Disentangling the effects of age and APOE on neuropathology and late life cognitive decline
Open accessAbstract
Age and APOE are the most robust risk factors for dementia and cognitive decline, but the underlying neurobiology remains unclear. We examined the extent to which the hallmark pathologies of Alzheimer's disease, Lewy body disease, and cerebrovascular diseases account for the association of age and APOE with decline in episodic memory versus nonepisodic cognitive abilities. Up to 20 waves of longitudinal cognitive data were collected from 858 autopsied participants in 2 ongoing clinical-pathologic cohort studies of aging. Neuropathologic examinations quantified measures of beta amyloid (Aβ) plaque, mesial temporal and neocortical neurofibrillary tangles, macro- and microinfarcts, and neocortical Lewy bodies. Random coefficient models estimated person-specific slopes of decline in episodic memory and nonepisodic cognition. Path analysis examined the relation of age, APOE, and the 6 pathologic indices to the slopes of cognitive decline. The effect of age on decline in episodic memory was mediated by Aβ, mesial temporal and neocortical tau tangles, and macroscopic infarcts; age on decline in nonepisodic cognition was mediated by Aβ, neocortical tangles, and macroscopic infarcts. The effect of APOE on decline in episodic memory was mediated by Aβ, mesial temporal and neocortical tangles, and neocortical Lewy bodies; APOE on nonepisodic cognition was mediated by Aβ, neocortical tangles, and neocortical Lewy bodies. There were no direct effects of age and APOE on decline after accounting for these pathologic pathways.
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APOE ε4 has a unique role in Alzheimer's disease given its large effect size (OR>3 for one copy) and substantial frequency.
“The APOE ε4 haplotype has a unique role in the disease given its large effect size (odds ratio > 3 for one copy of the APOE ε4 haplotype) and substantial frequency in human populations28.”
From A molecular network of the aging human brain provides insights into the pathology and cognitive decline of Alzheimer’s disease (2018) · cites this paper as [28]
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- Authors
- Yu, L., Boyle, P. A., Leurgans, S., Schneider, J. A., & Bennett, D. A.
- Affiliations
- Rush University Medical Center (US)
- Corresponding author
- Yu, Lei
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 35
- Issue
- 4
- Pages
- 819-826
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC3882071
- OpenAlex
- W2143972213
- Cited by
- 71
- References
- 65
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 4 · 2022: 1 · 2021: 10 · 2020: 4 · 2019: 2 · 2018: 13 · 2017: 10 · 2016: 8 · 2015: 9 · 2014: 5
- FWCI
- 5.21
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P30AG10161, R01AG15819, R01AG17917, R01AG34374)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Social Sciences › Psychology › Neuropsychology and Physiological Psychology › Aging and Gerontology Research
- Keywords
- apolipoprotein E, aging, cognitive decline, episodic memory, Alzheimer's disease, Lewy body disease, amyloid plaques, neurofibrillary tangles, cerebral infarction, neuropathology, dementia risk factors, mediation analysis
- MeSH terms
- Aged, Aged, 80 and over, Aging, Apolipoproteins E, Brain, Cognition Disorders, Female, Humans, Male, Cohort Studies, Amyloid beta-Peptides, Neurofibrillary Tangles, tau Proteins, Plaque, Amyloid
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