Finch Caleb E, Austad Steven N
Davis School of Gerontology and Department of Biological Sciences, University of Southern California, Los Angeles, CA, USA.
Department of Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
Neurobiol Aging. 2015 Feb;36(2):553-5. doi: 10.1016/j.neurobiolaging.2014.10.025. Epub 2014 Oct 23.
That Alzheimer's disease (AD) might be a human-specific disease was hypothesized by Rapoport in 1989. Apes and humans share an identical amyloid beta (Aβ) peptide amino acid sequence and accumulate considerable Aβ deposits after age 40 years, an age when amyloid plaques are uncommon in humans. Despite their early Aβ buildup, ape brains have not shown evidence dystrophic neurites near plaques. Aging great ape brains also have few neurofibrillary tangles, with one exception of 1 obese chimpanzee euthanized after a stroke who displayed abundant neurofibrillary tangles, but without the typical AD distribution. We discuss the need for more exacting evaluation of neuron density with age, and note husbandry issues that may allow great apes to live to greater ages. We remain reserved about expectations for fully developed AD-like pathology in the great apes of advanced ages and cautiously support Rapoport's hypothesis.
1989年，拉波波特提出阿尔茨海默病（AD）可能是人类特有的疾病这一假说。猿类和人类的β淀粉样蛋白（Aβ）肽氨基酸序列相同，并且在40岁之后会积累大量Aβ沉积物，而这个年龄在人类中淀粉样斑块并不常见。尽管猿类大脑早期就有Aβ积累，但在斑块附近并未显示出营养不良性神经突的证据。衰老的大猩猩大脑中神经原纤维缠结也很少，只有一只肥胖的黑猩猩在中风后被安乐死，其显示出大量神经原纤维缠结，但没有典型的AD分布。我们讨论了随着年龄增长对神经元密度进行更严格评估的必要性，并指出了可能使大猩猩活到更高年龄的饲养问题。对于老年大猩猩中完全发展的类AD病理学的预期，我们仍持保留态度，并谨慎支持拉波波特的假说。
