Several research studies point to the fact that sensory and cognitive reductions like cataracts, deafness, macular degeneration, or even lack of activity after job retirement, precede the onset of Alzheimer’s disease. To simulate Alzheimer’s disease earlier stages, which manifest in sensory cortices, we used a computational model of the koniocortex that is the first cortical stage processing sensory information. The architecture and physiology of the modeled koniocortex resemble those of its cerebral counterpart being capable of continuous learning. This model allows one to analyze the initial phases of Alzheimer’s disease by “aging” the artificial koniocortex through synaptic pruning, by the modification of acetylcholine and GABA-A signaling, and by reducing sensory stimuli, among other processes. The computational model shows that during aging, a GABA-A deficit followed by a reduction in sensory stimuli leads to a dysregulation of neural excitability, which in the biological brain is associated with hypermetabolism, one of the earliest symptoms of Alzheimer’s disease.

中文翻译：

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阿尔茨海默病是 GABA-A 缺陷大脑中刺激减少的结果：神经计算模型

几项研究表明，在阿尔茨海默病发病之前，感觉和认知能力下降，如白内障、耳聋、黄斑变性，甚至退休后缺乏活动。为了模拟阿尔茨海默病的早期阶段，这在感觉皮层中表现出来，我们使用了第一个皮质阶段处理感觉信息的 koniocortex 的计算模型。建模的角膜皮质的结构和生理学类似于能够持续学习的大脑对应物的结构和生理学。该模型允许人们通过突触修剪、乙酰胆碱和 GABA-A 信号的修饰以及减少感官刺激等过程来“老化”人工角膜皮质，从而分析阿尔茨海默病的初始阶段。计算模型表明，在老化过程中，