg, M., Asendorf, T., Esselmann, H., Hassan, M. M., Hansen, N., Celano, C. M., Heinemann, S., Kutschka, I., et al. (2026) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.70362 · Cited by 1
Atherosclerosis and dementia - causal aspects and preventive potential
Rasmussen, I. J., Luo, J., Rasmussen, K. L., Kjeldsen, E. W., Schneider, L. S., Sandau, N., Thomassen, J. Q., & Frikke‐Schmidt, R. (2026) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2026.120745 · Cited by 2
Self-citationChen, J., Liou, Y., & Chang, K. (2019) · Cardiology · doi:10.1159/000500825 · Cited by 1
Apolipoprotein ɛ4 Allele and Subjective Cognitive Functioning in Parents of Adults With Disabilities
Song, J., Seltzer, M. M., & Greenberg, J. S. (2020) · The Journals of Gerontology Series B · doi:10.1093/geronb/gbaa061 · Cited by 2
Metadata
- Authors
- Rasmussen, K. L.
- Affiliations
- Herlev Hospital (DK)
- Corresponding author
- Rasmussen, Katrine Laura
- Venue
- Atherosclerosis
- Publisher
- Elsevier BV
- Published
- 2016-12
- Volume
- 255
- Pages
- 145-155
- ISSN
- 0021-9150 (ISSN-L)
- OpenAlex
- W2538539323
- Semantic Scholar
- e7c03178a5a28d575d81f22bf67525d67017350e
- Cited by
- 125
- References
- 129
- Citations by year
- 2026: 14 · 2025: 17 · 2024: 9 · 2023: 14 · 2022: 17 · 2021: 21 · 2020: 11 · 2019: 13 · 2018: 7 · 2017: 2
- FWCI
- 1.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Atherosclerosis (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- apolipoprotein E, APOE polymorphism, APOE ε4, dementia, ischemic heart disease, Alzheimer's disease, LDL receptor, LDL receptor-related protein, triglyceride-rich lipoproteins, lipoprotein metabolism, amyloid-beta clearance, genetic risk factors
- MeSH terms
- Adult, Aged, Aged, 80 and over, Animals, Apolipoproteins E, Brain, Dementia, Female, Humans, Liver, Male, Middle Aged, Phenotype, Polymorphism, Genetic, Protein Conformation, Risk Factors, Structure-Activity Relationship, Biomarkers, Myocardial Ischemia, Risk Assessment, Genetic Predisposition to Disease, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-31, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-31 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
