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Cited by 98Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

A nonhuman primate model of early Alzheimer's disease pathologic change: Implications for disease pathogenesis

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Latimer, Caitlin S., Shively, Carol A., Keene, C. Dirk, Jorgensen, Matthew J., Andrews, Rachel N., Register, Thomas C., Montine, Thomas J., Wilson, Angela M. +6 more·2019·Alzheimer's & Dementia
DOI 10.1016/j.jalz.2018.06.3057PMC PMC6383152
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Abstract

Introduction: Nonhuman primates may serve as excellent models of sporadic age‐associated brain β‐amyloid deposition and Alzheimer's disease pathologic changes. We examined whether a vervet nonhuman primate model recapitulated pathologic, physiologic, and behavioral features of early Alzheimer's disease. Methods: Nine middle‐aged (mean = 11.2 years) and nine aged (mean = 21.7 years) female vervet/African green monkeys underwent cerebrospinal fluid collection, gait speed measurement, and neuroimaging before neuropathologic assessment. Results: β‐amyloid plaques were identified in all aged vervets and paired helical filament tau immunoreactivity was observed in all animals. Cerebrospinal fluid β‐amyloid 42 and gait speed correlated negatively with age and plaque density. Greater plaque and paired helical filament tau burden predicted reduced volumes and CMRg in several brain regions. Discussion: We observed a coordinated set of relationships among neuropathologic, cerebrospinal fluid, imaging, and behavioral modalities consistent with early Alzheimer's disease. Our results support future use of the vervet model to explore disease mechanisms, biomarkers, and novel therapeutic strategies.

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  • Vervets show amyloid deposits but do not have neurofibrillary tangles or tauopathy, so they do not present generalized neurodegeneration.

    “However, there are several limitations; vervets show amyloid deposits but do not have neurofibrillary tangles or tauopathy; therefore, they do not present generalized neurodegeneration.”

    From Alzheimer's Disease: Treatment Strategies and Their Limitations. (2022) · cites this paper as [153]

    The Results (Neuropathology; page not provided) report amyloid plaques and no classic neurofibrillary tangles in the examined vervets, but also report tau immunoreactivity in all animals. The Discussion (Limitations and future directions; page not provided) says vervets lack prominent humanoid tauopathy and widespread neurodegeneration, but only suggests that the latter may be associated with the lack of tauopathy; it does not establish the claim’s categorical absence of tauopathy or its causal “therefore.” (LLM, conf=0.90)

    Experimental — accuracy not yet measured

  • Vervets are best considered a pattern of early amyloid pathology and corresponding behavioral and biomarker changes, making them important for studying early AD stages.

    “Vervets are best considered a pattern of early amyloid pathology and corresponding behavioral and biomarker changes, making them important for the study of the early stages of AD [153].”

    From Alzheimer's Disease: Treatment Strategies and Their Limitations. (2022) · cites this paper as [153]

  • Vervets and other NHP are promising models for exploring early-stage disease mechanisms and biomarkers and testing new therapeutic strategies.

    “Recently, Latimer et al. showed that vervets and other NHP are promising models for exploring early-stage disease mechanisms and biomarkers and testing new therapeutic strategies [153].”

    From Alzheimer's Disease: Treatment Strategies and Their Limitations. (2022) · cites this paper as [153]

  • Non-human primates can model sporadic age-associated brain β-amyloid deposition and pathological changes in AD.

    “Non-human primates (NHP) can be used as models of sporadic age-associated brain β-amyloid deposition and pathological changes in AD.”

    From Alzheimer's Disease: Treatment Strategies and Their Limitations. (2022) · cites this paper as [153]

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References 52 · Cited by 98

Research works printed but not linked: 48

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Authors
Latimer, C. S., Shively, C. A., Keene, C. D., Jorgensen, M. J., Andrews, R. N., Register, T. C., Montine, T. J., Wilson, A. M., Neth, B. J., Mintz, A., Maldjian, J. A., Whitlow, C. T., Kaplan, J. R., & Craft, S.
Affiliations
  • University of Washington (US)
  • Wake Forest University Health Sciences (US)
  • Stanford Medicine (US)
  • Columbia University Irving Medical Center (US)
  • The University of Texas Southwestern Medical Center (US)
Corresponding author
Craft, Suzanne
ORCID
Venue
Alzheimer's & Dementia
Publisher
Wiley
Published
2018-11-19
Volume
15
Issue
1
Pages
93-105
ISSN
  • 1552-5260 (ISSN-L)
  • 1552-5279
DOI
10.1016/j.jalz.2018.06.3057
PMC
PMC6383152
OpenAlex
W2900542217
Cited by
98
References
52
Citations by year
2026: 3 · 2025: 20 · 2024: 13 · 2023: 14 · 2022: 9 · 2021: 20 · 2020: 13 · 2019: 6
FWCI
6.70
Type
journal article
Language
en
Open access
Licence
Locations
  • Alzheimer s & Dementia (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion, other-oa)
  • PubMed Central (acceptedVersion, cc-by-nc-nd)
Funders
  • Wake Forest Alzheimer's Disease Core Center (P30- AG049638)
  • Vervet Research Colony (P40-OD010965)
  • Roena B. Kulynych Center
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
MeSH terms
Alzheimer Disease, Animals, Brain, Chlorocebus aethiops, Disease Models, Animal, Female, Biomarkers, Plaque, Amyloid, Neuroimaging

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