Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
Open accessAbstract
Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain. APOE polymorphic alleles are the main genetic determinants of Alzheimer disease (AD) risk: individuals carrying the ε4 allele are at increased risk of AD compared with those carrying the more common ε3 allele, whereas the ε2 allele decreases risk. Presence of the APOE ε4 allele is also associated with increased risk of cerebral amyloid angiopathy and age-related cognitive decline during normal ageing. Apo-E-lipoproteins bind to several cell-surface receptors to deliver lipids, and also to hydrophobic amyloid-β (Aβ) peptide, which is thought to initiate toxic events that lead to synaptic dysfunction and neurodegeneration in AD. Apo-E isoforms differentially regulate Aβ aggregation and clearance in the brain, and have distinct functions in regulating brain lipid transport, glucose metabolism, neuronal signalling, neuroinflammation, and mitochondrial function. In this Review, we describe current knowledge on Apo-E in the CNS, with a particular emphasis on the clinical and pathological features associated with carriers of different Apo-E isoforms. We also discuss Aβ-dependent and Aβ-independent mechanisms that link Apo-E4 status with AD risk, and consider how to design effective strategies for AD therapy by targeting Apo-E.
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Equivalent expression of E2 almost cancels out the deleterious effect of the E4 allele.
“and equivalent expression of E2 almost cancels out the deleterious effect of the E4 allele.6,14,15”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [15]
In “APOE ε4 as a strong risk factor for AD” (page unavailable), the review reports an Alzheimer disease odds ratio of 2.6 for ε2/ε4, versus 3.2 for ε3/ε4 and 1 for the ε3/ε3 reference group. That suggests some attenuation, not near-cancellation of ε4-associated risk. The passage compares genotypes; it does not establish equivalent expression of the two isoforms. (LLM, conf=0.87)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredE2/E4 heterozygotes have only double the risk of E3/E3 homozygotes.
“E2/E4 heterozygotes have only double the risk of E3/E3 homozygotes”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [15]
The “APOE ε4 as a strong risk factor for AD” section reports an odds ratio of 2.6 for ε2/ε4 compared with ε3/ε3 among Caucasian subjects. This supports an elevated Alzheimer disease risk, but not the stated figure of only double the risk; the reported measure is also an odds ratio, not a risk ratio. (LLM, conf=0.88)
Experimental — accuracy not yet measuredapoE2 exerts a protective effect against Aβ pathology and AD morbidity.
“Epidemiological evidence and evidence from neuropathological assessment of the impact of apoE isoforms on the brain Aβ load, have suggested that apoE2 exerts a protective effect against Aβ pathology and AD morbidity [3,9,10], while apoE4, in contrast, markedly enhances the disease process [7,8,30].”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [3]
The “APOE and Aβ deposition” section states that APOE ε2 reduces dementia risk, supporting the AD-morbidity part. It does not establish protection against Aβ pathology: in individuals older than 90, ε2 was associated with greater amyloid burden than ε3, and the authors suggest its protective effect against AD might not be associated with Aβ deposition. Page numbers are not available in the supplied copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAn APOE ε2 allele halves AD risk relative to 2 copies of ε3.
“A single copy of the APOE ε4 allele endows a ~3 fold increase in AD risk, and 2 APOE ε4 copies result in a ~15 fold risk increase, while an APOE ε2 allele halves AD risk relative to 2 copies of ε3 (reviewed in [4]).”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [4]
The “APOE ε4 as a strong risk factor for AD” section reports that, among Caucasian subjects, ε2/ε3 carriers had lower AD odds than ε3/ε3 carriers. It gives an odds ratio of 0.6—not a halving of risk—and the citing sentence omits the population qualifier. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTwo APOE ε4 copies result in a ~15 fold risk increase.
“A single copy of the APOE ε4 allele endows a ~3 fold increase in AD risk, and 2 APOE ε4 copies result in a ~15 fold risk increase, while an APOE ε2 allele halves AD risk relative to 2 copies of ε3 (reviewed in [4]).”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [4]
In “APOE ε4 as a strong risk factor for AD,” the review reports an odds ratio of 14.9 for people with two ε4 copies versus ε3/ε3, but that estimate is for Caucasian subjects. The same section reports different estimates for other populations, so the unqualified ~15-fold claim is broader than the source supports. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Recently identified functional siRNA sequences target Apolipoprotein E (ApoE), implicated in several neurodegenerative diseases.
“Recently, we identified functional siRNA sequences targeting Apolipoprotein E (ApoE), implicated in several neurodegenerative diseases, including Alzheimer’s disease and Amyotrophic Lateral Sclerosis26–28 (Ferguson et al., manuscript in preparation).”
From A divalent siRNA chemical scaffold for potent and sustained modulation of gene expression throughout the central nervous system (2019) · cites this paper as [26]
The Introduction (page unavailable) identifies APOE ε4 as a risk factor for late-onset Alzheimer’s disease, and “APOE and other types of dementia” discusses associations with other disorders. That section says APOE genotypes do not seem to influence the risk of amyotrophic lateral sclerosis, so the ALS example is not supported. The siRNA identification is attributed to the citing authors’ own work, not to this source. (LLM, conf=0.88)
Experimental — accuracy not yet measuredEstablished risk factors for AD include advanced age >65 years, female sex, and most importantly, the Apolipoprotein E ε4 allele.
“Established risk factors for AD include advanced age > 65 years, female sex, and most importantly, the Apolipoprotein E (ApoE) ε4 allele [20,23].”
From Clonal Hematopoiesis of Indeterminate Potential as an Emerging Interdisciplinary Risk Factor in Alzheimer’s Disease: Current Evidence and Future Directions (2026) · cites this paper as [23]
The Introduction reports that AD prevalence rises from about 13% after age 65 to 45% after age 85. The section “APOE ε4 as a strong risk factor for AD” calls ε4 the strongest *genetic* risk factor, not the most important risk factor overall. Our copy does not establish female sex as an AD risk factor (searched: female sex, women, female). Page numbers were not available in the indexed passages. (LLM, conf=0.88)
Experimental — accuracy not yet measuredApoE ε4 elevates risk of AD by about three-four-fold, ApoE ε2 is associated with a protective effect, and ApoE ε3 is considered largely neutral.
“While ApoE ε4 eleveates risk of AD by about three–four-fold, ApoE ε2 is associated with a protective effect, and ApoE ε3, as the most prevalent isoform in the general population, is considered largely neutral [23].”
From Clonal Hematopoiesis of Indeterminate Potential as an Emerging Interdisciplinary Risk Factor in Alzheimer’s Disease: Current Evidence and Future Directions (2026) · cites this paper as [23]
The Introduction reports ε3 as the most prevalent allele (77.9%), and the ‘APOE ε4 as a strong risk factor for AD’ section uses ε3/ε3 as the risk reference and reports a protective association for ε2. Its approximately threefold ε4 estimate applies to one-copy carriers among Caucasian subjects (ε3/ε4 OR 3.2); the estimate for ε4/ε4 is OR 14.9. The unqualified three–four-fold figure therefore does not cover all ε4 carriers. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIncreasing apoE lipidation, either through genetic or pharmacological approaches, promotes Aβ clearance and improves cognitive performance in mice.
“In addition, several studies have demonstrated that increasing apoE lipidation, either through genetic or pharmacological approaches, promotes Aβ clearance and improves cognitive performance in mice (27, 44, 45).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [27]
The Aβ metabolism and aggregation section says LXR or RXR stimulation facilitates Aβ clearance, probably by increasing ApoE levels and lipidation. The Regulation of ApoE expression section reports improved cognition or memory after receptor-agonist treatment in amyloid mouse models. The paper does not establish that increased lipidation caused both benefits, and its genetic evidence concerns ABCA1 deficiency worsening clearance and memory deficits in ApoE4 mice, not a genetic approach that increases lipidation and improves performance. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn the central nervous system, neurons are the primary source of extracellular Aβ, generated through amyloidogenic processing of APP, while non-neuronal cells, particularly astrocytes, play important roles in Aβ uptake and clearance.
“In the central nervous system, neurons are the primary source of extracellular Aβ, which is generated through amyloidogenic processing of amyloid precursor protein (APP), while non-neuronal cells, particularly astrocytes, play important roles in Aβ uptake and clearance from the extracellular space (Liu et al., 2013).”
From Isogenic human stem cell models reveal mutation-dependent protective mechanisms of APOE3 Christchurch (2026) · cites this paper as Liu et al., 2013
The Introduction states that Aβ is generated by cleavage of APP. The “Aβ metabolism and aggregation” section discusses Aβ clearance, possible cellular uptake of ApoE–Aβ complexes, and degradation by microglia. It does not identify neurons as the primary source of extracellular Aβ or specifically establish astrocytes as important cells for its uptake and clearance; its statement that astrocytes primarily produce ApoE concerns a different protein. The indexed passages provide section labels but no page numbers. (LLM, conf=0.86)
Experimental — accuracy not yet measuredBesides AD, APOE has been associated with at least eighteen other diseases, including heart disease and high cholesterol.
“Besides AD43, APOE has been associated with at least eighteen other diseases, including heart disease and high cholesterol44.”
From Proteogenomic analysis of human cerebrospinal fluid identifies neurologically relevant regulation and implicates causal proteins for Alzheimer’s disease (2024) · cites this paper as [43]
The Introduction states that ApoE4 is associated with hypercholesterolemia and coronary heart disease, supporting both examples. The paper does not state that APOE is associated with at least eighteen other diseases, so it does not support the claimed count. (LLM, conf=0.89)
Experimental — accuracy not yet measuredApoE4 exists in about 20% of the population but comprises nearly 65% of Alzheimer's disease cases.
“In contrast, ApoE4 exists in 20% of the population; however it comprises nearly 65% of AD cases (Kim et al., 2009;Liu et al., 2013).”
From Human ApoE Isoforms Differentially Modulate Brain Glucose and Ketone Body Metabolism: Implications for Alzheimer's Disease Risk Reduction and Early Intervention (2018) · cites this paper as Liu et al., 2013
The Introduction (page not available) supports the underlying point that APOE ε4 is more common in AD: it reports an allele frequency of 13.7% worldwide and about 40% among patients with AD. It does not give the claimed percentages of people carrying APOE ε4 (20% of the population or nearly 65% of AD cases); allele frequency and carrier prevalence are different measures. The 65% in the Aβ deposition section refers to patients with positive PiB-PET scans, not to all AD cases. (LLM, conf=0.83)
Experimental — accuracy not yet measuredEach ApoE4 allele increases AD risk by 3- to 4-fold while lowering the age at onset by ~8 years.
“Each ApoE4 allele increases AD risk by 3- to 4-fold while lowering the age at onset by ~8 years (Liu et al., 2013).”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Liu et al., 2013
The “APOE ε4 as a strong risk factor for AD” section reports mean onset ages of 84, 76, and 68 years for noncarriers, heterozygotes, and homozygotes—an eight-year difference at each step. It also reports approximately threefold higher odds for one ε4 copy and 14.9-fold higher odds for two copies versus ε3/ε3, but those figures are for Caucasian subjects; the section notes that the association varies across populations. Thus, a universal 3- to 4-fold increase in risk per allele overstates the reported figures. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAPOE4 is the major genetic risk factor for sporadic AD.
“Apolipoprotein E4 ( APOE4 ) is the major genetic risk factor for sporadic AD (258, 368, 612, 681).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [368]
There is strong experimental evidence that the APOE isoforms are major determinants of the amount and quality of amyloid-β peptide (Aβ) and amyloid burden in the brain that develops during aging.
“There is strong experimental evidence that the APOE isoforms are major determinants of the amount and quality of amyloid-β peptide (Aβ) and amyloid burden in the brain that develops during aging.15–17”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [15]
Previous human and animal studies have established the baseline consequences of APOE3 and APOE4 in the absence of amyloid pathology.
“Previous human and animal studies have already established the baseline consequences of APOE3 and APOE4 in the absence of amyloid pathology. 60 , 61 , 62 , 63”
From Apolipoprotein ε4 exacerbates white matter impairment in a mouse model of Aβ amyloidosis by decreasing actively myelinating oligodendrocytes (2025) · cites this paper as [62]
APOE4 is the major genetic risk factor for sporadic, late-onset AD.
