APOE ε2 is associated with milder clinical and pathological A lzheimer disease

Serrano‐Pozo, Alberto; Qian, Jing; Monsell, Sarah E.; Betensky, Rebecca A.; Hyman, Bradley T.

doi:10.1002/ana.24369

Cited by 177Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

APOE ε2 is associated with milder clinical and pathological A lzheimer disease

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Serrano‐Pozo, Alberto, Qian, Jing, Monsell, Sarah E., Betensky, Rebecca A., Hyman, Bradley T.·2015·Annals of Neurology

DOI 10.1002/ana.24369PMC PMC4447539

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Abstract

Objective: The Alzheimer disease (AD) APOE ε4 risk allele associates with an earlier age at onset and increased amyloid‐β deposition, whereas the protective APOE ε2 allele delays the onset and appears to prevent amyloid‐β deposition. Yet the clinical and pathological effects of APOE ε2 remain uncertain because of its relative rarity. We investigated the effects of APOE ε2 and ε4 alleles on AD pathology and cognition in a large US data set of well‐characterized AD patients. Methods: We studied individuals from the National Alzheimer's Coordinating Center autopsy cohort across the entire clinicopathological continuum of AD. Multivariate models were built to examine the associations between APOE alleles and AD neuropathological changes, using the APOE ε3/ε3 group as comparator. Mediation analysis was used to estimate the direct and indirect effects of APOE alleles on AD pathology and cognition (Clinical Dementia Rating Sum of Boxes and Mini‐Mental State Examination). Results: Compared to APOE ε3/ε3, APOE ε2 is independently associated with lower Braak neurofibrillary tangle (NFT) stages and possibly fewer neuritic plaques, but has no direct effect on cerebral amyloid angiopathy (CAA) severity, whereas APOE ε4 is associated with more neuritic plaques and CAA, but has no independent effect on Braak NFT stage. Unadjusted analyses showed marked differences among APOE genotypes with respect to cognitive performance (ε2 > ε3 > ε4). Mediation analysis suggests that this is largely explained through effects on pathology. Interpretation: Even when adjusted for age at onset, symptom duration, and other demographic variables, APOE ε2 is associated with milder AD pathology and less severe antemortem cognitive impairment compared to APOE ε3 and ε4 alleles, suggesting a relative neuroprotective effect of APOE ε2 in AD. Ann Neurol 2015;77:917–929

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Relative to the APOEε3 homozygote reference group, carrying one or two APOEε4 alleles is independently associated with a higher Aβ plaque burden and more severe cerebral amyloid angiopathy, whereas APOEε2/ε2 and ε2/ε3 individuals have fewer Aβ plaques but are more likely to have cerebral amyloid angiopathy.
“Relative to the APOEε3 homozygote reference group, carrying one or two APOEε4 alleles is independently associated with a higher Aβ plaque burden and more severe cerebral amyloid angiopathy (CAA), whereas APOEε2/ε2 and ε2/ε3 individuals have fewer Aβ plaques46–50 but are more likely to have CAA51.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [48]
Split into 2 atoms — 1 confirmed, 0 partially supported, 1 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
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Homozygous APOE4 individuals have a 6 to 18-fold increase in AD risk compared to APOE2/3 individuals.
“Homozygous APOE4 individuals have a 6 to 18-fold increase in AD risk compared to APOE2/3 individuals [9, 10].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [9]
The Introduction reports that carrying two APOE ε4 alleles increases lifetime AD risk 8–12 times compared with the ε3 allele. It does not give the claimed 6–18-fold range or use APOE ε2/ε3 individuals as the comparator; it separately says ε2 reduces risk relative to ε3. No page number is available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measured
The study supports known effects of APOE genotypes on standard measures of neuritic Aβ plaque and tau tangle severity.
“The study supports known effects of APOE genotypes on standard measures of neuritic Aβ plaque and tau tangle severity13”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [13]
APOE4 is the strongest genetic risk factor for late-onset Alzheimer's disease.
“Apolipoprotein E ε4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer’s disease (LOAD).”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [9]
Most studies agree that the APOEε4-linked effect on tau neurofibrillary tangles is primarily indirect, mediated through its increase of Aβ plaque burden.
“In contrast to Aβ pathology, the existence of a direct effect of APOE genotype on the severity of tau neurofibrillary tangle pathology remains controversial, with most studies agreeing that APOEε4-linked effect on tangles is primarily indirect, mediated through its increase of Aβ plaque burden46–48,53.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [48]

