The DOI matches its Crossref record; 13 of the 14 references it cites were found in a registry or an index.
Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition
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Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“ApoE is strongly associated with the amount of fibrillar amyloid that deposits into plaques (28).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [28]
In the citing paper
“In addition to isoform status, it appears that the amount of apoE also plays a role in determining the extent of Aβ accumulation in the brain.”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Bales et al., 1997
In the citing paper
“Initial studies clearly indicated that the deletion of the endogenous murine Apoe gene causes a dramatic decrease in fibrillar and total Aβ deposition in APP transgenic mouse models (Bales et al., 1997).”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Bales et al., 1997
In the citing paper
“Previous studies demonstrated that the lack of apoE led to a dramatic decrease of amyloid deposition in APP transgenic mouse models (Bales et al., 1997; Holtzman et al., 2000b).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Bales et al., 1997
In the citing paper
“Previous studies demonstrated that the absence of apoE leads to a dramatic decrease in the levels of fibrillar Aβ deposits in APP transgenic mouse models (Bales et al., 1999; Bales et al., 1997; Holtzman et al., 2000a; Holtzman et al., 2000b).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Bales et al., 1997
In the citing paper
“Later, in vivo studies demonstrated that the lack of apoE led to a dramatic reduction of fibrillar Aβ deposition in APP transgenic mouse models (Bales et al., 1999; Bales et al., 1997; Holtzman et al., 2000a; Holtzman et al., 2000b).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Bales et al., 1997
In the citing paper
“Reducing ApoE in mouse models of amyloidosis greatly reduces plaque formation (7, 8, 33, 34).”
From The E3 ubiquitin ligase Idol controls brain LDL receptor expression, ApoE clearance, and Aβ amyloidosis (2015) · cites this paper as [33]
In the citing paper
“Both genetic deletion and pharmacological reduction of APOE reduced Aβ deposition in mouse models of AD. 3 , 4 , 5 , 6 , 7 , 8 , 9”
From Deletion of neuronal Idol ameliorates Alzheimer's disease–related pathologies via APOE receptors (2025) · cites this paper as [3]
In the citing paper
“Notably, deletion of Apoe reduces amyloid deposition in transgenic mouse models of AD. 3 , 4”
From Deletion of neuronal Idol ameliorates Alzheimer's disease–related pathologies via APOE receptors (2025) · cites this paper as [3]
In the citing paper
“Our findings remain consistent with the effects of apoE knock-out noted in several AD Tg mouse models, where lack of apoE was associated with absence of fibrillar Aβ deposits and prevented neurodegeneration [13,29,31,32].”
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 [31]
In the citing paper
“Independent of apoE isoform, the amount of apoE in the brain appears to be critical for determining the extent of amyloid deposition [25,26].”
From Measurement of apolipoprotein E and amyloid β clearance rates in the mouse brain using bolus stable isotope labeling (2012) · cites this paper as [25]
In the citing paper
“ApoE gene deletion in APP transgenic mice leads to dramatically decreased amyloid plaques without affecting Aβ production (Bales et al., 1997).”
From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as Bales et al., 1997
In the citing paper
“The pivotal role of ApoE in brain Ab accumulation was confirmed by showing a marked reduction in Ab plaque and CAA deposits associated with the Apoe gene knockout (KO) in AD transgenic (Tg) mice.14”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [14]
In the citing paper
“Similar effects of the ApoE KO were previously reported in APP V717F and APP SW lines, representing more latent models of Ab pathology in which thioflavin-S detects the first plaques around the age of 1 year.14,55”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [14]
In the citing paper
“Reducing ApoE levels is generally protective in AD models1,4–6.”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [4]
In the citing paper
“Previous studies showed that apoE is co-deposited in senile plaques and plays a crucial role in fibrillar plaque formation (23, 24).”
From APOE3 -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [23]
In the citing paper
“In amyloid precursor proteineexpressing transgenic mice, deletion of mouse apoE gene inhibits development of fibrillar amyloid plaques [80,81].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [80]
In the citing paper
“ApoE strongly regulates brain amyloid-β (Aβ) deposition in a dose- and isoform-dependent manner (E4>E3>E2) (Bales et al., 1997; Holtzman et al., 2000; Schmechel et al., 1993).”