“APOE4 is the major genetic risk factor for sporadic, late-onset AD (199, 368, 580, 612).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [368]
The APOE ε4 allele is the strongest genetic risk factor for sporadic Alzheimer's disease.
“For these cases, the strongest genetic risk factor is the apolipoprotein E (ΑPOE) ε4 allele. 2 , 3”
From Deletion of miR-33, a regulator of the ABCA1–APOE pathway, ameliorates neuropathological phenotypes in APP/PS1 mice (2024) · cites this paper as [3]
ApoE is a crucial factor in development of AD.
“ApoE is also a crucial factor in the development of AD (5, 6, 31, 32).”
From The E3 ubiquitin ligase Idol controls brain LDL receptor expression, ApoE clearance, and Aβ amyloidosis (2015) · cites this paper as [32]
Inheritance of apolipoprotein E isoforms is the strongest genetic factor modulating overall risk of sporadic Alzheimer's disease and age of onset.
“In the far more prevalent sporadic AD, the mechanism(s) underlying disturbance of Aβ homeostasis are less obvious, but inheritance of the apolipoprotein (apo) E isoforms has been thus far established by numerous independent studies as the strongest genetic factor modulating overall risk of occurrence of the disease and age of onset (reviewed in [3]).”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [3]
ApoE isoforms produce a differential effect on Aβ clearance and Aβ aggregation and deposition.
“To provide a mechanistic explanation for the variable effect of apoE isoforms on Aβ accumulation and overall disease risk, it has been proposed that they produce a differential effect on Aβ clearance and Aβ aggregation and deposition [3].”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [3]
A single copy of the APOE ε4 allele endows a ~3 fold increase in AD risk.
“A single copy of the APOE ε4 allele endows a ~3 fold increase in AD risk, and 2 APOE ε4 copies result in a ~15 fold risk increase, while an APOE ε2 allele halves AD risk relative to 2 copies of ε3 (reviewed in [4]).”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [4]
Susceptibility to sporadic Alzheimer's disease is foremost modulated by APOE genotype.
“Susceptibility to sporadic AD is foremost modulated by APOE genotype, which also influences the load of Aβ parenchymal plaques and vascular Aβ (VAβ) deposits.”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [4]
ApoE independently influences several key factors that drive pathogenesis of Alzheimer's disease, including β-amyloidosis, tauopathy, and synaptic dysfunction.
“ApoE has been shown to independently influence several key factors that drive pathogenesis of AD, including 𝛃 -amyloidosis, tauopathy, and synaptic dysfunction (1-3).”
From Therapeutic Idol reduction ameliorates amyloidosis and improves cognitive function in APP/PS1 mice (2020) · cites this paper as [2]
APOE4 is the strongest genetic risk factor for late-onset Alzheimer's disease.
“As stated, APOE4 is the strongest genetic risk factor for late-onset AD (5, 27).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [27]
The three common ApoE isoforms differ at two residues: ApoE2 carries Cys112/Cys158, ApoE3 carries Cys112/Arg158, and ApoE4 carries Arg112/Arg158.
“The three isoforms differ at two residues: ApoE2 carries Cys112/Cys158, ApoE3 carries Cys112/Arg158, and ApoE4 carries Arg112/Arg158.”
APOE mainly exists in three allelic variants, APOE2, E3, and E4, which differ in a single amino acid change at position 112 or 158: APOE2 (Cys112, Cys158), APOE3 (Cys112, Arg158), and APOE4 (Arg112, Arg158).
“APOE mainly exists in three allelic variants, APOE2, E3, and E4, which differ in a single amino acid change at position 112 or 158: APOE2 (Cys112, Cys158), APOE3 (Cys112, Arg158), and APOE4 (Arg112, Arg158) (Liu et al., 2013).”
From APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytes (2022) · cites this paper as Liu et al., 2013
The ε4 allele is the strongest common genetic risk factor for sporadic AD.
“The ε4 allele is the strongest common genetic risk factor for sporadic AD”
From Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era (2026) · cites this paper as [6]
The ε4 allele influences disease risk, age at onset, and multiple aspects of the biological phenotype in a dose-dependent manner.
“influencing disease risk, age at onset, and multiple aspects of the biological phenotype in a dose-dependent manner [6, 7].”
From Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era (2026) · cites this paper as [6]
ApoE4 is the strongest genetic risk factor for late-onset AD.
“the ε4 isoform (ApoE4) is the strongest genetic risk factor for the predominant, late-onset form of Alzheimer’s disease (AD).”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Liu et al., 2013
ApoE4 increases risk for Alzheimer's disease.
“ApoE4 increases risk for AD”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [9]
ApoE4 lowers the age of onset of Alzheimer's disease.
“lowers the age of onset [4–14]”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [9]
ApoE4 is less efficient than ApoE3 in transporting brain cholesterol.
“ApoE4 was also suggested to be less efficient than ApoE3 in transporting brain cholesterol [33]”
From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [33]
In humans, the APOE4 and APOE2 alleles are codominant.
“In humans, the APOE4 and APOE2 alleles are codominant”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [15]
The “APOE ε4 as a strong risk factor for AD” section reports an ε2/ε4 genotype and its associated AD risk, but does not say whether the two alleles are codominant. Searches for codominance and expression in heterozygotes found no passage addressing that point; page numbers were not available in our copy. (LLM, conf=0.75)
Experimental — accuracy not yet measuredApoE2 is protective against AD, while ApoE3 is risk-neutral.
“Conversely, ApoE2 is considered to be protective against AD, while ApoE3 is considered risk-neutral”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [13]
The allele frequency of ApoE4 is 15-20%, with some variation in incidence between populations.
“The allele frequency of ApoE4 is 15–20%, with some variation in incidence between populations [13].”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [13]
APOE ε4 allele is potently associated with late AD onset.
“Compelling evidence demonstrates that the ε4 allele is potently associated with late AD onset [318, 443, 451].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [451]
APOEε4 may be the missing link connecting Aβ to tau via actions of αSyn.
“Hence, APOEε4, which has been implicated in AD pathophysiology and pathogenesis by processes mainly linked to Aβ but also associated with Aβ-independent pathways [15], may be the missing link connecting Aβ to tau via actions of αSyn.”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [15]
The apoE3 and apoE4 amino acid sequences differ only at position 112, where apoE4 has an arginine instead of a cysteine.
“The apoE3 and apoE4 amino acid sequences differ only at position 112 where apoE4 has an Arg instead of a Cys.”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [6]
Apolipoprotein E4 is the major genetic risk factor for late-onset familial and sporadic Alzheimer's disease.
“Apolipoprotein (apo) E4, an isoform of the APOE gene in humans, is the major genetic risk factor for late-onset familial and sporadic AD [4–8], which account for most AD cases.”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [6]
Both amyloid-β plaque and neurofibrillary tangle pathologies are exacerbated by the presence of apoE4.
“Both of these pathologies are exacerbated by the presence of apoE4 [4–7, 12].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [6]
ApoE4 increases the risk and decreases the age of onset of Alzheimer's disease in a gene dose dependent manner.
“ApoE4 increases the risk and decreases the age of onset of AD in a gene dose dependent manner [4–11].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [6]
ApoE plays major roles in Alzheimer's disease pathogenesis in both an amyloid-β-dependent and independent manner.
“Overall, it has been demonstrated, both in vivo and in vitro, that apoE plays major roles in AD pathogenesis in both an Aβ-dependent and independent manner, and different cellular sources of apoE4 may contribute in distinct ways to AD pathogenesis [4–8, 12–14, 21, 22].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [6]
APOEε3 is the most common allele in all human populations, present in almost 80% of individuals.
“Of the three alleles, APOEε3 is the most common in all human populations, present in almost 80% of individuals [57].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [57]
APOEε4 is less frequent (~14%) among the general population but drastically increases risk for Alzheimer's disease in a dose-dependent manner.
“APOEε4 is less frequent (~14%) among the general population but drastically increases risk for AD in a dose-dependent manner [54, 57]”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [57]
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Cites
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864 · see citing works
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 · see citing works
Mild Cognitive Impairment: Clinical Characterization and Outcome
Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J., Tangalos, E. G., & Kokmen, E. (1999) · Archives of Neurology · doi:10.1001/archneur.56.3.303 · Cited by 8,980 · see citing works
Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B
Klunk, W. E., Engler, H., Nordberg, A., Wang, Y., Blomqvist, G., Holt, D. P., Bergström, M., Savitcheva, I., Huang, G., Estrada, S., et al. (2004) · Annals of Neurology · doi:10.1002/ana.20009 · Cited by 4,496 · see citing works
Alzheimer's Disease Is a Synaptic Failure
Selkoe, D. J. (2002) · Science · doi:10.1126/science.1074069 · Cited by 4,420 · see citing works
Harold, D., Abraham, R., Hollingworth, P., Sims, R., Gerrish, A., Hamshere, M. L., Pahwa, J. S., Moskvina, V., Dowzell, K., Williams, A., et al. (2009) · Nature Genetics · doi:10.1038/ng.440 · Cited by 3,326 · see citing works
Blennow, K., de Leon, M. J., & Zetterberg, H. (2006) · The Lancet · doi:10.1016/s0140-6736(06)69113-7 · Cited by 3,134 · see citing works
Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease
the European Alzheimer's Disease Initiative Investigators, Lambert, J.-C., Heath, S., Even, G., Campion, D., Sleegers, K., Hiltunen, M., Combarros, O., Zelenika, D., Bullido, M. J., et al. (2009) · Nature Genetics · doi:10.1038/ng.439 · Cited by 2,234 · see citing works
Decreased Clearance of CNS β-Amyloid in Alzheimer’s Disease
Mawuenyega, K. G., Sigurdson, W., Ovod, V., Munsell, L., Kasten, T., Morris, J. C., Yarasheski, K. E., & Bateman, R. J. (2010) · Science · doi:10.1126/science.1197623 · Cited by 2,078 · see citing works
Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model
Roberson, E. D., Scearce-Levie, K., Palop, J. J., Yan, F., Cheng, I. H., Wu, T., Gerstein, H., Yu, G.-Q., & Mucke, L. (2007) · Science · doi:10.1126/science.1141736 · Cited by 1,892 · see citing works
Apolipoprotein E: Far More Than a Lipid Transport Protein
Mahley, R. W., & Rall, S. C. (2000) · Annual Review of Genomics and Human Genetics · doi:10.1146/annurev.genom.1.1.507 · Cited by 1,836 · see citing works
Mild Cognitive Impairment Represents Early-Stage Alzheimer Disease
Morris, J. C., Storandt, M., Miller, J. P., McKeel, D. W., Price, J. L., Rubin, E. H., & Berg, L. (2001) · Archives of Neurology · doi:10.1001/archneur.58.3.397 · Cited by 1,833 · see citing works
Alzheimer Mechanisms and Therapeutic Strategies
Huang, Y., & Mucke, L. (2012) · Cell · doi:10.1016/j.cell.2012.02.040 · Cited by 1,758 · see citing works
CNS synaptogenesis promoted by glia-derived cholesterol
Mauch, D. H., Nägler, K., Schumacher, S., Göritz, C., Müller, E.-C., Otto, A., & Pfrieger, F. W. (2001) · Science · doi:10.1126/science.294.5545.1354 · Cited by 1,711 · see citing works
The role of apolipoprotein E in Alzheimer's disease
Kim, J., Basak, J. M., & Holtzman, D. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.06.026 · Cited by 1,661 · see citing works
Distinct patterns of brain activity in young carriers of the <i>APOE</i> -ε4 allele
Filippini, N., MacIntosh, B. J., Hough, M. G., Goodwin, G. M., Frisoni, G. B., Smith, S. M., Matthews, P. M., Beckmann, C. F., & Mackay, C. E. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0811879106 · Cited by 1,613 · see citing works
Schmechel, D. E., Saunders, A. M., Strittmatter, W. J., Crain, B. J., Hulette, C. M., Joo, S. H., Pericak-Vance, M. A., Goldgaber, D., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.20.9649 · Cited by 1,525 · see citing works
Reiman, E. M., Caselli, R. J., Yun, L. S., Chen, K., Bandy, D., Minoshima, S., Thibodeau, S. N., & Osborne, D. (1996) · New England Journal of Medicine · doi:10.1056/nejm199603213341202 · Cited by 1,366 · see citing works
A PPARγ-LXR-ABCA1 Pathway in Macrophages Is Involved in Cholesterol Efflux and Atherogenesis
Chawla, A., Boisvert, W. A., Lee, C.-H., Laffitte, B. A., Barak, Y., Joseph, S. B., Liao, D., Nagy, L., Edwards, P. A., Curtiss, L. K., et al. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00164-2 · Cited by 1,347 · see citing works
Patterns of Brain Activation in People at Risk for Alzheimer's Disease
Bookheimer, S. Y., Strojwas, M. H., Cohen, M. S., Saunders, A. M., Pericak-Vance, M. A., Mazziotta, J. C., & Small, G. W. (2000) · New England Journal of Medicine · doi:10.1056/nejm200008173430701 · Cited by 1,328 · see citing works
Apolipoprotein E controls cerebrovascular integrity via cyclophilin A
Bell, R. D., Winkler, E. A., Singh, I., Sagare, A. P., Deane, R., Wu, Z., Holtzman, D. M., Betsholtz, C., Armulik, A., Sallstrom, J., et al. (2012) · Nature · doi:10.1038/nature11087 · Cited by 1,293 · see citing works
Synaptic Activity Regulates Interstitial Fluid Amyloid-β Levels In Vivo
Cirrito, J. R., Yamada, K. A., Finn, M. B., Sloviter, R. S., Bales, K. R., May, P. C., Schoepp, D. D., Paul, S. M., Mennerick, S., & Holtzman, D. M. (2005) · Neuron · doi:10.1016/j.neuron.2005.10.028 · Cited by 1,265 · see citing works
Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance
Castellano, J. M., Kim, J., Stewart, F. R., Jiang, H., DeMattos, R. B., Patterson, B. W., Fagan, A. M., Morris, J. C., Mawuenyega, K. G., Cruchaga, C., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002156 · Cited by 1,227 · see citing works
Type 2 Diabetes, APOE Gene, and the Risk for Dementia and Related Pathologies
Peila, R., Rodriguez, B. L., & Launer, L. J. (2002) · Diabetes · doi:10.2337/diabetes.51.4.1256 · Cited by 1,207 · see citing works
Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy
Bu, G. (2009) · Nature Reviews Neuroscience · doi:10.1038/nrn2620 · Cited by 1,168 · see citing works
Self-citationNamba, Y., Tomonaga, M., Kawasaki, H., Otomo, E., & Ikeda, K. (1991) · Brain Research · doi:10.1016/0006-8993(91)91092-f · Cited by 1,157 · see citing works
Apolipoprotein E in sporadic Alzheimer's disease: Allelic variation and receptor interactions
William Rebeck, G., Reiter, J. S., Strickland, D. K., & Hyman, B. T. (1993) · Neuron · doi:10.1016/0896-6273(93)90070-8 · Cited by 1,107 · see citing works
Cerebral amyloid angiopathy. A critical review.
