Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy
Open accessAbstract
Nonhuman primates are useful for the study of age-associated changes in the brain and behavior in a model that is biologically proximal to humans. The Aβ and tau proteins, two key players in the pathogenesis of Alzheimer's disease (AD), are highly homologous among primates. With age, all nonhuman primates analyzed to date develop senile (Aβ) plaques and cerebral β-amyloid angiopathy. In contrast, significant tauopathy is unusual in simians, and only humans manifest the profound tauopathy, neuronal degeneration and cognitive impairment that characterize Alzheimer's disease. Primates thus are somewhat paradoxical models of AD-like pathology; on the one hand, they are excellent models of normal aging and naturally occurring Aβ lesions, and they can be useful for testing diagnostic and therapeutic agents targeting aggregated forms of Aβ. On the other hand, the resistance of monkeys and apes to tauopathy and AD-related neurodegeneration, in the presence of substantial cerebral Aβ deposition, suggests that a comparative analysis of human and nonhuman primates could yield informative clues to the uniquely human predisposition to Alzheimer's disease.
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Memory impairments in great apes appear mild, more similar to typical age-related memory decline than the extensive cognitive decline seen in AD.
“Also, memory impairments appear to be mild; appearing more similar to typical age-related memory decline, rather than the extensive cognitive decline seen in AD[57].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [57]
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Cystatin C Mutation in an Elderly Man With Sporadic Amyloid Angiopathy and Intracerebral Hemorrhage
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- Authors
- Heuer, E., F. Rosen, R., Cintron, A., & C. Walker, L.
- Affiliations
- Emory University (US)
- ORCID
- Heuer, Eric
- Venue
- Current Pharmaceutical Design
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2012-03-01
- Volume
- 18
- Issue
- 8
- Pages
- 1159-1169
- ISSN
- 1381-6128 (ISSN-L)
- PMC
- PMC3381739
- OpenAlex
- W2152340197
- Cited by
- 169
- References
- 143
- Citations by year
- 2026: 3 · 2025: 18 · 2024: 15 · 2023: 16 · 2022: 10 · 2021: 14 · 2020: 14 · 2019: 17 · 2018: 7 · 2017: 12 · 2016: 17 · 2015: 10 · 2014: 8 · 2013: 4 · 2012: 1
- FWCI
- 4.93
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Current Pharmaceutical Design (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (P51OD011132)
- National Institute on Aging (P01AG026423, P50AG025688)
- National Institute of Neurological Disorders and Stroke (R21NS077049)
- National Center for Research Resources (RR-00 165, P51RR000165)
- 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, non-human primates, amyloid-beta, tau protein, amyloid plaques, tauopathy, neurodegeneration, primate aging, comparative neurobiology, animal models of Alzheimer's disease
- MeSH terms
- Aging, Alzheimer Disease, Animals, Behavior, Animal, Brain, Disease Models, Animal, Humans, Primates, Species Specificity, Amyloid beta-Peptides, tau Proteins
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.
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