From Overexpressing low‐density lipoprotein receptor reduces tau‐associated neurodegeneration in relation to apoE‐linked mechanisms (2021) · cites this paper as Bales et al., 1997
In the citing paper
“APP transgenic mice lacking endogenous mouse apoE display a significant decrease of amyloid pathology”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Bales et al 1997
In the citing paper
“apoE-deficient APP transgenic mice display virtually no fibrillar Aβ deposits nor neuritic degeneration”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Bales et al 1997
In the citing paper
“Initial studies using the PDAPP and Tg2576 APP transgenic mouse models that develop Aβ deposition demonstrated that the lack of murine apoE resulted in a significant decrease in Aβ deposition, along with an almost complete lack of true amyloid plaques and neuritic dystrophy (Bales et al., 1997; Holtzman et al., 2000; Holtzman et al., 1999).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Bales et al., 1997
In the citing paper
“Data from transgenic mouse models produced more conflicting results with impaired plaque deposition seen in mice lacking murine APOE (Bales et al., 1997; Holtzman et al., 2000), but also in animals overexpressing the human APOE3 or APOE4 isoforms (Holtzman et al., 1999).”
From The Pro-Neurotrophin Receptor Sortilin Is a Major Neuronal Apolipoprotein E Receptor for Catabolism of Amyloid-β Peptide in the Brain (2013) · cites this paper as Bales et al., 1997
In the citing paper
“Murine Apoe deletion reduced Aβ deposition in various transgenic APP mouse models (Bales, Verina et al. 1997, Bales, Verina et al. 1999, Holtzman, Fagan et al. 2000, Irizarry, Cheung et al. 2000, Ulrich, Ulland et al. 2018)”
From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Bales, Verina et al. 1997
In the citing paper
“ApoE has a major impact on the generation of amyloid deposits in the AD mouse brain and deletion of ApoE in most AD mouse models significantly inhibits amyloid plaque formation [6], [7], [8].”
From Lack of LDL receptor enhances amyloid deposition and decreases glial response in an Alzheimer's disease mouse model (2011) · cites this paper as [8]
In the citing paper
“APP transgenic mice deficient for ApoE show a dramatic decrease in fibrillary amyloid deposits [5], [6], [7], [8], [9].”
From Lack of LDL receptor enhances amyloid deposition and decreases glial response in an Alzheimer's disease mouse model (2011) · cites this paper as [8]
In the citing paper
“Total body apoE knockout as well as astrocyte specific ApoE knockout results in markedly decreased fibrillar amyloid deposition and in less compact Aβ plaques as well as decreasing neuronal loss and reactive gliosis in a tauopathy model [96, 99, 100].”
From ApoE lipoproteins in the central nervous system under homeostasis and role in Alzheimer’s disease and related disorders (2026) · cites this paper as [100]
In the citing paper
“In addition, the strongest genetic risk factor for LOAD, apolipoprotein E, APOE, in large part appears to increase risk via influencing Aβ seeding and clearance”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Bales et al., 1997
In the citing paper
“To date, substantial evidence has demonstrated ApoE affects amyloid-β deposition in a dosage and isoform-specific fashion (ApoE4>ApoE3>ApoE2)96–100”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [96]
In the citing paper
“Transgenic mouse studies confirmed that ApoE was necessary for the formation of fibrillar amyloid plaques and CAA [4, 5, 41, 61], however they also identified important differences between mouse and human ApoE.”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [5]
Citations
Cites
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516
Self-citationSpontaneous Hypercholesterolemia and Arterial Lesions in Mice Lacking Apolipoprotein E
Zhang, S. H., Reddick, R. L., Piedrahita, J. A., & Maeda, N. (1992) · Science · doi:10.1126/science.1411543 · Cited by 2,237
Apolipoprotein E polymorphism and Alzheimer's disease
Poirier, J., Bertrand, P., Poirier, J., Kogan, S., Gauthier, S., Poirier, J., Gauthier, S., Davignon, J., Bouthillier, D., & Davignon, J. (1993) · The Lancet · doi:10.1016/0140-6736(93)91705-q · Cited by 1,108
Ma, J., Yee, A., Brewer, H. B., Das, S., & Potter, H. (1994) · Nature · doi:10.1038/372092a0 · Cited by 871
Normal and Abnormal Biology of the Beta-Amyloid Precursor Protein
Selkoe, D. J. (1994) · Annual Review of Neuroscience · doi:10.1146/annurev.ne.17.030194.002421 · Cited by 834
Reduction of β‐amyloid peptide42 in the cerebrospinal fluid of patients with Alzheimer's disease
Motter, R., Vigo‐Pelfrey, C., Kholodenko, D., Barbour, R., Johnson‐Wood, K., Galasko, D., Chang, L., Miller, B., Clark, C., Green, R., et al. (1995) · Annals of Neurology · doi:10.1002/ana.410380413 · Cited by 701
Apolipoprotein E and Alzheimer disease.