Vinters, H. V. (1987) · Stroke · doi:10.1161/01.str.18.2.311 · Cited by 1,070 · see citing works
ApoE-Directed Therapeutics Rapidly Clear β-Amyloid and Reverse Deficits in AD Mouse Models
Cramer, P. E., Cirrito, J. R., Wesson, D. W., Lee, C. Y. D., Karlo, J. C., Zinn, A. E., Casali, B. T., Restivo, J. L., Goebel, W. D., James, M. J., et al. (2012) · Science · doi:10.1126/science.1217697 · Cited by 1,050 · see citing works
Adult hippocampal neurogenesis and its role in Alzheimer’s disease
Mu, Y., & Gage, F. H. (2011) · Molecular Neurodegeneration · doi:10.1186/1750-1326-6-85 · Cited by 1,021 · see citing works
2012 Alzheimer's disease facts and figures Alzheimer's Association ∗
Thies, W. H., & Bleiler, L. (2012) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2012.02.001 · Cited by 984 · see citing works
Mahley, R. W., Weisgraber, K. H., & Huang, Y. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0600549103 · Cited by 912 · see citing works
Neuronal activity regulates the regional vulnerability to amyloid-β deposition
Bero, A. W., Yan, P., Roh, J. H., Cirrito, J. R., Stewart, F. R., Raichle, M. E., Lee, J.-M., & Holtzman, D. M. (2011) · Nature Neuroscience · doi:10.1038/nn.2801 · Cited by 880 · see citing works
ApoE Promotes the Proteolytic Degradation of Aβ
Jiang, Q., Lee, C. Y. D., Mandrekar, S., Wilkinson, B., Cramer, P., Zelcer, N., Mann, K., Lamb, B., Willson, T. M., Collins, J. L., et al. (2008) · Neuron · doi:10.1016/j.neuron.2008.04.010 · Cited by 876 · see citing works
Apolipoprotein E in Alzheimer’s disease and other neurological disorders
Verghese, P. B., Castellano, J. M., & Holtzman, D. M. (2011) · The Lancet Neurology · doi:10.1016/s1474-4422(10)70325-2 · Cited by 857 · see citing works
Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition
Bales, K. R., Verina, T., Dodel, R. C., Du, Y., Altstiel, L., Bender, M., Hyslop, P., Johnstone, E. M., Little, S. P., Cummins, D. J., et al. (1997) · Nature Genetics · doi:10.1038/ng1197-263 · Cited by 830 · see citing works
<i>APOE</i> predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging
Morris, J. C., Roe, C. M., Xiong, C., Fagan, A. M., Goate, A. M., Holtzman, D. M., & Mintun, M. A. (2010) · Annals of Neurology · doi:10.1002/ana.21843 · Cited by 830 · see citing works
Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer’s disease
Small, G. W., Ercoli, L. M., Silverman, D. H. S., Huang, S.-C., Komo, S., Bookheimer, S. Y., Lavretsky, H., Miller, K., Siddarth, P., Rasgon, N. L., et al. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.090106797 · Cited by 790 · see citing works
Pike, K. E., Savage, G., Villemagne, V. L., Ng, S., Moss, S. A., Maruff, P., Mathis, C. A., Klunk, W. E., Masters, C. L., & Rowe, C. C. (2007) · Brain · doi:10.1093/brain/awm238 · Cited by 789 · see citing works
Reiman, E. M., Chen, K., Liu, X., Bandy, D., Yu, M., Lee, W., Ayutyanont, N., Keppler, J., Reeder, S. A., Langbaum, J. B. S., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0900345106 · Cited by 785 · see citing works
Petersen, R. C. (1995) · JAMA · doi:10.1001/jama.1995.03520400044042 · Cited by 783 · see citing works
apoE isoform–specific disruption of amyloid β peptide clearance from mouse brain
Deane, R., Sagare, A., Hamm, K., Parisi, M., Lane, S., Finn, M. B., Holtzman, D. M., & Zlokovic, B. V. (2008) · Journal of Clinical Investigation · doi:10.1172/jci36663 · Cited by 771 · see citing works
McKeith, I. G. (2004) · Europe PMC (PubMed Central) · Cited by 756 · see citing works
Fleminger, S. (2003) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.74.7.857 · Cited by 719 · see citing works
Weller, R. O., Massey, A., Newman, T. A., Hutchings, M., Kuo, Y.-M., & Roher, A. E. (1998) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)65616-7 · Cited by 679 · see citing works
Small, G. W. (1995) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.1995.03520360056039 · Cited by 604 · see citing works
Barthel, H., Gertz, H., Dresel, S. H. J., Peters, O., Bartenstein, P., Büerger, K., Hiemeyer, F. J., Wittemer‐Rump, S., Seibyl, J. P., Reininger, C. B., et al. (2011) · The Lancet Neurology · doi:10.1016/s1474-4422(11)70077-1 · Cited by 588 · see citing works
Ellis, R. J., Olichney, J. M., Thal, L. J., Mirra, S. S., Morris, J. C., Beekly, D., & Heyman, A. (1996) · Neurology · doi:10.1212/wnl.46.6.1592 · Cited by 561 · see citing works
Isoform-specific binding of apolipoprotein E to beta-amyloid.
LaDu, M. J., Falduto, M. T., Manelli, A. M., Reardon, C. A., Getz, G. S., & Frail, D. E. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)31529-6 · Cited by 540 · see citing works
Longitudinal Modeling of Age-Related Memory Decline and the<i>APOE</i>ε4 Effect
Caselli, R. J., Dueck, A. C., Osborne, D., Sabbagh, M. N., Connor, D. J., Ahern, G. L., Baxter, L. C., Rapcsak, S. Z., Shi, J., Woodruff, B. K., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0809437 · Cited by 528 · see citing works
Reelin, lipoprotein receptors and synaptic plasticity
Herz, J., & Chen, Y. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn2009 · Cited by 524 · see citing works
Apolipoprotein E, Dementia, and Cortical Deposition of β-Amyloid Protein
Polvikoski, T., Sulkava, R., Haltia, M., Kainulainen, K., Vuorio, A., Verkkoniemi, A., Niinistö, L., Halonen, P., & Kontula, K. (1995) · New England Journal of Medicine · doi:10.1056/nejm199511093331902 · Cited by 493 · see citing works
Apolipoprotein E ε4 allele is associated with deposition of amyloid β-protein following head injury
Nicoll, J. A. R., Roberts, G. W., & Graham, D. I. (1995) · Nature Medicine · doi:10.1038/nm0295-135 · Cited by 486 · see citing works
Advances in the early detection of Alzheimer's disease
Nestor, P. J., Scheltens, P., & Hodges, J. R. (2004) · Nature Medicine · doi:10.1038/nrn1433 · Cited by 465 · see citing works
ApoE and Clusterin Cooperatively Suppress Aβ Levels and Deposition
DeMattos, R. B., Cirrito, J. R., Parsadanian, M., May, P. C., O'Dell, M. A., Taylor, J. W., Harmony, J. A. K., Aronow, B. J., Bales, K. R., Paul, S. M., et al. (2004) · Neuron · doi:10.1016/s0896-6273(03)00850-x · Cited by 459 · see citing works
Haan, M. N. (1999) · JAMA · doi:10.1001/jama.282.1.40 · Cited by 457 · see citing works
Cholesterol homeostasis and function in neurons of the central nervous system
Pfrieger, F. W. (2003) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-003-3018-7 · Cited by 453 · see citing works
Chartier‐Harlin, M., Parfitt, M., Legrain, S., Pérez‐Tur, J., Brousseau, T., Evans, A., Berr, C., Vldal, O., Roques, P. K., Gourlet, V., et al. (1994) · Human Molecular Genetics · doi:10.1093/hmg/3.4.569 · Cited by 437 · see citing works
Insulin resistance is associated with the pathology of Alzheimer disease: The Hisayama Study
Matsuzaki, T., Sasaki, K., Tanizaki, Y., Hata, J., Fujimi, K., Matsui, Y., Sekita, A., Suzuki, S. O., Kanba, S., Kiyohara, Y., et al. (2010) · Neurology · doi:10.1212/wnl.0b013e3181eee25f · Cited by 432 · see citing works
Sheline, Y. I., Morris, J. C., Snyder, A. Z., Price, J. L., Yan, Z., D’Angelo, G., Liu, C., Dixit, S., Benzinger, T. L. S., Fagan, A. M., et al. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.3987-10.2010 · Cited by 430 · see citing works
Self-citationBrecht, W. J., Harris, F. M., Chang, S., Tesseur, I., Yu, G.-Q., Xu, Q., Dee Fish, J., Wyss-Coray, T., Buttini, M., Mucke, L., et al. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.4315-03.2004 · Cited by 403 · see citing works
Reiman, E. M., Chen, K., Alexander, G. E., Caselli, R. J., Bandy, D., Osborne, D., Saunders, A. M., & Hardy, J. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0500579102 · Cited by 401 · see citing works
Lynch, J. R., Tang, W., Wang, H., Vitek, M. P., Bennett, E. R., Sullivan, P. M., Warner, D. S., & Laskowitz, D. T. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m306923200 · Cited by 394 · see citing works
A TOMM40 variable-length polymorphism predicts the age of late-onset Alzheimer's disease
Roses, A. D., Lutz, M. W., Amrine‐Madsen, H., Saunders, A. M., Crenshaw, D. G., Sundseth, S. S., Huentelman, M. J., Welsh-Bohmer, K. A., & Reiman, E. M. (2009) · The Pharmacogenomics Journal · doi:10.1038/tpj.2009.69 · Cited by 391 · see citing works
fMRI evidence of compensatory mechanisms in older adults at genetic risk for Alzheimer disease
Bondi, M. W., Houston, W. S., Eyler, L. T., & Brown, G. G. (2005) · Neurology · doi:10.1212/01.wnl.0000150885.00929.7e · Cited by 372 · see citing works
Chen, Y., Durakoglugil, M. S., Xian, X., & Herz, J. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0914984107 · Cited by 368 · see citing works
Biology and pathophysiology of the amyloid precursor protein
Zheng, H., & Koo, E. H. (2011) · Molecular Neurodegeneration · doi:10.1186/1750-1326-6-27 · Cited by 346 · see citing works
