Cited by 57Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchGenetics, Aging, and Longevity in Model Organisms

The Age of Biosenescence and the Incidence of Cerebral β‐Amyloidosis in Aged Captive Rhesus Monkeys a

UNO, H., WALKER, L. C.·1993·Annals of the New York Academy of Sciences

Abstract

Autopsy surveillance of 186 rhesus monkeys aged 20 to 36 years revealed that development of major geriatric diseases such as emphysema, coronary sclerosis, and cancer increased rapidly after the age of 25 years, and nearly 70% of the monkeys in each cohort group died by 30 years. According to our 12‐year longitudinal survey, the age of biosenescence in captive rhesus monkeys begins around 25 years and the maximum longevity is 36 years. The incidence of cerebral β‐amyloidosis associated with plaque formation and cerebral angiopathy was observed in 51 brains of rhesus monkeys aged 25 to 36 years. Lesions were found in 31 of 51 aged brains (60%) and 6 monkeys over 34 years of age were all severely affected. Despite the size of the plaque, nearly all of them showed immunopositive β‐amyloid. Cerebral angiopathy coexisted in 10 of 31 plaque‐positive brains. The basal prefrontal gyms was the most common site and contained the highest density of plaques, followed by the amygdala region. The amyloid in the liver, spleen, adrenal and pancreatic islets in visceral amyloidosis showed no positivity to the β‐amyloid demonstrated in the brain. As in aged human brains, the incidence of age‐dependent cerebral β‐amyloidosis in captive rhesus monkeys showed great individual variation.

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Crossref · 10.1111/j.1749-6632.1993.tb23058.x

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8 of 8 references verified0 citation errors · 0 not checkable

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  • The two largest studies examining the presence of plaques in rhesus monkeys found that approximately 40% of aged animals (25-31 years) did not have any evidence of plaques or CAA after death of natural causes.

    “The two largest studies examining the presence of plaques in rhesus monkeys found that approximately 40% of aged animals (25–31 years) did not have any evidence of plaques or CAA after death of natural causes [164, 165].”

    From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [165]

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Authors
UNO, H., & WALKER, L. C.
Affiliations
  • University of Wisconsin–Madison (US)
  • Johns Hopkins University (US)
Corresponding author
UNO, H.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
1993-09
Volume
695
Issue
1
Pages
232-235
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W2150501036
Cited by
57
References
8
Citations by year
2026: 4 · 2025: 5 · 2024: 7 · 2023: 3 · 2022: 2 · 2021: 5 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 2 · 2012: 2
FWCI
1.11
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Center for Research Resources (RR 00167, P51RR000167)
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 › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
rhesus monkeys, amyloid plaques, cerebral angiopathy, aging, longevity, geriatric diseases, emphysema, coronary sclerosis, cancer, amygdala
MeSH terms
Aging, Animals, Animals, Laboratory, Brain, Longitudinal Studies, Macaca mulatta, Monkey Diseases, Amyloid beta-Peptides, Neurites, Amyloid beta-Protein Precursor, Cerebral Amyloid Angiopathy

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