Giannakopoulos P, Silhol S, Jallageas V, Mallet J, Bons N, Bouras C, Delaère P
Neuromorphologie Fonctionnelle, Ecole Pratique des Hautes Etudes, Université de Montpellier II, France.
Acta Neuropathol. 1997 Aug;94(2):131-9. doi: 10.1007/s004010050684.
Recent studies have revealed the presence of tau protein-immunoreactive accumulations and beta amyloid protein (A beta) deposits in the cerebral cortex of the aged mouse lemur, Microcebus murinus. To examine the age-related evolution of these changes and compare their regional distribution to that reported for humans and nonhuman primates with Alzheimer's disease lesions, we performed a quantitative analysis of a large series of mouse lemurs aged from 1 to 13 years. The prevalence and density of tau protein-immunoreactive accumulations in the neocortex of this prosimian increased steadily with age. Neocortical areas were frequently affected even in young mouse lemurs, whereas the subiculum and entorhinal cortex were only involved occasionally in animals older than 8 years. As in anthropoid primates, diffuse A beta deposits were often observed in the cerebral cortex and amygdala of old mouse lemurs. Although all animals with diffuse A beta deposits had tau protein-immunoreactive accumulations in the neocortex, no correlation was found between the densities of these lesions in each area and among the areas studied. The age-dependent progression of tau protein-immunoreactive accumulations indicates that this prosimian may represent a valuable model for the study of the biochemical mechanisms of brain aging, while the relative sparing of hippocampus in mouse lemurs contrasts sharply with previous reports on neurofibrillary tangle formation in humans, and suggests that this animal may also be useful to investigate the biological characteristics of neuroprotection in this area. Furthermore, the present data indicate that A beta deposition in mouse lemurs is not age dependent, but occurs in a few vulnerable old animals.
最近的研究显示，在老年小鼠狐猴（Microcebus murinus）的大脑皮层中存在tau蛋白免疫反应性积聚和β淀粉样蛋白（Aβ）沉积。为了研究这些变化与年龄相关的演变，并将其区域分布与患有阿尔茨海默病病变的人类和非人类灵长类动物的情况进行比较，我们对大量年龄在1至13岁之间的小鼠狐猴进行了定量分析。这种原猴新皮层中tau蛋白免疫反应性积聚的患病率和密度随年龄稳步增加。即使在年轻的小鼠狐猴中，新皮层区域也经常受到影响，而在8岁以上的动物中，下托和内嗅皮层只是偶尔受累。与类人猿灵长类动物一样，在老年小鼠狐猴的大脑皮层和杏仁核中经常观察到弥漫性Aβ沉积。虽然所有有弥漫性Aβ沉积的动物在新皮层中都有tau蛋白免疫反应性积聚，但在每个区域以及所研究的区域之间，这些病变的密度之间没有发现相关性。tau蛋白免疫反应性积聚的年龄依赖性进展表明，这种原猴可能是研究大脑老化生化机制的有价值模型，而小鼠狐猴海马相对较少受累与先前关于人类神经原纤维缠结形成的报道形成鲜明对比，并表明这种动物也可能有助于研究该区域神经保护的生物学特性。此外，目前的数据表明，小鼠狐猴中的Aβ沉积不依赖于年龄，而是发生在少数易患的老年动物中。