Strittmatter, W. J., & Roses, A. D. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.11.4725 · Cited by 701
(1997) · doi:10.1073/pnas.94.4.1550 · Cited by 535
Human apolipoprotein E: the Alzheimer's disease connection
Weisgraber, K. H., & Mahley, R. W. (1996) · The FASEB Journal · doi:10.1096/fasebj.10.13.8940294 · Cited by 333
Hyman, B. T., West, H. L., Rebeck, G. W., Buldyrev, S. V., Mantegna, R. N., Ukleja, M., Havlin, S., & Stanley, H. E. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.8.3586 · Cited by 212
Purification of Apolipoprotein E Attenuates Isoform-specific Binding to β-Amyloid
LaDu, M. J., Pederson, T. M., Frail, D. E., Reardon, C. A., Getz, G. S., & Falduto, M. T. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.16.9039 · Cited by 189
Hyman, B. T., Tanzi, R. E., Marzloff, K., Barbour, R., & Schenk, D. (1992) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-199201000-00009 · Cited by 135
Normal Scores, Normal Plots Tests for Normality
Brown, B. M., & Hettmansperger, T. P. (1996) · Journal of the American Statistical Association · doi:10.1080/01621459.1996.10476736 · Cited by 35
Flagged first, then by citations
1 of the 14 references couldn’t be matched to a known paper.
Research works printed but not linked: 2
- Kim, K.S. et al. Neurosci. Res. Comm. 51, 113–122 (1990).
- Brown, B.M. & Hettmansperger, T.P. J. Am. Stat. Assoc. 91, 1668–1675 (1996).
Cited by
Sorted by citations
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
Alzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
Liu, C.-C., Kanekiyo, T., Xu, H., & Bu, G. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2012.263 · Cited by 3,459
Alzheimer Disease: An Update on Pathobiology and Treatment Strategies
Long, J. M., & Holtzman, D. M. (2019) · Cell · doi:10.1016/j.cell.2019.09.001 · Cited by 3,204
PLEIOTROPIC EFFECTS OF STATINS
Liao, J. K., & Laufs, U. (2005) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.45.120403.095748 · Cited by 1,994
Metadata
- Authors
- 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., Piccardo, P., Ghetti, B., & Paul, S. M.
- Affiliations
- Eli Lilly (United States) (US)
- Indiana University School of Medicine (US)
- Philipps University of Marburg (DE)
- Venue
- Nature Genetics
- Published
- 1997-11
- Volume
- 17
- Issue
- 3
- Pages
- 263-264
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W1981554609
- Cited by
- 830
- References
- 14
- Citations by year
- 2026: 11 · 2025: 8 · 2024: 27 · 2023: 18 · 2022: 25 · 2021: 19 · 2020: 27 · 2019: 24 · 2018: 16 · 2017: 21 · 2016: 20 · 2015: 19 · 2014: 21 · 2013: 16 · 2012: 20
- FWCI
- 26.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- apolipoprotein E, amyloid-beta, amyloid deposition, Alzheimer's disease, APOE genotype, apolipoprotein E deficiency
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Apolipoproteins E, Brain, Humans, Immunohistochemistry, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Transgenic, RNA, Messenger, Polymerase Chain Reaction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice, Knockout, Mice
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