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Aging-related Alzheimer's disease-like neuropathology and functional decline in captive vervet monkeys (Chlorocebus aethiops sabaeus)

期刊

AMERICAN JOURNAL OF PRIMATOLOGY
卷 83, 期 11, 页码 -

出版社

WILEY
DOI: 10.1002/ajp.23260

关键词

African green monkey; Alzheimer' s disease; cognitive decline; gait speed; vervet

类别

资金

  1. National Institutes of Health (NIH) [K08 AG065426, R01HL087103, RF1AG058829, P30 AG049638]
  2. Department of Pathology, Wake Forest School of Medicine Intramural Grant
  3. Wake Forest Claude D. Pepper Older Americans Independence Center [P30 AG21332]
  4. Wake Forest Clinical and Translational Science Institute [NCATS UL1TR001420]
  5. Nancy and Buster Alvord Endowment
  6. Vervet Research Colony [P40-OD010965]

向作者/读者索取更多资源

The study highlights the vervet monkey as a suitable model for age-related Alzheimer's disease, with traits related to cognitive function, physical function, glucose handling, and more. Evidence suggests that aging vervets exhibit characteristics consistent with early AD, making them a valuable model for LOAD research. Studies show relationships between AD-like neuropathology in vervets and modifiable risk factors, shaping future research to understand mechanisms underlying divergent neurocognitive aging trajectories and develop interventions for LOAD.
Age-related neurodegeneration characteristic of late-onset Alzheimer's disease (LOAD) begins in middle age, well before symptoms. Translational models to identify modifiable risk factors are needed to understand etiology and identify therapeutic targets. Here, we outline the evidence supporting the vervet monkey (Chlorocebus aethiops sabaeus) as a model of aging-related AD-like neuropathology and associated phenotypes including cognitive function, physical function, glucose handling, intestinal physiology, and CSF, blood, and neuroimaging biomarkers. This review provides the most comprehensive multisystem description of aging in vervets to date. This review synthesizes a large body of evidence that suggests that aging vervets exhibit a coordinated suite of traits consistent with early AD and provide a powerful, naturally occurring model for LOAD. Notably, relationships are identified between AD-like neuropathology and modifiable risk factors. Gaps in knowledge and key limitations are provided to shape future studies to illuminate mechanisms underlying divergent neurocognitive aging trajectories and to develop interventions that increase resilience to aging-associated chronic disease, particularly, LOAD.

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