Comparative analyses can yield useful insights into human diseases (the interplay of prion research in nonhumans and humans is just one example). Barnes and colleagues' nice analysis of behavior and neuropathology in aging rhesus monkeys is recommended reading for anyone interested in the comparative neurobiology of senescence and Alzheimer's disease.
The scientists undertook their investigation in the context of widely used staging schemes (ATN, ABC) for defining the pathology of AD. They found that some behavioral decline was only evident in animals with the most extreme ATN and ABC scores or abundant cerebral Aβ amyloid angiopathy (CAA). Importantly, by comparing immunohistochemical evidence of abnormal tau with classical stains (thioflavin and silver) for neurofibrillary tangles, they conclude that fully developed tangles were essentially absent in their simian subjects. In short, none displayed complete evidence of human-like AD.
Will fully manifest Alzheimer's disease ever be found in a monkey? The jury is still out, but current evidence suggests that it is at least much less likely than in humans. Aged monkeys deposit impressive amounts of aberrant Aβ in the brain, but neither a multidomain dementia-like disorder nor abundant, widespread, fully developed neurofibrillary tangles has yet been documented.
Elucidating the apparent disconnect in monkeys between Aβ deposition and tangles—which contribute strongly to dementia—could reveal new therapeutic objectives for AD. One might also ask (e.g., using various omic approaches) whether neuroinflammation differs in aged monkeys and humans, and if so, how? Much has been written about the failure of nonhuman animals to model AD, but perhaps we should also consider how they might model the neurobiology of resilience.
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Emory University
Comparative analyses can yield useful insights into human diseases (the interplay of prion research in nonhumans and humans is just one example). Barnes and colleagues' nice analysis of behavior and neuropathology in aging rhesus monkeys is recommended reading for anyone interested in the comparative neurobiology of senescence and Alzheimer's disease.
The scientists undertook their investigation in the context of widely used staging schemes (ATN, ABC) for defining the pathology of AD. They found that some behavioral decline was only evident in animals with the most extreme ATN and ABC scores or abundant cerebral Aβ amyloid angiopathy (CAA). Importantly, by comparing immunohistochemical evidence of abnormal tau with classical stains (thioflavin and silver) for neurofibrillary tangles, they conclude that fully developed tangles were essentially absent in their simian subjects. In short, none displayed complete evidence of human-like AD.
Will fully manifest Alzheimer's disease ever be found in a monkey? The jury is still out, but current evidence suggests that it is at least much less likely than in humans. Aged monkeys deposit impressive amounts of aberrant Aβ in the brain, but neither a multidomain dementia-like disorder nor abundant, widespread, fully developed neurofibrillary tangles has yet been documented.
Elucidating the apparent disconnect in monkeys between Aβ deposition and tangles—which contribute strongly to dementia—could reveal new therapeutic objectives for AD. One might also ask (e.g., using various omic approaches) whether neuroinflammation differs in aged monkeys and humans, and if so, how? Much has been written about the failure of nonhuman animals to model AD, but perhaps we should also consider how they might model the neurobiology of resilience.
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