In the absence of disease, ageing in the human brain is accompanied by mild cognitive dysfunction, gradual volumetric atrophy, a lack of significant cell loss, moderate neuroinflammation, and an increase in the amyloid beta (Aβ) and tau proteins. Conversely, pathologic age-related conditions, particularly Alzheimer's disease (AD), result in extensive neocortical and hippocampal atrophy, neuron death, substantial Aβ plaque and tau-associated neurofibrillary tangle pathologies, glial activation and severe cognitive decline. Humans are considered uniquely susceptible to neurodegenerative disorders, although recent studies have revealed Aβ and tau pathology in non-human primate brains. Here, we investigate the effect of age and AD-like pathology on cell density in a large sample of postmortem chimpanzee brains (n = 28, ages 12–62 years). Using a stereologic, unbiased design, we quantified neuron density, glia density and glia:neuron ratio in the dorsolateral prefrontal cortex, middle temporal gyrus, and CA1 and CA3 hippocampal subfields. Ageing was associated with decreased CA1 and CA3 neuron densities, while AD pathologies were not correlated with changes in neuron or glia densities. Differing from cerebral ageing and AD in humans, these data indicate that chimpanzees exhibit regional neuron loss with ageing but appear protected from the severe cell death found in AD.

This article is part of the theme issue ‘Evolution of the primate ageing process’.

在没有疾病的情况下，人脑的衰老伴随着轻度认知功能障碍、逐渐体积萎缩、明显细胞损失缺乏、中度神经炎症以及β淀粉样蛋白（ Aβ ）和tau蛋白的增加。相反，与年龄相关的病理性疾病，特别是阿尔茨海默病 (AD)，会导致广泛的新皮质和海马萎缩、神经元死亡、大量 A β斑块和 tau 相关神经原纤维缠结病理、神经胶质活化和严重认知能力下降。尽管最近的研究揭示了非人类灵长类动物大脑中的 A β和 tau 蛋白病理学，但人类被认为特别容易受到神经退行性疾病的影响。在这里，我们研究了年龄和 AD 样病理对大量死后黑猩猩大脑样本（ n = 28，年龄 12-62 岁）细胞密度的影响。使用体视学、无偏见的设计，我们量化了背外侧前额叶皮层、颞中回以及 CA1 和 CA3 海马亚区的神经元密度、神经胶质密度和神经胶质与神经元比率。衰老与 CA1 和 CA3 神经元密度下降有关，而 AD 病理与神经元或神经胶质细胞密度的变化无关。与人类的大脑老化和 AD 不同，这些数据表明，黑猩猩随着衰老表现出局部神经元损失，但似乎免受 AD 中严重细胞死亡的影响。

本文是主题“灵长类动物衰老过程的进化”的一部分。