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Gene Transfer of Human Apoe Isoforms Results in Differential Modulation of Amyloid Deposition and Neurotoxicity in Mouse Brain
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The apolipoprotein E varepsilon2 allele and decline in episodic memory
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APOEɛ4 influences the pathological phenotype of Alzheimer's disease by favouring cerebrovascular over parenchymal accumulation of Aβ protein
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APOE , vascular pathology, and the AD brain
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Apolipoprotein E genotype does not influence rates of cognitive decline in Alzheimer's disease
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Accelerated decline in apolipoprotein E-ϵ4 homozygotes with Alzheimer's disease
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APOE associations with severe CAA-associated vasculopathic changes: collaborative meta-analysis
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Association between severe cerebral amyloid angiopathy and cerebrovascular lesions in Alzheimer disease is not a spurious one attributable to apolipoprotein E4.
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The absence of an apolipoprotein ϵ4 allele is associated with a more aggressive form of Alzheimer's disease
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Frequency of the apolipoprotein E ε2 allele is diminished in sporadic Alzheimer disease
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Mild to moderate Alzheimer dementia with insufficient neuropathological changes
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Apolipoprotein E isoforms and the development of low and high Braak stages of Alzheimer’s disease-related lesions
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Apolipoprotein E Genotype and Rate of Decline in Probable Alzheimer's Disease
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Most rapid cognitive decline in APOE ε4 negative Alzheimer's disease with early onset
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Examination of the Clinicopathologic Continuum of Alzheimer Disease in the Autopsy Cohort of the National Alzheimer Coordinating Center
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Amyloid mediates the association of apolipoprotein E e4 allele to cognitive function in older people
Bennett, D. A. (2005) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.2004.054445 · Cited by 99 · see citing works
Apolipoprotein E ε4 Allele Is Unrelated to Cognitive or Functional Decline in Alzheimer’s Disease: Retrospective and Prospective Analysis
Kleiman, T., Zdanys, K. F., Black, B. T., Rightmer, T., Grey, M. A., Garman, K. S., MacAvoy, M. G., Gelernter, J. E., & van Dyck, C. H. (2006) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000093316 · Cited by 90 · see citing works
No association between apolipoprotein E epsilon 4 allele and rate of decline in Alzheimer's disease
Murphy, G. M., Taylor, J. L., KRAEMER, H. C., Yesavage, J. A., & Tinklenberg, J. R. (1997) · American Journal of Psychiatry · doi:10.1176/ajp.154.5.603 · Cited by 89 · see citing works
Apolipoprotein E epsilon 4 allele, cognitive decline, and deterioration of everyday performance in Alzheimer's disease
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Amyloid load in nondemented brains correlates with APOE e4
Caselli, R. J., Walker, D. G., Sue, L. I., Sabbagh, M. N., & Beach, T. G. (2010) · Neuroscience Letters · doi:10.1016/j.neulet.2010.02.016 · Cited by 83 · see citing works
Individual Growth Curve Analysis of APOE ε4–Associated Cognitive Decline in Alzheimer Disease
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Differential Binding of Apolipoprotein E Isoforms to Tau and Other Cytoskeletal Proteins
Fleming, L. M., Weisgraber, K. H., Strittmatter, W. J., Troncoso, J. C., & Johnson, G. V. W. (1996) · Experimental Neurology · doi:10.1006/exnr.1996.0064 · Cited by 82 · see citing works
Apolipoprotein E-epsilon 2 and Alzheimer's disease
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Protective effect of apoE ∈2 in Alzheimer's disease
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A 2-process model for neuropathology of Alzheimer's disease
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ApoE3 binding to tau tandem repeat I is abolished by tau serine262 phosphorylation
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Apolipoprotein E Genotype and Deposits of Aβ40 and Aβ42 in Alzheimer Disease
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Effect of apolipoprotein E genotype on Alzheimer's disease neuropathology in a cohort of elderly Norwegians
