Details

Autor(en) / Beteiligte

• Latimer, Caitlin S.
• Shively, Carol A.
• Keene, C. Dirk
• Jorgensen, Matthew J.
• Andrews, Rachel N.
• Register, Thomas C.
• Montine, Thomas J.
• Wilson, Angela M.
• Neth, Bryan J.
• Mintz, Akiva
• Maldjian, Joseph A.
• Whitlow, Christopher T.
• Kaplan, Jay R.
• Craft, Suzanne

Titel

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

Ist Teil von

• Alzheimer's & dementia, 2019-01, Vol.15 (1), p.93-105

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2019

Link zum Volltext

Quelle

Wiley Online Library All Journals

Beschreibungen/Notizen

• 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. 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. β-amyloid plaques were identified in all aged vervets and paired helical filament tau immunoreactivity was observed in all animals. Cerebrospinal fluid β-amyloid42 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. 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. •First nonhuman primate study applying human National Institute on Aging-Alzheimer's Association guidelines to study neuropathologic changes together with cerebrospinal fluid and imaging biomarkers and behavior.•Observed a coordinated set of relationships in this model consistent with early amyloidosis observed in Alzheimer's disease.•Results provide support for future studies using this model to explore sporadic Alzheimer's disease.