Impact of Apolipoprotein E (ApoE) Polymorphism on Brain ApoE Levels
Riddell, D. R., Zhou, H., Atchison, K., Warwick, H. K., Atkinson, P. J., Jefferson, J., Xu, L., Aschmies, S., Kirksey, Y., Hu, Y., et al. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.1972-08.2008 · Cited by 342 · see citing works
Medial temporal lobe atrophy on MRI predicts dementia in patients with mild cognitive impairment
Korf, E. S. C., Wahlund, L., Visser, P. J., & Scheltens, P. (2004) · Neurology · doi:10.1212/01.wnl.0000133114.92694.93 · Cited by 342 · see citing works
Svennerholm, L. T., & Gottfries, C. (1994) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1994.62031039.x · Cited by 327 · see citing works
Andrews-Zwilling, Y., Bien-Ly, N., Xu, Q., Li, G., Bernardo, A., Yoon, S. Y., Zwilling, D., Yan, T. X., Chen, L., & Huang, Y. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.4040-10.2010 · Cited by 326 · see citing works
Apolipoprotein E genotype and cardiovascular disease in the Framingham Heart Study
Lahoz, C., Schaefer, E. J., Cupples, L. A., Wilson, P. W. F., Levy, D. A., Osgood, D. P., Parpos, S., Pedro‐Botet, J., Daly, J. A., & Ordovás, J. M. (2001) · Atherosclerosis · doi:10.1016/s0021-9150(00)00570-0 · Cited by 317 · see citing works
Enhanced Risk for Alzheimer Disease in Persons With Type 2 Diabetes and APOE ε4
Irie, F., Fitzpatrick, A. L., López, O. L., Kuller, L. H., Peila, R., Newman, A. B., & Launer, L. J. (2008) · Archives of Neurology · doi:10.1001/archneurol.2007.29 · Cited by 304 · see citing works
Alzheimer's disease: synapses gone cold
Koffie, R. M., Hyman, B. T., & Spires‐Jones, T. L. (2011) · Molecular Neurodegeneration · doi:10.1186/1750-1326-6-63 · Cited by 302 · see citing works
Apolipoprotein E–dependent accumulation of Alzheimer disease–related lesions begins in middle age
Kok, E., Haikonen, S., Luoto, T., Huhtala, H., Goebeler, S., Haapasalo, H., & Karhunen, P. J. (2009) · Annals of Neurology · doi:10.1002/ana.21696 · Cited by 299 · see citing works
Longitudinal fMRI in elderly reveals loss of hippocampal activation with clinical decline
O’Brien, J. L., O’Keefe, K., LaViolette, P. S., DeLuca, A. N., Blacker, D., Dickerson, B. C., & Sperling, R. A. (2010) · Neurology · doi:10.1212/wnl.0b013e3181e3966e · Cited by 297 · see citing works
Li, G., Bien-Ly, N., Andrews-Zwilling, Y., Xu, Q., Bernardo, A., Ring, K., Halabisky, B., Deng, C., Mahley, R. W., & Huang, Y. (2009) · Cell Stem Cell · doi:10.1016/j.stem.2009.10.015 · Cited by 288 · see citing works
Topology of human apolipoprotein E3 uniquely regulates its diverse biological functions
Chen, J., Li, Q., & Wang, J. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1106420108 · Cited by 283 · see citing works
Pre-Clinical Detection of Alzheimer's Disease Using FDG-PET, with or without Amyloid Imaging
Mosconi, L., Berti, V., Glodzik, L., Pupi, A., Santi, S. D., & de Leon, M. J. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-091504 · Cited by 279 · see citing works
Fryer, J. D., Simmons, K., Parsadanian, M., Bales, K. R., Paul, S. M., Sullivan, P. M., & Holtzman, D. M. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.5170-04.2005 · Cited by 278 · see citing works
Variants at APOE influence risk of deep and lobar intracerebral hemorrhage
Biffi, A., Sonni, A., Anderson, C. D., D, B. M. K. M., Jagiella, J. M., Schmidt, H., Jiménez-Conde, J., Hansen, B. M., Fernández‐Cadenas, I., Cortellini, L., et al. (2010) · Annals of Neurology · doi:10.1002/ana.22134 · Cited by 278 · see citing works
Kim, J., Castellano, J. M., Jiang, H., Basak, J. M., Parsadanian, M., Pham, V., Mason, S. M., Paul, S. M., & Holtzman, D. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.11.013 · Cited by 274 · see citing works
Human<i>APOE</i>Isoform-Dependent Effects on Brain β-Amyloid Levels in PDAPP Transgenic Mice
Bales, K. R., Liu, F., Wu, S., Lin, S., Koger, D., DeLong, C., Hansen, J. C., Sullivan, P. M., & Paul, S. M. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.0887-09.2009 · Cited by 274 · see citing works
Direct and Potent Regulation of γ-Secretase by Its Lipid Microenvironment
Osenkowski, P., Ye, W., Wang, R., Wolfe, M. S., & Selkoe, D. J. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m801925200 · Cited by 269 · see citing works
Liu, Q., Trotter, J., Zhang, J., Peters, M. M., Cheng, H., Bao, J., Han, X., Weeber, E. J., & Bu, G. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.4067-10.2010 · Cited by 268 · see citing works
Self-citationHead (2012) · doi:10.1001/archneurol.2011.845 · Cited by 267 · see citing works
Hippocampal volumes in cognitively normal persons at genetic risk for Alzheimer's disease
Reiman, E. M., Uecker, A., Caselli, R. J., Lewis, S., Bandy, D., De Leon, M. J., De Santi, S., Convit, A., Osborne, D., Weaver, A., et al. (1998) · Annals of Neurology · doi:10.1002/ana.410440226 · Cited by 266 · see citing works
Better Memory and Neural Efficiency in Young Apolipoprotein E 4 Carriers
Mondadori, C. R. A., de Quervain, D. J. ‐., Buchmann, A., Mustovic, H., Wollmer, M. A., Schmidt, C. F., Boesiger, P., Hock, C., Nitsch, R. M., Papassotiropoulos, A., et al. (2006) · Cerebral Cortex · doi:10.1093/cercor/bhl103 · Cited by 265 · see citing works
Greenberg, S. M., Briggs, M. E., Hyman, B. T., Kokoris, G. J., Takis, C. E., Kanter, D. S., Kase, C. S., & Pessin, M. S. (1996) · Stroke · doi:10.1161/01.str.27.8.1333 · Cited by 259 · see citing works
Putcha, D., Brickhouse, M. J., O’Keefe, K., Sullivan, C., Rentz, D. M., Marshall, G. A., Dickerson, B. C., & Sperling, R. A. (2011) · Journal of Neuroscience · doi:10.1523/jneurosci.4740-11.2011 · Cited by 258 · see citing works
Riddell, D. R., Zhou, H., Comery, T. A., Kouranova, E., Lo, C. F., Warwick, H. K., Ring, R. H., Kirksey, Y., Aschmies, S., Xu, J., et al. (2007) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2007.01.011 · Cited by 244 · see citing works
Meta-Analysis of APOE 4 Allele and Outcome after Traumatic Brain Injury
Zhou, W., Xu, D., Peng, X., Zhang, Q., Jia, J., & Crutcher, K. A. (2008) · Journal of Neurotrauma · doi:10.1089/neu.2007.0489 · Cited by 241 · see citing works
Longitudinal changes in cognition and behavior in asymptomatic carriers of the APOE e4 allele
Caselli, R. J., Reiman, E. M., Osborne, D., Hentz, J. G., Baxter, L. C., Hernandez, J. L., & Alexander, G. (2004) · Neurology · doi:10.1212/01.wnl.0000129533.26544.bf · Cited by 231 · see citing works
Clinical predictors of progression to Alzheimer disease in amnestic mild cognitive impairment
Fleisher, A., Sowell, B. B., Taylor, C., Gamst, A. C., Petersen, R. C., & Thal, L. J. (2007) · Neurology · doi:10.1212/01.wnl.0000258542.58725.4c · Cited by 230 · see citing works
Effect of APOE ε4 Status on Intrinsic Network Connectivity in Cognitively Normal Elderly Subjects
Machulda, M. M., Jones, D. T., Vemuri, P., McDade, E., Avula, R. T. V., Przybelski, S. A., Boeve, B. F., Knopman, D. S., Petersen, R. C., & Jack, C. R. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.108 · Cited by 223 · see citing works
ApoE4 Decreases Spine Density and Dendritic Complexity in Cortical Neurons<i>In Vivo</i>
Dumanis, S. B., Tesoriero, J. A., Babus, L. W., Nguyen, M. T., Trotter, J. H., Ladu, M. J., Weeber, E. J., Turner, R. S., Xu, B., Rebeck, G. W., et al. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.4026-09.2009 · Cited by 220 · see citing works
APOE ε4 allele predicts faster cognitive decline in mild Alzheimer disease
Cosentino, S., Scarmeas, N., Helzner, E., Glymour, M. M., Brandt, J., Albert, M., Blacker, D., & Stern, Y. (2008) · Neurology · doi:10.1212/01.wnl.0000304038.37421.cc · Cited by 214 · see citing works
Kanekiyo, T., Zhang, J., Liu, Q., Liu, C.-C., Zhang, L., & Bu, G. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.5491-10.2011 · Cited by 212 · see citing works
Self-citationAβ deposition is associated with enhanced cortical α-synuclein lesions in Lewy body diseases
Pletniková, O., West, N. C., Lee, M. K., Rudow, G. L., Skolasky, R. L., Dawson, T. M., Marsh, L., & Troncoso, J. C. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2004.10.006 · Cited by 209 · see citing works
NSAID use and dementia risk in the Cardiovascular Health Study*: Role of <i>APOE</i> and NSAID type
Szekely, C. A., Breitner, J. C. S., Fitzpatrick, A. L., Rea, T. D., Psaty, B. M., Kuller, L. H., & Zandi, P. P. (2008) · Neurology · doi:10.1212/01.wnl.0000284596.95156.48 · Cited by 204 · see citing works
Fleisher, A. S., Chen, K., Liu, X., Ayutyanont, N., Roontiva, A., Thiyyagura, P., Protas, H., Joshi, A. D., Sabbagh, M., Sadowsky, C. H., et al. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.04.017 · Cited by 202 · see citing works
Plasma Aβ in Alzheimer's disease—up or down?