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Pattern and Progression of Cognitive Decline in Alzheimer’s Disease: Role of Premorbid Intelligence and ApoE Genotype
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Apolipoprotein E Genotype and its Effect on Duration and Severity of Early and Late Onset Alzheimer's Disease
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Apolipoprotein E ɛ2 and Functional Decline in Amnestic Mild Cognitive Impairment and Alzheimer Disease
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Tau–amyloid interactions in the rTgTauEC model of early Alzheimer's disease suggest amyloid‐induced disruption of axonal projections and exacerbated axonal pathology
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Neocortical β‐amyloid area is associated with dementia and APOE in the oldest‐old
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Alzheimer disease
Knopman, D. S., Amieva, H., Petersen, R. C., Chételat, G., Holtzman, D. M., Hyman, B. T., Nixon, R. A., & Jones, D. T. (2021) · Nature Reviews Disease Primers · doi:10.1038/s41572-021-00269-y · Cited by 2,606 · see citing works
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Alzheimer's disease
Masters, C. L., Bateman, R., Blennow, K., Rowe, C. C., Sperling, R. A., & Cummings, J. L. (2015) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2015.56 · Cited by 1,853 · see citing works
Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies
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APOE and Alzheimer’s disease: Advances in genetics, pathophysiology, and therapeutic approaches
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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
Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study
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ApoE4: an emerging therapeutic target for Alzheimer’s disease
Safieh, M., Korczyn, A. D., & Michaelson, D. M. (2019) · BMC Medicine · doi:10.1186/s12916-019-1299-4 · Cited by 449 · see citing works
Amyloid toxicity in Alzheimer’s disease
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Apolipoprotein E, Receptors, and Modulation of Alzheimer’s Disease
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New Insights Into the Pathogenesis of Alzheimer's Disease
Fan, L., Mao, C.-Y., Hu, X., Zhang, S., Yang, Z.-H., Hu, Z., Sun, H.-F., Fan, Y., Dong, Y., Yang, J., et al. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2019.01312 · Cited by 294 · see citing works
APOE2: protective mechanism and therapeutic implications for Alzheimer’s disease
Li, Z., Shue, F., Zhao, N., Shinohara, M., & Bu, G. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00413-4 · Cited by 306 · see citing works
Deciphering the astrocyte reaction in Alzheimer's disease
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Microglia in Alzheimer Disease: Well-Known Targets and New Opportunities
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The role of APOE in cerebrovascular dysfunction
Tai, L. M., Thomas, R., Marottoli, F. M., Koster, K. P., Kanekiyo, T., Morris, A. W. J., & Bu, G. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1547-z · Cited by 231 · see citing works
Multifaceted roles of APOE in Alzheimer disease
Jackson, R. J., Hyman, B. T., & Serrano-Pozo, A. (2024) · Nature Reviews Neurology · doi:10.1038/s41582-024-00988-2 · Cited by 193 · see citing works
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Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease
Liao, F., Yoon, H., & Kim, J. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000383 · Cited by 191 · see citing works
Alzheimer's Disease Genetic Risk Factor APOE-ε4 Also Affects Normal Brain Function
Battista, A. M. D., Heinsinger, N. M., & Rebeck, G. W. (2016) · Current Alzheimer Research · doi:10.2174/1567205013666160401115127 · Cited by 184 · see citing works
Microglia and Astrocyte Function and Communication: What Do We Know in Humans?
Garland, E. F., Hartnell, I. J., & Boche, D. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.824888 · Cited by 165 · see citing works
Is Alzheimer’s Disease Risk Modifiable?
Serrano‐Pozo, A., & Growdon, J. H. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad181028 · Cited by 157 · see citing works
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APOE and cerebral amyloid angiopathy in community-dwelling older persons
Yu, L., Boyle, P. A., Nag, S., Leurgans, S., Buchman, A. S., Wilson, R. S., Arvanitakis, Z., Farfel, J. M., De Jager, P. L., Bennett, D. A., et al. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.08.008 · Cited by 123 · see citing works
The role of the immune system in Alzheimer’s disease
Wu, K., Zhang, Y.-R., Huang, Y., Dong, Q., Tan, L., & Yu, J. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101409 · Cited by 116 · see citing works
