Amyloidosis increase is not attenuated by long-term calorie restriction or related to neuron density in the prefrontal c
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ORIGINAL ARTICLE
Amyloidosis increase is not attenuated by long-term calorie restriction or related to neuron density in the prefrontal cortex of extremely aged rhesus macaques GA Stonebarger & HF Urbanski & RL Woltjer & KL Vaughan & DK Ingram & PL Schultz & SM Calderazzo & JA Siedeman & JA Mattison & DL Rosene & SG Kohama
Received: 8 May 2020 / Accepted: 24 August 2020 # American Aging Association 2020
Abstract As human lifespan increases and the population ages, diseases of aging such as Alzheimer’s disease (AD) are a major cause for concern. Although calorie restriction (CR) as an intervention has been shown to increase healthspan in many species, few studies have examined the effects of CR on brain aging in primates. Using postmortem tissue from a cohort of extremely aged rhesus monkeys (22–44 years old, average age 31.8 years) from a longitudinal CR study, we measured immunohistochemically labeled amyloid beta plaques in Brodmann areas 32 and 46 of the prefrontal cortex, areas that play key roles in cognitive processing, are sensitive to aging and, in humans, are also susceptible to AD pathogenesis. We also evaluated these areas for cortical neuron loss, which has not been observed in younger cohorts of aged monkeys. We found a
significant increase in plaque density with age, but this was unaffected by diet. Moreover, there was no change in neuron density with age or treatment. These data suggest that even in the oldest-old rhesus macaques, amyloid beta plaques do not lead to overt neuron loss. Hence, the rhesus macaque serves as a pragmatic animal model for normative human aging but is not a complete model of the neurodegeneration of AD. This model of aging may instead prove most useful for determining how even the oldest monkeys are protected from AD, and this information may therefore yield valuable information for clinical AD treatments.
Keywords Aging . Alzheimer’s disease . Amyloid plaques . Diet . Neurodegeneration . Neuron number
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11357-020-00259-0) contains supplementary material, which is available to authorized users. G. Stonebarger : H. Urbanski Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR 97239, USA G. Stonebarger : H. Urbanski : S. Kohama (*) Division of Neuroscience, Oregon National Primate Research Center, 505 NW 185th Avenue, Beaverton, OR 97006, USA e-mail: [email protected] R. Woltjer Department of Pathology, Oregon Health & Science University, Portland, OR 97239, USA
K. Vaughan : J. Mattison Translational Gerontology Branch, National Institute on Aging Intramural Research Program, NIH, Dickerson, MD 20842, USA K. Vaughan Charles River, Wilmington, MA 01867, USA D. Ingram Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA P. Schultz : S. Calderazzo : J. Siedeman : D. Rosene Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MD 02218, USA
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Abbreviations Aβ Amylo
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