Zetterberg, H., & Blennow, K. (2006) · The Lancet Neurology · doi:10.1016/s1474-4422(06)70503-8 · Cited by 200 · see citing works
Donkin, J. J., Stukas, S., Hirsch-Reinshagen, V., Namjoshi, D., Wilkinson, A., May, S., Chan, J., Fan, J., Collins, J., & Wellington, C. L. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.108100 · Cited by 200 · see citing works
Kim, J., Jiang, H., Park, S., Eltorai, A. E. M., Stewart, F. R., Yoon, H., Basak, J. M., Finn, M. B., & Holtzman, D. M. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.3773-11.2011 · Cited by 199 · see citing works
Impact of APOE in mild cognitive impairment
Farlow, M. R., He, Y., Tekin, S., Xu, J., Lane, R. M., & Charles, H. C. (2004) · Neurology · doi:10.1212/01.wnl.0000144279.21502.b7 · Cited by 199 · see citing works
Effect of apolipoprotein E on biomarkers of amyloid load and neuronal pathology in Alzheimer disease
Vemuri, P., Wiste, H. J., Weigand, S. D., Knopman, D. S., Shaw, L. M., Trojanowski, J. Q., Aisen, P. S., Weiner, M., Petersen, R. C., Jack, C. R., et al. (2010) · Annals of Neurology · doi:10.1002/ana.21953 · Cited by 195 · see citing works
Biffi, A., Anderson, C. D., Jagiella, J. M., Schmidt, H., D, B. M. K. M., Hansen, B. M., Jiménez-Conde, J., Pires, C. R., Ayres, A. M., Schwab, K. M., et al. (2011) · The Lancet Neurology · doi:10.1016/s1474-4422(11)70148-x · Cited by 194 · see citing works
Ji, Y., Gong, Y., Gan, W., Beach, T., Holtzman, D. M., & Wisniewski, T. (2003) · Neuroscience · doi:10.1016/j.neuroscience.2003.08.007 · Cited by 189 · see citing works
Lynch, J., Morgan, D., Mance, J., Matthew, W. D., & Laskowitz, D. T. (2001) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(00)00459-8 · Cited by 188 · see citing works
APOE ε2 is associated with intact cognition but increased Alzheimer pathology in the oldest old
Berlau, D. J., Corrada, M. M., Head, E., & Kawas, C. H. (2009) · Neurology · doi:10.1212/01.wnl.0000343853.00346.a4 · Cited by 185 · see citing works
Buttini, M., Yu, G.-Q., Shockley, K., Huang, Y., Jones, B., Masliah, E., Mallory, M., Yeo, T., Longo, F. M., & Mucke, L. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-24-10539.2002 · Cited by 183 · see citing works
Oxysterols, cholesterol homeostasis, and Alzheimer disease
Vaya, J., & Schipper, H. M. (2007) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2007.04689.x · Cited by 181 · see citing works
Aβ-independent roles of apolipoprotein E4 in the pathogenesis of Alzheimer's disease
Huang, Y. (2010) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2010.04.004 · Cited by 170 · see citing works
Bien-Ly, N., Gillespie, A. K., Walker, D., Yoon, S. Y., & Huang, Y. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.0033-12.2012 · Cited by 170 · see citing works
Sadowski, M. J., Pankiewicz, J., Scholtzova, H., Mehta, P. D., Prelli, F., Quartermain, D., & Wisniewski, T. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0604011103 · Cited by 167 · see citing works
Smith, G. E., Bohac, D. L., Waring, S. C., Kokmen, E., Tangalos, E. G., Ivnik, R. J., & Petersen, R. C. (1998) · Neurology · doi:10.1212/wnl.50.2.355 · Cited by 167 · see citing works
The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations
Tuminello, E. R., & Han, S. D. (2011) · International Journal of Alzheimer s Disease · doi:10.4061/2011/726197 · Cited by 166 · see citing works
Chen, H.-K., Liu, Z., Meyer-Franke, A., Brodbeck, J., Miranda, R. D., McGuire, J. G., Pleiss, M. A., Ji, Z.-S., Balestra, M. E., Walker, D. W., et al. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.276162 · Cited by 163 · see citing works
Understanding the association of apolipoprotein E4 with Alzheimer disease: clues from its structure
Zhong, N., & Weisgraber, K. H. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.r800009200 · Cited by 159 · see citing works
Kalmijn, S., Feskens, E. J. M., Launer, L. J., & Kromhout, D. (1996) · Stroke · doi:10.1161/01.str.27.12.2230 · Cited by 159 · see citing works
Predictive value of APOE- 4 allele for progression from MCI to AD-type dementia: a meta-analysis
Elias-Sonnenschein, L. S., Viechtbauer, W., Ramakers, I. H. G. B., Verhey, F. R. J., & Visser, P. J. (2011) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.2010.231555 · Cited by 154 · see citing works
Liver X receptor activation restores memory in aged AD mice without reducing amyloid
Vanmierlo, T., Rutten, K., Dederen, J., Bloks, V. W., van Vark-van der Zee, L. C., Kuipers, F., Kiliaan, A., Blokland, A., Sijbrands, E. J. G., Steinbusch, H., et al. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.07.005 · Cited by 154 · see citing works
Ries, M. L., Carlsson, C. M., Rowley, H. A., Sager, M. A., Gleason, C. E., Asthana, S., & Johnson, S. C. (2008) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.2008.01684.x · Cited by 151 · see citing works
Morphologic diagnosis of “vascular dementia” — A critical update
Jellinger, K. A. (2008) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2008.03.006 · Cited by 150 · see citing works
Plasma apolipoprotein E and Alzheimer disease risk: The AIBL study of aging
Gupta, V. B., Laws, S. M., Villemagne, V. L., Ames, D., Bush, A. I., Ellis, K. A., Lui, J. K., Masters, C., Rowe, C. C., Szoeke, C., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e318211c352 · Cited by 149 · see citing works
Caselli, R. J., Reiman, E. M., Locke, D. E. C., Hutton, M. L., Hentz, J. G., Hoffman‐Snyder, C., Woodruff, B. K., Alexander, G. E., & Osborne, D. (2007) · Archives of Neurology · doi:10.1001/archneur.64.9.1306 · Cited by 149 · see citing works
Bales, K. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00143-3 · Cited by 143 · see citing works
Apolipoprotein E ε4 and the pattern of regional brain atrophy in Alzheimer’s disease
Hashimoto, M., Yasuda, M., Tanimukai, S., Matsui, M., Hirono, N., Kazui, H., & Mori, E. (2001) · Neurology · doi:10.1212/wnl.57.8.1461 · Cited by 143 · see citing works
Beffert, U., Cohn, J. S., Petit-Turcotte, C., Tremblay, M., Aumont, N., Ramassamy, C., Davignon, J., & Poirier, J. (1999) · Brain Research · doi:10.1016/s0006-8993(99)01894-6 · Cited by 142 · see citing works
Accelerated age-related cortical thinning in healthy carriers of apolipoprotein E ɛ4
Espeseth, T., Westlye, L. T., Fjell, A. M., Walhovd, K. B., Rootwelt, H., & Reinvang, I. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.10.030 · Cited by 138 · see citing works
Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology.
Wang, C., Wilson, W. A., Moore, S. D., Mace, B. E., Maeda, N., Schmechel, D. E., & Sullivan, P. M. (2005) · Neurobiology of Disease · doi:10.1016/j.nbd.2004.10.013 · Cited by 138 · see citing works
Fitz, N. F., Cronican, A. A., Saleem, M., Fauq, A. H., Chapman, R., Lefterov, I. M., & Koldamova, R. P. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.1937-12.2012 · Cited by 138 · see citing works
McKeith, I. G., Burn, D. J., Ballard, C. G., Collerton, D., Jaros, E., Morris, C. M., McLaren, A., Perry, E. K., Perry, R., Piggott, M. A., et al. (2003) · Seminars in Clinical Neuropsychiatry · doi:10.1053/scnp.2003.50006 · Cited by 134 · see citing works
Frieden, C., & Garai, K. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1207022109 · Cited by 133 · see citing works
<i>APOE</i> ε4 allele is associated with reduced cerebrospinal fluid levels of Aβ42
Prince, J. A., Zetterberg, H., Andreasen, N., Marcusson, J., & Blennow, K. (2004) · Neurology · doi:10.1212/01.wnl.0000128088.08695.05 · Cited by 128 · see citing works
Harrington, C. R., Louwagie, J., Rossau, R., Vanmechelen, E., Perry, R. H., Perry, E. K., Xuereb, J. H., Roth, M., & Wischik, C. M. (1994) · PubMed Central · doi:10.25405/ncl.34087548 · Cited by 127 · see citing works
Rapp, A., Gmeiner, B. M. K., & Hüttinger, M. (2005) · Biochimie · doi:10.1016/j.biochi.2005.10.007 · Cited by 127 · see citing works
APOE-ε4 is associated with memory decline in cognitively impaired elderly
Dik, M. G., Jonker, C., Bouter, L. M., Geerlings, M. I., van Kamp, G. J., & Deeg, D. J. H. (2000) · Neurology · doi:10.1212/wnl.54.7.1492 · Cited by 126 · see citing works
Farrer, L. A. (1997) · JAMA · doi:10.1001/jama.1997.03550160069041 · Cited by 124 · see citing works
LaDu, M. J., Shah, J. A., Reardon, C. A., Getz, G. S., Bu, G., Hu, J., Guo, L., & Van Eldik, L. J. (2001) · Neurochemistry International · doi:10.1016/s0197-0186(01)00050-x · Cited by 118 · see citing works
Self-citationReduced levels of human apoE4 protein in an animal model of cognitive impairment
Sullivan, P. M., Han, B., Liu, F., Mace, B. E., Ervin, J. F., Wu, S., Koger, D., Paul, S., & Bales, K. R. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.05.011 · Cited by 113 · see citing works
APOE and cognitive decline in preclinical Alzheimer disease and non-demented aging
Bunce, D. J., Fratiglioni, L., Small, B. J., Winblad, B. G., & Bäckman, L. (2004) · Neurology · doi:10.1212/01.wnl.0000137041.86153.42 · Cited by 111 · see citing works
ApoE is required for maintenance of the dentate gyrus neural progenitor pool
Yang, C.-P., Gilley, J. A., Zhang, G., & Kernie, S. G. (2011) · Development · doi:10.1242/dev.065540 · Cited by 109 · see citing works
Increased Expression of Neuronal Apolipoprotein E in Human Brain With Cerebral Infarction
Aoki, K., Uchihara, T., Sanjo, N., Nakamura, A., Ikeda, K., Tsuchiya, K., & Wakayama, Y. (2003) · Stroke · doi:10.1161/01.str.0000064320.73388.c6 · Cited by 108 · see citing works
A large study reveals no association between APOE and Parkinson's disease
Federoff, M., Jimenez‐Rolando, B., Nalls, M. A., & Singleton, A. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.02.002 · Cited by 106 · see citing works
Cruchaga, C. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.155 · Cited by 104 · see citing works
Keene, C. D., Cudaback, E., Li, X., Montine, K. S., & Montine, T. J. (2011) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2011.08.002 · Cited by 103 · see citing works
Longitudinal modeling of frontal cognition in APOE ε4 homozygotes, heterozygotes, and noncarriers
Caselli, R. J., Dueck, A. C., Locke, D. E. C., Hoffman‐Snyder, C. R., Woodruff, B. K., Rapcsak, S. Z., & Reiman, E. M. (2011) · Neurology · doi:10.1212/wnl.0b013e3182167147 · Cited by 99 · see citing works
Li, F., Sempowski, G. D., McKenna, S., Laskowitz, D. T., Colton, C. A., & Vitek, M. P. (2006) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.106.103671 · Cited by 97 · see citing works
Altered cholesterol metabolism in human apolipoprotein E4 knock-in mice
Hamanaka, H. (2000) · Human Molecular Genetics · doi:10.1093/hmg/9.3.353 · Cited by 96 · see citing works
Clinical‐neuroimaging characteristics of dysexecutive mild cognitive impairment
Pa, J., Boxer, A. L., Chao, L. L., Gazzaley, A. H., Freeman, K. M., Kramer, J. H., Miller, B. L., Weiner, M. W., Neuhaus, J. M., & Johnson, J. K. (2009) · Annals of Neurology · doi:10.1002/ana.21591 · Cited by 96 · see citing works
APOE ε4 differentially influences change in memory performance depending on age. The SMART-MR study
Jochemsen, H. M., Muller, M., van der Graaf, Y., & Geerlings, M. I. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.07.016 · Cited by 92 · see citing works
Measurement of Apolipoprotein E (apoE) in Cerebrospinal Fluid
Hesse, C., Larsson, H. E., Fredman, P., Minthon, L., Andreasen, N., Davidsson, P., & Blennow, K. (2000) · Neurochemical Research · doi:10.1023/a:1007516210548 · Cited by 89 · see citing works
Yin, Y.-W., Li, J.-C., Wang, J.-Z., Li, B.-H., Pi, Y., Yang, Q.-W., Fang, C.-Q., Gao, C.-Y., & Zhang, L.-L. (2012) · Neuroscience Letters · doi:10.1016/j.neulet.2012.02.031 · Cited by 84 · see citing works
Apolipoprotein E levels in cerebrospinal fluid and the effects of ABCA1polymorphisms
Wahrle, S. E., Shah, A. R., Fagan, A. M., Smemo, S., Kauwe, J. S., Grupe, A., Hinrichs, A., Mayo, K., Jiang, H., Thal, L. J., et al. (2007) · Molecular Neurodegeneration · doi:10.1186/1750-1326-2-7 · Cited by 84 · see citing works
Li, F., Fowler, K. A., Neil, J. E., Colton, C. A., & Vitek, M. P. (2010) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.110.167882 · Cited by 84 · see citing works
Distinct patterns of brain activity in young carriers of the APOE e4 allele
Filippini, N., MacIntosh, B., Hough, M., Goodwin, G. M., Frisoni, G. B., Ebmeier, K. P., Smith, S. M., Matthews, P. M., Beckmann, C. F., & Mackay, C. (2009) · NeuroImage · doi:10.1016/s1053-8119(09)71381-3 · Cited by 81 · see citing works
Buttini, M., Masliah, E., Yu, G.-Q., Palop, J. J., Chang, S., Bernardo, A., Lin, C., Wyss-Coray, T., Huang, Y., & Mucke, L. (2010) · The American Journal of Pathology · doi:10.2353/ajpath.2010.090973 · Cited by 80 · see citing works
How can elderly apolipoprotein E ε4 carriers remain free from dementia?