Aβ profiles generated by Alzheimer’s disease causing PSEN1 variants determine the pathogenicity of the mutation and predict age at disease onset
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APOE2 eases cognitive decline during Aging: Clinical and preclinical evaluations
Shinohara, M., Kanekiyo, T., Yang, L., Linthicum, D., Shinohara, M., Fu, Y., Price, L., Frisch‐Daiello, J. L., Han, X., Fryer, J. D., et al. (2016) · Annals of Neurology · doi:10.1002/ana.24628 · Cited by 111 · see citing works
Association between tau deposition and antecedent amyloid-β accumulation rates in normal and early symptomatic individuals
Tosun, D., Landau, S. M., Aisen, P. S. S., Petersen, R. C., Mintun, M. A., Jagust, W., Weiner, M. W., & Initiative, A. D. N. (2017) · Brain · doi:10.1093/brain/awx046 · Cited by 108 · see citing works
Plaque-associated local toxicity increases over the clinical course of Alzheimer disease
Serrano-Pozo, A., Betensky, R. A., Frosch, M. P., & Hyman, B. T. (2016) · The American Journal of Pathology · doi:10.1016/j.ajpath.2015.10.010 · Cited by 100 · see citing works
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Roles of ApoE4 on the Pathogenesis in Alzheimer’s Disease and the Potential Therapeutic Approaches
Sun, Y.-Y., Wang, Z., & Huang, H. (2023) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-023-01365-1 · Cited by 95 · see citing works
Aβ propagation and strains: Implications for the phenotypic diversity in Alzheimer's disease
Condello, C., & Stöhr, J. (2017) · Neurobiology of Disease · doi:10.1016/j.nbd.2017.03.014 · Cited by 87 · see citing works
APOE2 gene therapy reduces amyloid deposition and improves markers of neuroinflammation and neurodegeneration in a mouse model of Alzheimer disease
Jackson, R. J., Keiser, M. S., Meltzer, J. C., Fykstra, D. P., Dierksmeier, S. E., Hajizadeh, S., Kreuzer, J., Morris, R., Melloni, A., Nakajima, T., et al. (2024) · Molecular Therapy · doi:10.1016/j.ymthe.2024.03.024 · Cited by 86 · see citing works
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Apolipoprotein E in Alzheimer’s disease: molecular insights and therapeutic opportunities
Belaidi, A. A., Bush, A. I., & Ayton, S. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00843-y · Cited by 91 · see citing works
Association of APOE e2 genotype with Alzheimer’s and non-Alzheimer’s neurodegenerative pathologies
Goldberg, T. E., Huey, E. D., & Devanand, D. P. (2020) · Nature Communications · doi:10.1038/s41467-020-18198-x · Cited by 82 · see citing works
Predictors of cognitive impairment in primary age-related tauopathy: an autopsy study
Iida, M. A., Farrell, K. W., Walker, J. M., Richardson, T. E., Marx, G. A., Bryce, C., Purohit, D. P., Ayalon, G., Beach, T. G., Bigio, E. H., et al. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01233-3 · Cited by 78 · see citing works
APOE effects on regional tau in preclinical Alzheimer’s disease
Young, C. B., Johns, E., Kennedy, G., Belloy, M. E., Insel, P. S., Greicius, M. D., Sperling, R. A., Johnson, K. A., Poston, K. L., Mormino, E. C., et al. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00590-4 · Cited by 80 · see citing works
Association of APOE Genotype With Heterogeneity of Cognitive Decline Rate in Alzheimer Disease
Qian, J., Betensky, R. A., Hyman, B. T., & Serrano-Pozo, A. (2021) · Neurology · doi:10.1212/wnl.0000000000011883 · Cited by 71 · see citing works
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APOE2 orchestrated differences in transcriptomic and lipidomic profiles of postmortem AD brain
Lefterov, I., Wolfe, C. M., Fitz, N. F., Nam, K. N., Letronne, F., Biedrzycki, R. J., Kofler, J., Han, X., Wang, J., Schug, J., et al. (2019) · Alzheimer's Research & Therapy · doi:10.1186/s13195-019-0558-0 · Cited by 74 · see citing works
Parkinson Disease and Dementia
Ptacek, S. G., & Kramberger, M. G. (2016) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/0891988716654985 · Cited by 73 · see citing works
Apolipoprotein E in Alzheimer’s disease trajectories and the next-generation clinical care pathway
Narasimhan, S., Holtzman, D. M., Apostolova, L. G., Cruchaga, C., Masters, C. L., Hardy, J., Villemagne, V. L., Bell, J. S., Cho, M., & Hampel, H. J. (2024) · Nature Neuroscience · doi:10.1038/s41593-024-01669-5 · Cited by 70 · see citing works
Treatment of Alzheimer’s Disease: The Legacy of the Cholinergic Hypothesis, Neuroplasticity, and Future Directions
Ashford, J. W. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150381 · Cited by 66 · see citing works
APOE2 Is Associated with Spatial Navigational Strategies and Increased Gray Matter in the Hippocampus