Ferrari, C., Xu, W., Wang, H., Winblad, B. G., Sorbi, S., Qiu, C., & Fratiglioni, L. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.03.003 · Cited by 78 · see citing works
Presence of ApoE ε4 Allele Associated with Thinner Frontal Cortex in Middle Age
Fennema‐Notestine, C., Panizzon, M. S., Thompson, W., Chen, C., Eyler, L. T., Fischl, B. R., Franz, C. E., Grant, M. D., Jak, A. J., Jernigan, T. L., et al. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-0002 · Cited by 76 · see citing works
Aono, M., Bennett, E. R., Kim, K. S., Lynch, J., Myers, J., Pearlstein, R. D., Warner, D. S., & Laskowitz, D. T. (2003) · Neuroscience · doi:10.1016/s0306-4522(02)00709-1 · Cited by 72 · see citing works
New Perspectives on Amyloid-β Dynamics After Acute Brain Injury
Magnoni, S., & Brody, D. L. (2010) · Archives of Neurology · doi:10.1001/archneurol.2010.214 · Cited by 72 · see citing works
Whitehair, D. C., Sherzai, A., Emond, J. A., Raman, R., Aisen, P. S. S., Petersen, R. C., Fleisher, A., & Study, A. D. C. (2010) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2009.12.003 · Cited by 70 · see citing works
Sen, A., Alkon, D. L., & Nelson, T. J. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.312710 · Cited by 69 · see citing works
Klein, R. C., Mace, B. E., Moore, S. D., & Sullivan, P. M. (2010) · Neuroscience · doi:10.1016/j.neuroscience.2010.10.027 · Cited by 67 · see citing works
ApoE genotype is a risk factor in nonpresenilin early-onset alzheimer's disease families
Houlden, H., Crook, R., Backhovens, H., Prihar, G., Baker, M. C., Hutton, M., Rossor, M. N., Martin, J. J., Broeckhoven, C. V., & Hardy, J. (1998) · American Journal of Medical Genetics · doi:10.1002/(sici)1096-8628(19980207)81:1 · Cited by 64 · see citing works
Decreased Cognition in Children with Risk Factors for Alzheimer's Disease
Bloss, C. S., Delis, D. C., Salmon, D. P., & Bondi, M. W. (2008) · Biological Psychiatry · doi:10.1016/j.biopsych.2008.07.004 · Cited by 61 · see citing works
Lack of association of APOE and tau polymorphisms with dementia in Parkinson’s disease
Ezquerra, M., Campdelacreu, J., Gaig, C., Compta, Y., Muñoz, E., Martı́, M. J., Valldeoriola, F., & TOLOSA, E. S. (2008) · Neuroscience Letters · doi:10.1016/j.neulet.2008.10.018 · Cited by 60 · see citing works
The association between APOE and dementia does not seem to be mediated by vascular factors
Prince, M. J., Lovestone, S., Cervilla, J. A., Joels, S., Powell, J. F., Russ, C., & MANN, A. H. (2000) · Neurology · doi:10.1212/wnl.54.2.397 · Cited by 60 · see citing works
Bender, A. R., & Raz, N. (2012) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2011.12.025 · Cited by 56 · see citing works
Plasma Signaling Proteins in Persons at Genetic Risk for Alzheimer Disease
Ringman, J. M., Elashoff, D. A., Geschwind, D. H., Welsh, B. T., Gylys, K. H., Lee, C., Cummings, J. L., & Cole, G. M. (2012) · Archives of Neurology · doi:10.1001/archneurol.2012.277 · Cited by 55 · see citing works
Ramakers, I. H. G. B., Visser, P. J., Aalten, P., Bekers, O., Sleegers, K., Broeckhoven, C. V., Jolles, J., & Verhey, F. R. J. (2008) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000144072 · Cited by 52 · see citing works
Meta-analysis of APOE genotype and subarachnoid hemorrhage
Lanterna, L. A., Ruigrok, Y. M., Alexander, S. A., Tang, J., Biroli, F., Dunn, L., & Poon, W. S. (2007) · Neurology · doi:10.1212/01.wnl.0000267640.03300.6b · Cited by 52 · see citing works
The Association of APOE Genotype with Cognitive Function in Persons Aged 35 Years or Older
Izaks, G. J., Gansevoort, R. T., van der Knaap, A. M., Navis, G. J., Dullaart, R. P. F., & Slaets, J. P. J. (2011) · PLoS ONE · doi:10.1371/journal.pone.0027415 · Cited by 41 · see citing works
Lin, A., Laird, A. R., Fox, P. T., & Gao, J. (2011) · Neurology Research International · doi:10.1155/2012/907409 · Cited by 34 · see citing works
Apolipoprotein epsilon 3 alleles are associated with indicators of neuronal resilience
Aboud, O., Mrak, R. E., Boop, F. A., & Griffin, S. T. (2012) · BMC Medicine · doi:10.1186/1741-7015-10-35 · Cited by 34 · see citing works
Apolipoprotein E genotypes do not influence the age of onset in Huntington's disease
Carsten Saft, C. (2004) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2003.022756 · Cited by 32 · see citing works
The APOE Gene Locus in Frontotemporal Dementia and Primary Progressive Aphasia
Seripa, D., Bizzarro, A., Panza, F., et al. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.90 · Cited by 31 · see citing works
Mann, Brown, Owen, Baba, & Iwatsubo, T. (1998) · Neuropathology and Applied Neurobiology · doi:10.1046/j.1365-2990.1998.00112.x · Cited by 30 · see citing works
Does apolipoprotein E genotype modify the clinical expression of ALS?
Jawaid, A., Poon, M., Strutt, A. M., Rice, L., McDowell, E. J., Salamone, A. R., Qureshi, S. U., Simpson, E. P., Appel, S. H., York, M. K., et al. (2010) · European Journal of Neurology · doi:10.1111/j.1468-1331.2010.03225.x · Cited by 24 · see citing works
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Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission
Livingston, G., Huntley, J., Liu, K. Y., Costafreda, S. G., Selbæk, G., Alladi, S., Ames, D., Banerjee, S., Burns, A., Brayne, C., et al. (2024) · The Lancet · doi:10.1016/s0140-6736(24)01296-0 · Cited by 3,860 · see citing works
Ageing as a risk factor for neurodegenerative disease
Hou, Y., Dan, X., Babbar, M., Wei, Y., Hasselbalch, S. G., Croteau, D. L., & Bohr, V. A. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-019-0244-7 · Cited by 3,310 · see citing works
Comprehensive Review on Alzheimer’s Disease: Causes and Treatment
Breijyeh, Z., & Karaman, R. (2020) · Molecules · doi:10.3390/molecules25245789 · Cited by 2,789 · see citing works
Jansen, I. E., Savage, J. E., Watanabe, K., Bryois, J., Williams, D. M., Steinberg, S., Sealock, J., Karlsson, I. K., Hägg, S., Athanasiu, L., et al. (2019) · Nature Genetics · doi:10.1038/s41588-018-0311-9 · Cited by 2,277 · see citing works
Inflammation as a central mechanism in Alzheimer's disease
Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T. (2018) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.06.014 · Cited by 2,253 · see citing works
Blood-Brain Barrier: From Physiology to Disease and Back
Sweeney, M. D., Zhao, Z., Montagne, A., Nelson, A. R., & Zlokovic, B. V. (2019) · Physiological Reviews · doi:10.1152/physrev.00050.2017 · Cited by 2,294 · see citing works
The Amyloid-β Pathway in Alzheimer’s Disease
Hampel, H., Hardy, J., Blennow, K., Chen, C., Perry, G., Kim, S. H., Villemagne, V. L., Aisen, P., Vendruscolo, M., Iwatsubo, T., et al. (2021) · Molecular Psychiatry · doi:10.1038/s41380-021-01249-0 · Cited by 1,952 · see citing works
The cholinergic system in the pathophysiology and treatment of Alzheimer’s disease
Hampel, H., Mesulam, M.-M., Cuello, A. C., Farlow, M. R., Giacobini, E., Grossberg, G. T., Khachaturian, A. S., Vergallo, A., Cavedo, E., Snyder, P. J., et al. (2018) · Brain · doi:10.1093/brain/awy132 · Cited by 1,918 · see citing works
Clearance systems in the brain—implications for Alzheimer disease
Tarasoff-Conway, J. M., Carare, R. O., Osorio, R. S., Glodzik, L., Butler, T., Fieremans, E., Axel, L., Rusinek, H., Nicholson, C., Zlokovic, B. V., et al. (2015) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.119 · Cited by 1,678 · see citing works
Role of neuroinflammation in neurodegeneration development
Zhang, W., Xiao, D., Mao, Q., & Xia, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01486-5 · Cited by 1,668 · see citing works
“A single amino acid difference between APOE3 and APOE4 leads to the changing of protein conformation which affects the binding of APOE with its receptors, lipids, and Aβ.(167) Carrying one APOE4 allele increases the risk of AD by 3–4 times, and carrying two alleles increases the risk by 9–15 times.”
BackgroundApolipoprotein E and Alzheimer disease: pathobiology and targeting strategies
Yamazaki, Y., Zhao, N., Caulfield, T. R., Liu, C.-C., & Bu, G. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-019-0228-7 · Cited by 1,425 · see citing works
Self-citationDisease-Associated Microglia: A Universal Immune Sensor of Neurodegeneration
Deczkowska, A., Keren-Shaul, H., Weiner, A., Colonna, M., Schwartz, M., & Amit, I. (2018) · Cell · doi:10.1016/j.cell.2018.05.003 · Cited by 1,474 · see citing works
Single App knock-in mouse models of Alzheimer’s disease
Saito, T., Matsuba, Y., Mihira, N., Takano, J., Nilsson, P., Itohara, S., Iwata, N., & Saido, T. C. (2014) · Nature Neuroscience · doi:10.1038/nn.3697 · Cited by 1,447 · see citing works
Lin, Y.-T., Seo, J., Gao, F., Feldman, H. M., Wen, H.-L., Penney, J., Cam, H. P., Gjoneska, E., Raja, W. K., Cheng, J., et al. (2018) · Neuron · doi:10.1016/j.neuron.2018.05.008 · Cited by 1,125 · see citing works
Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
Guo, T., Zhang, D., Zeng, Y., Huang, T. Y., Xu, H., & Zhao, Y. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00391-7 · Cited by 994 · see citing works
Self-citationAlzheimer’s Disease Risk Gene CD33 Inhibits Microglial Uptake of Amyloid Beta
Griciuc, A., Serrano-Pozo, A., Parrado, A. R., Lesinski, A. N., Asselin, C. N., Mullin, K., Hooli, B., Choi, S. H., Hyman, B. T., & Tanzi, R. E. (2013) · Neuron · doi:10.1016/j.neuron.2013.04.014 · Cited by 1,004 · see citing works
A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease
Panza, F., Lozupone, M., Logroscino, G., & Imbimbo, B. P. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-018-0116-6 · Cited by 965 · see citing works
β-Amyloid accumulation in the human brain after one night of sleep deprivation
Shokri-Kojori, E., Wang, G.-J., Wiers, C. E., Demiral, S. B., Guo, M., Kim, S. W., Lindgren, E., Ramirez, V., Zehra, A., Freeman, C., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1721694115 · Cited by 893 · see citing works
ApoE in Alzheimer’s disease: pathophysiology and therapeutic strategies
Raulin, A.-C., Doss, S. V., Trottier, Z. A., Ikezu, T. C., Bu, G., & Liu, C.-C. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00574-4 · Cited by 756 · see citing works
Self-citationFriedman, B. A., Srinivasan, K., Ayalon, G., Meilandt, W. J., Lin, H., Huntley, M. A., Cao, Y., Lee, S.-H., Haddick, P. C. G., Ngu, H., et al. (2018) · Cell Reports · doi:10.1016/j.celrep.2017.12.066 · Cited by 662 · see citing works
History and progress of hypotheses and clinical trials for Alzheimer’s disease
Liu, P.-P., Xie, Y., Meng, X.-Y., & Kang, J.-S. (2019) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-019-0063-8 · Cited by 723 · see citing works
Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis
Neu, S. C., Pa, J., Kukull, W., Beekly, D., Kuzma, A., Gangadharan, P., Wang, L.-S., Romero, K., Arneric, S. P., Redolfi, A., et al. (2017) · JAMA Neurology · doi:10.1001/jamaneurol.2017.2188 · Cited by 674 · see citing works
Age, APOE and sex: triad of risk of Alzheimer’s disease.
Riedel, B. C., Thompson, P. M., & Brinton, R. D. (2016) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2016.03.012 · Cited by 627 · see citing works
Apolipoprotein E Is a Ligand for Triggering Receptor Expressed on Myeloid Cells 2 (TREM2)
Atagi, Y., Liu, C.-C., Painter, M. M., Chen, X.-F., Verbeeck, C., Zheng, H., Li, X., Rademakers, R., Kang, S. S., Xu, H., et al. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.679043 · Cited by 587 · see citing works
Self-citationNagpal, R., Neth, B. J., Wang, S., Craft, S., & Yadav, H. (2019) · EBioMedicine · doi:10.1016/j.ebiom.2019.08.032 · Cited by 653 · see citing works
ApoE and Aβ in Alzheimer’s Disease: Accidental Encounters or Partners?
Kanekiyo, T., Xu, H., & Bu, G. (2014) · Neuron · doi:10.1016/j.neuron.2014.01.045 · Cited by 608 · see citing works
Self-citationAlzheimer's Disease: Treatment Strategies and Their Limitations.
Passeri, E., Elkhoury, K., Morsink, M., Broersen, K., Linder, M., Tamayol, A., Malaplate, C., Yen, F. T., & Arab-Tehrany, E. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232213954 · Cited by 592 · see citing works
“The ε4 has been linked to changes in neurotoxic and neuroprotective mechanisms, including Aβ peptide metabolism, aggregation, toxicity, tauopathy, synaptic plasticity, lipid transport, vascular integrity, and neuroinflammation [96].”
BackgroundAmyloid-β-independent regulators of tau pathology in Alzheimer disease
van der Kant, R., Goldstein, L. S. B., & Ossenkoppele, R. (2020) · Nature reviews. Neuroscience · doi:10.1038/s41583-019-0240-3 · Cited by 580 · see citing works
Blood–Brain Barrier Dysfunction as a Cause and Consequence of Alzheimer's Disease
Erickson, M. A., & Banks, W. A. (2013) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2013.135 · Cited by 572 · see citing works
Drug treatments in Alzheimer’s disease
Briggs, R., Kennelly, S. P., & O’Neill, D. (2016) · Clinical Medicine · doi:10.7861/clinmedicine.16-3-247 · Cited by 571 · see citing works
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 · see citing works
Central Nervous System Lipoproteins: ApoE and Regulation of Cholesterol Metabolism
Mahley, R. W. (2016) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.116.307023 · Cited by 516 · see citing works
The probabilistic model of Alzheimer disease: the amyloid hypothesis revised
Frisoni, G. B., Altomare, D., Thal, D. R., Ribaldi, F., van der Kant, R., Ossenkoppele, R., Blennow, K., Cummings, J., van Duijn, C., Nilsson, P. M., et al. (2022) · Nature Reviews Neuroscience · doi:10.1038/s41583-021-00533-w · Cited by 513 · see citing works
ApoE4 Accelerates Early Seeding of Amyloid Pathology
Liu, C.-C., Zhao, N., Fu, Y., Wang, N., Linares, C., Tsai, C.-W., & Bu, G. (2017) · Neuron · doi:10.1016/j.neuron.2017.11.013 · Cited by 451 · see citing works
Self-citationModeling Alzheimer’s disease with iPSC-derived brain cells
Penney, J., Ralvenius, W. T., & Tsai, L.-H. (2020) · Molecular Psychiatry · doi:10.1038/s41380-019-0468-3 · Cited by 471 · see citing works
Alcohol use and dementia: a systematic scoping review
Rehm, J., Hasan, O. S. M., Black, S. E., Shield, K. D., & Schwarzinger, M. (2019) · Alzheimer's Research & Therapy · doi:10.1186/s13195-018-0453-0 · Cited by 450 · see citing works
Lee, C. Y. D., Daggett, A., Gu, X., Jiang, L.-L., Langfelder, P., Li, X., Wang, N., Zhao, Y., Park, C. S., Cooper, Y., et al. (2018) · Neuron · doi:10.1016/j.neuron.2018.02.002 · Cited by 396 · see citing works
Self-citationEstrogens, Neuroinflammation, and Neurodegeneration
Villa, A., Vegeto, E., Poletti, A., & Maggi, A. (2016) · Endocrine Reviews · doi:10.1210/er.2016-1007 · Cited by 423 · see citing works
Wang, C., Najm, R., Xu, Q., Jeong, D.-E., Walker, D., Balestra, M. E., Yoon, S. Y., Yuan, H., Li, G., Miller, Z. A., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0004-z · Cited by 428 · see citing works
Slot, R. E. R., Sikkes, S. A. M., Berkhof, J., Brodaty, H., Buckley, R., Cavedo, E., Dardiotis, E., Guillo‐Benarous, F., Hampel, H., Kochan, N. A., et al. (2019) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.10.003 · Cited by 428 · see citing works
Modifiable pathways in Alzheimer’s disease: Mendelian randomisation analysis
Larsson, S. C., Traylor, M., Malik, R., Dichgans, M., Burgess, S., & Markus, H. S. (2017) · BMJ · doi:10.1136/bmj.j5375 · Cited by 382 · see citing works
α-synuclein in the pathophysiology of Alzheimer’s disease
Twohig, D., & Nielsen, H. M. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0320-x · Cited by 374 · see citing works
Apolipoprotein E in Alzheimer's Disease: An Update
Yu, J.-T., Tan, L., & Hardy, J. (2014) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-071013-014300 · Cited by 394 · see citing works
Do glia drive synaptic and cognitive impairment in disease?
Chung, W.-S., Welsh, C. A., Barres, B. A., & Stevens, B. (2015) · Nature Neuroscience · doi:10.1038/nn.4142 · Cited by 385 · see citing works
ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism
Qi, G., Mi, Y., Shi, X., Gu, H., Brinton, R. D., & Yin, F. (2021) · Cell Reports · doi:10.1016/j.celrep.2020.108572 · Cited by 379 · see citing works
Chakrabarty, P., Li, A., Ceballos-Diaz, C., Eddy, J. A., Funk, C. C., Moore, B., DiNunno, N., Rosario, A. M., Cruz, P. E., Verbeeck, C., et al. (2015) · Neuron · doi:10.1016/j.neuron.2014.11.020 · Cited by 354 · see citing works
Sex-Specific Association of Apolipoprotein E With Cerebrospinal Fluid Levels of Tau
Hohman, T. J., Dumitrescu, L., Barnes, L. L., Thambisetty, M., Beecham, G., Kunkle, B., Gifford, K. A., Bush, W. S., Chibnik, L. B., Mukherjee, S., et al. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.0821 · Cited by 340 · see citing works
van der Kant, R., Langness, V. F., Herrera, C. M., Williams, D. A., Fong, L. K., Leestemaker, Y., Steenvoorden, E., Rynearson, K. D., Brouwers, J. F., Helms, J. B., et al. (2019) · Cell Stem Cell · doi:10.1016/j.stem.2018.12.013 · Cited by 350 · see citing works
Immune Signaling in Neurodegeneration
Hammond, T. R., Marsh, S. E., & Stevens, B. (2019) · Immunity · doi:10.1016/j.immuni.2019.03.016 · Cited by 336 · see citing works
Continuous evolution of base editors with expanded target compatibility and improved activity
Thuronyi, B. W., Koblan, L. W., Levy, J. M., Yeh, W.-H., Zheng, C., Newby, G. A., Wilson, C., Bhaumik, M., Shubina-Oleinik, O., Holt, J. R., et al. (2019) · Nature Biotechnology · doi:10.1038/s41587-019-0193-0 · Cited by 347 · see citing works
Mechanisms of Molecular Mimicry Involving the Microbiota in Neurodegeneration
Friedland, R. P. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-142841 · Cited by 338 · see citing works
<i>APOE</i> ε4: The most prevalent yet understudied risk factor for Alzheimer's disease
Michaelson, D. M. (2014) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.06.015 · Cited by 331 · see citing works
Michailidis, M., Moraitou, D., Tata, D. A., Kalinderi, K., Papamitsou, T., & Papaliagkas, V. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23052687 · Cited by 330 · see citing works
Lipid accumulation induced by APOE4 impairs microglial surveillance of neuronal-network activity
Victor, M. B., Leary, N., Luna, X., Meharena, H. S., Scannail, A. N., Bozzelli, P. L., Samaan, G., Murdock, M. H., von Maydell, D., Effenberger, A. H., et al. (2022) · Cell Stem Cell · doi:10.1016/j.stem.2022.07.005 · Cited by 316 · see citing works
Microglial translational profiling reveals a convergent APOE pathway from aging, amyloid, and tau
Kang, S. S., Ebbert, M. T. W., Baker, K. E., Cook, C., Wang, X., Sens, J. P., Kocher, J.-P., Petrucelli, L., & Fryer, J. D. (2018) · Journal of Experimental Medicine · doi:10.1084/jem.20180653 · Cited by 260 · see citing works
Apolipoprotein E4 Impairs Neuronal Insulin Signaling by Trapping Insulin Receptor in the Endosomes
Zhao, N., Liu, C.-C., Van Ingelgom, A. J., Martens, Y. A., Linares, C., Knight, J. A., Painter, M. M., Sullivan, P. M., & Bu, G. (2017) · Neuron · doi:10.1016/j.neuron.2017.09.003 · Cited by 289 · see citing works
Self-citationShinohara, M., Tachibana, M., Kanekiyo, T., & Bu, G. (2017) · Journal of Lipid Research · doi:10.1194/jlr.r075796 · Cited by 297 · see citing works
Self-citationMa, Q., Zhao, Z., Sagare, A. P., Wu, Y., Wang, M., Owens, N. C., Verghese, P. B., Herz, J., Holtzman, D. M., & Zlokovic, B. V. (2018) · Molecular Neurodegeneration · doi:10.1186/s13024-018-0286-0 · Cited by 281 · see citing works