Konishi, K., Bhat, V., Banner, H., Poirier, J., Joober, R., & Bohbot, V. D. (2016) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2016.00349 · Cited by 63 · see citing works
Integrative brain transcriptome analysis links complement component 4 and HSPA2 to the APOE ε2 protective effect in Alzheimer disease
Panitch, R., Hu, J., Chung, J., Zhu, C., Meng, G., Xia, W., Bennett, D. A., Lunetta, K. L., Ikezu, T., Au, R., et al. (2021) · Molecular Psychiatry · doi:10.1038/s41380-021-01266-z · Cited by 58 · see citing works
Effects of APOE Genotype on Brain Proteomic Network and Cell Type Changes in Alzheimer's Disease
Dai, J., Johnson, E. C. B., Dammer, E. B., Duong, D. M., Gearing, M., Lah, J. J., Levey, A. I., Wingo, T. S., & Seyfried, N. T. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00454 · Cited by 62 · see citing works
Large multi-ethnic genetic analyses of amyloid imaging identify new genes for Alzheimer disease
Ali, M., Archer, D. B., Gorijala, P., Western, D., Timsina, J., Fernández, M. V., Wang, T., Satizábal, C. L., Yang, Q., Beiser, A., et al. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01563-4 · Cited by 59 · see citing works
Brain Lipids and Lipid Droplet Dysregulation in Alzheimer’s Disease and Neuropsychiatric Disorders
Zhao, X., Zhang, S., Sanders, A. R., & Duan, J. (2023) · Complex Psychiatry · doi:10.1159/000535131 · Cited by 54 · see citing works
Differential associations of APOE-ε2 and APOE-ε4 alleles with PET-measured amyloid-β and tau deposition in older individuals without dementia
Salvadó, G., Grothe, M. J., Groot, C., Moscoso, A., Schöll, M., Gispert, J. D., Ossenkoppele, R., & Initiative, A. D. N. (2021) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-021-05192-8 · Cited by 54 · see citing works
Clinical phenotype, atrophy, and small vessel disease in APOE ε2 carriers with Alzheimer disease
Groot, C., Sudre, C. H., Barkhof, F., Teunissen, C. E., van Berckel, B. N. M., Seo, S. W., Sebastien Ourselin, A., Scheltens, P., Cardoso, M. J., van der Flier, W. M., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000006503 · Cited by 53 · see citing works
Effect of APOE alleles on the glial transcriptome in normal aging and Alzheimer’s disease
Serrano-Pozo, A., Li, Z., Noori, A., Nguyen, H. N., Mezlini, A., Li, L., Hudry, E., Jackson, R. J., Hyman, B. T., & Das, S. (2021) · Nature Aging · doi:10.1038/s43587-021-00123-6 · Cited by 49 · see citing works
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Early- and Late-Onset Alzheimer’s Disease: Two Sides of the Same Coin?
Valdez-Gaxiola, C. A., Rosales-Leycegui, F., Gaxiola-Rubio, A., Moreno-Ortíz, J. M., & Figuera, L. E. (2024) · Diseases · doi:10.3390/diseases12060110 · Cited by 50 · see citing works
Protective effects of APOE e2 against disease progression in subcortical vascular mild cognitive impairment patients: A three-year longitudinal study
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APOEε2 Is Associated With Milder Clinical and Pathological Alzheimer’s Disease (S16.005)
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Epidemiological, Clinical, and Neuropathological Study of Apolipoprotein E Genotype in Alzheimer's Disease
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Authors: Serrano‐Pozo, A., Qian, J., Monsell, S. E., Betensky, R. A., & Hyman, B. T.
Affiliations: University of Iowa Hospitals and Clinics (US)
University of Massachusetts Amherst (US)
University of Washington (US)
Harvard University (US)
Massachusetts General Hospital (US)
Corresponding author: Hyman, Bradley T.
ORCID: Serrano‐Pozo, Alberto
Qian, Jing
Monsell, Sarah E.
Betensky, Rebecca A.
Hyman, Bradley T.
Venue: Annals of Neurology
Publisher: Wiley
Published: 2015-05-27
Volume: 77
Issue: 6
Pages: 917-929
ISSN: 0364-5134 (ISSN-L)
1531-8249
DOI: 10.1002/ana.24369
PMC: PMC4447539
OpenAlex: W1958554455
Cited by: 176
References: 96
Citations by year: 2026: 13 · 2025: 24 · 2024: 17 · 2023: 20 · 2022: 20 · 2021: 22 · 2020: 11 · 2019: 7 · 2018: 8 · 2017: 9 · 2016: 16 · 2015: 9
FWCI: 10.32
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Annals of Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (P50 AG005134)
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: Alzheimer's disease, APOE ε2, APOE ε4, APOE ε3, risk alleles, neurofibrillary tangles, neuritic plaques, cerebral amyloid angiopathy, amyloid-beta deposition, cognitive impairment, neuropathology, neuroprotection, age of onset
MeSH terms: Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Female, Humans, Male, Severity of Illness Index, Cohort Studies, Apolipoprotein E3, Apolipoprotein E4, Apolipoprotein E2

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APOE ε2 is associated with milder clinical and pathological A lzheimer disease

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