The dual roles of cytokines in Alzheimer’s disease: update on interleukins, TNF-α, TGF-β and IFN-γ
Zheng, C., Zhou, X.-W., & Wang, J.-Z. (2016) · Translational Neurodegeneration · doi:10.1186/s40035-016-0054-4 · Cited by 292 · see citing works
Kanekiyo, T., & Bu, G. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00093 · Cited by 281 · see citing works
Self-citationLipid droplets in the nervous system
Ralhan, I., Chang, C.-L., Lippincott-Schwartz, J., & Ioannou, M. S. (2021) · Journal of Cell Biology · doi:10.1083/jcb.202102136 · Cited by 281 · see citing works
Microglial genes regulating neuroinflammation in the progression of Alzheimer's disease
Villegas-Llerena, C., Phillips, A., Garcia-Reitboeck, P., Hardy, J., & Pocock, J. M. (2016) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2015.10.004 · Cited by 270 · see citing works
The Genetics of Aging: A Vertebrate Perspective
Singh, P. P., Demmitt, B. A., Nath, R. D., & Brunet, A. (2019) · Cell · doi:10.1016/j.cell.2019.02.038 · Cited by 259 · see citing works
D’Amato, A., Di Cesare Mannelli, L., Lucarini, E., Man, A. L., Le Gall, G., Branca, J. J. V., Ghelardini, C., Amedei, A., Bertelli, E., Regoli, M., et al. (2020) · Microbiome · doi:10.1186/s40168-020-00914-w · Cited by 269 · see citing works
Astrocytic LRP1 Mediates Brain Aβ Clearance and Impacts Amyloid Deposition
Liu, C.-C., Hu, J., Zhao, N., Wang, J., Wang, N., Cirrito, J. R., Kanekiyo, T., Holtzman, D. M., & Bu, G. (2017) · The Journal of Neuroscience · doi:10.1523/jneurosci.3442-16.2017 · Cited by 267 · see citing works
Self-citationSnyder, H. M., Asthana, S., Bain, L., Brinton, R., Craft, S., Dubal, D. B., Espeland, M. A., Gatz, M., Mielke, M. M., Raber, J., et al. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.08.004 · Cited by 262 · see citing works
Michinaga, S., & Koyama, Y. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20030571 · Cited by 263 · see citing works
Amyloid-β Receptors: The Good, the Bad, and the Prion Protein
Jarosz-Griffiths, H. H., Noble, E., Rushworth, J. V., & Hooper, N. M. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.r115.702704 · Cited by 256 · see citing works
HDL and cholesterol handling in the brain
Vitali, C., Wellington, C. L., & Calabresi, L. (2014) · Cardiovascular Research · doi:10.1093/cvr/cvu148 · Cited by 254 · see citing works
Down Syndrome, Partial Trisomy 21, and Absence of Alzheimer’s Disease: The Role of APP
Doran, E., Keator, D., Head, E., Phelan, M. J., Kim, R., Totoiu, M., Barrio, J. R., Small, G. W., Potkin, S. G., & Lott, I. T. (2017) · Journal of Alzheimer’s Disease · doi:10.3233/jad-160836 · Cited by 244 · see citing works
Jazvinšćak Jembrek, M., Hof, P. R., & Šimić, G. (2015) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2015/346783 · Cited by 244 · see citing works
Brain Endothelial Cells Are Exquisite Sensors of Age-Related Circulatory Cues
Chen, M. B., Yang, A. C., Yousef, H., Lee, D., Chen, W., Schaum, N., Lehallier, B., Quake, S. R., & Wyss-Coray, T. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.03.012 · Cited by 233 · see citing works
“, Stmn2, Prnp, Nos3, Sod1, Apoe, Vwf, Alpl, Ctsd, Alpl2, App Sqstm1, and Clstn1) and brain aging (Cuyvers et al., 2015; Dahiyat et al., 1999; Guerreiro et al., 2014; Liu et al., 2013; Vardy et al., 2012; Wolters et al., 2018), highlighting the potential for BECs to contribute to molecular mechanisms and functional def…”
Mancuso, C., & Santangelo, R. (2018) · Pharmacological Research · doi:10.1016/j.phrs.2017.12.009 · Cited by 232 · see citing works
Prevention of dementia in an ageing world: Evidence and biological rationale
Grande, G., Qiu, C., & Fratiglioni, L. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101045 · Cited by 229 · see citing works
Marzi, S. J., Leung, S. K., Ribarska, T., Hannon, E., Smith, A. R., Pishva, E., Poschmann, J., Moore, K., Troakes, C., Al-Sarraj, S., et al. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0253-7 · Cited by 232 · see citing works
Alterman, J. F., Godinho, B. M. D. C., Hassler, M. R., Ferguson, C. M., Echeverria, D., Sapp, E., Haraszti, R. A., Coles, A. H., Conroy, F., Miller, R., et al. (2019) · Nature Biotechnology · doi:10.1038/s41587-019-0205-0 · Cited by 227 · see citing works
Cholesterol and Alzheimer’s Disease; From Risk Genes to Pathological Effects
Feringa, F. M., & van der Kant, R. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.690372 · Cited by 226 · see citing works
Ochalek, A., Mihalik, B., Avci, H. X., Chandrasekaran, A., Téglási, A., Bock, I., Giudice, M. L., Táncos, Z., Molnár, K., László, L., et al. (2017) · Alzheimer's Research & Therapy · doi:10.1186/s13195-017-0317-z · Cited by 225 · see citing works
Uddin, M. S., Kabir, M. T., Al Mamun, A., Abdel-Daim, M. M., Barreto, G. E., & Ashraf, G. M. (2019) · Molecular Neurobiology · doi:10.1007/s12035-018-1237-z · Cited by 212 · see citing works
Blood–Brain Barrier Breakdown in Alzheimer’s Disease: Mechanisms and Targeted Strategies
Alkhalifa, A. E., Al-Ghraiybah, N. F., Odum, J., Shunnarah, J. G., Austin, N., & Kaddoumi, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242216288 · Cited by 212 · see citing works
Brkic, M., Balusu, S., Libert, C., & Vandenbroucke, R. E. (2015) · Mediators of Inflammation · doi:10.1155/2015/620581 · Cited by 205 · see citing works
Modeling Sporadic Alzheimer's Disease in Human Brain Organoids under Serum Exposure
Chen, X., Sun, G., Tian, E., Zhang, M., Davtyan, H., Beach, T. G., Reiman, E. M., Blurton‐Jones, M., Holtzman, D. M., & Shi, Y. (2021) · Advanced Science · doi:10.1002/advs.202101462 · Cited by 200 · see citing works
Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease
Najm, R., Jones, E. A., & Huang, Y. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0324-6 · Cited by 183 · see citing works
Chen, J. C., Alvarez, M. J., Talos, F., Dhruv, H., Rieckhof, G. E., Iyer, A., Diefes, K. L., Aldape, K., Berens, M., Shen, M. M., et al. (2014) · Cell · doi:10.1016/j.cell.2014.09.021 · Cited by 188 · see citing works
TREM2 dependent and independent functions of microglia in Alzheimer’s disease
Hou, J., Chen, Y., Grajales-Reyes, G., & Colonna, M. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00588-y · Cited by 191 · see citing works
The Alzheimer’s Disease Amyloid-Beta Hypothesis in Cardiovascular Aging and Disease
Stakos, D. A., Stamatelopoulos, K., Bampatsias, D., Sachse, M., Zormpas, E., Vlachogiannis, N. I., Tual-Chalot, S., & Stellos, K. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.12.033 · Cited by 188 · see citing works
Targeting microglia for the treatment of Alzheimer’s Disease
Wes, P. D., Sayed, F. A., Bard, F., & Gan, L. (2016) · Glia · doi:10.1002/glia.22988 · Cited by 185 · see citing works
Wu, L., Zhang, X., & Zhao, L. (2018) · The Journal of Neuroscience · doi:10.1523/jneurosci.2262-17.2018 · Cited by 185 · see citing works
Park, C., Ha, J., & Park, S. (2020) · Expert Systems with Applications · doi:10.1016/j.eswa.2019.112873 · Cited by 184 · see citing works
TREM2 in CNS homeostasis and neurodegenerative disease
Painter, M. M., Atagi, Y., Liu, C.-C., Rademakers, R., Xu, H., Fryer, J. D., & Bu, G. (2015) · Molecular Neurodegeneration · doi:10.1186/s13024-015-0040-9 · Cited by 169 · see citing works
Self-citationMicroglia and C9orf72 in neuroinflammation and ALS and frontotemporal dementia
Lall, D., & Baloh, R. H. (2017) · Journal of Clinical Investigation · doi:10.1172/jci90607 · Cited by 175 · see citing works
Amyloid‐β immunotherapy for alzheimer disease: Is it now a long shot?
Panza, F., Lozupone, M., Seripa, D., & Imbimbo, B. P. (2019) · Annals of Neurology · doi:10.1002/ana.25410 · Cited by 178 · see citing works
Xiong, M., Jiang, H., Serrano, J. R., Gonzales, E. R., Wang, C., Gratuze, M., Hoyle, R., Bien-Ly, N., Silverman, A. P., Sullivan, P. M., et al. (2021) · Science Translational Medicine · doi:10.1126/scitranslmed.abd7522 · Cited by 179 · see citing works
Magistri, M., Velmeshev, D., Makhmutova, M., & Faghihi, M. A. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-150398 · Cited by 175 · see citing works
Alzheimer’s Disease: Exploring the Landscape of Cognitive Decline
Tenchov, R., Sasso, J. M., & Zhou, Q. A. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.4c00339 · Cited by 170 · see citing works
AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease
Rosenberg, J. B., Kaplitt, M. G., De, B. P., Chen, A., Flagiello, T., Salami, C., Pey, E., Zhao, L., Ricart Arbona, R. J., Monette, S., et al. (2018) · Human Gene Therapy Clinical Development · doi:10.1089/humc.2017.231 · Cited by 169 · see citing works
Brain cell type-specific cholesterol metabolism and implications for learning and memory
Li, D., Zhang, J., & Liu, Q. (2022) · Trends in Neurosciences · doi:10.1016/j.tins.2022.01.002 · Cited by 163 · see citing works
Martínez-Morillo, E., Hansson, O., Atagi, Y., Bu, G., Minthon, L., Diamandis, E. P., & Nielsen, H. M. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1266-2 · Cited by 168 · see citing works
Self-citationApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease
Lane-Donovan, C., & Herz, J. (2017) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2016.12.001 · Cited by 157 · see citing works
“The allele frequency of ApoE4 is 15–20%, with some variation in incidence between populations [13].”
BackgroundTai, L. M., Ghura, S., Koster, K. P., Liakaite, V., Maienschein‐Cline, M., Kanabar, P., Collins, N., Ben‐Aissa, M., Lei, A. Z., Bahroos, N., et al. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13072 · Cited by 165 · see citing works
- Authors
- Liu, C.-C., Kanekiyo, T., Xu, H., & Bu, G.
- Affiliations
- Xiamen University (CN)
- Mayo Clinic (US)
- Corresponding author
- Bu, Guojun
- Venue
- Nature Reviews Neurology
- Published
- 2013-01-08
- Volume
- 9
- Issue
- 2
- Pages
- 106-118
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- PMC
- PMC3726719
- OpenAlex
- W2140718540
- Cited by
- 3,459
- References
- 180
- Citations by year
- 2026: 273 · 2025: 343 · 2024: 332 · 2023: 277 · 2022: 331 · 2021: 341 · 2020: 321 · 2019: 291 · 2018: 278 · 2017: 206 · 2016: 171 · 2015: 128 · 2014: 123 · 2013: 41
- FWCI
- 17.01
- Type
- journal article
- Language
- en
- Update notices
- correction (2013-03-26)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- American Health Assistance Foundation
- Xiamen University
- National Institutes of Health
- National Institute on Aging (P01AG030128, R01AG044420, R01AG038710, R01AG027924, R01AG021173, R01AG031784, RF1AG046205, R01AG035355)
- National Institute of Neurological Disorders and Stroke (P01NS074969)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- apolipoprotein E, APOE ε4, Alzheimer's disease, genetic risk factors, amyloid-beta, neurodegeneration, cerebral amyloid angiopathy, neurovascular function, neuroinflammation, mitochondrial function
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Brain, Brain Injuries, Dementia, Humans, Immunotherapy, Inflammation, Neuronal Plasticity, Predictive Value of Tests, Risk, Vascular Diseases, Amyloid beta-Peptides, tau Proteins, Dendritic Spines, Lipid Metabolism, Neurogenesis, Cognitive Dysfunction
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.
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 ›
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