Aging impact on amyloid precursor protein neuronal trafficking
Aging impact on amyloid precursor protein neuronal trafficking
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DOI：
10.1016/j.conb.2022.102524
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发表时间：
2022-03-15
影响因子：
5.7
通讯作者：
Almeida, Claudia Guimas
中科院分区：
文献类型：
--
作者：
Burrinha, Tatiana;Almeida, Claudia Guimas
神经元寿命很长。神经元老化可能会增加阿尔茨海默病的风险。神经元膜运输如何在衰老过程中维持突触功能？在正常的老年大脑中，神经元内β-淀粉样蛋白（Ab）积累而没有阿尔茨海默病突变或风险变体。然而，神经元老化的变化是否会增强抗体的积累？我们回顾了淀粉样前体蛋白在神经元中的膜运输，并强调了其在抗体产生中的重要性。重要的是，我们回顾了支持衰老对神经元膜运输、APP加工以及随后的Ab产生的影响的证据。在神经元老化过程中，需要剖析APP运输的分子调节因子，以确定延迟突触衰退和预防阿尔茨海默病的策略。
Neurons live a lifetime. Neuronal aging may increase the risk of Alzheimer's disease. How does neuronal membrane trafficking maintain synapse function during aging? In the normal aged brain, intraneuronal beta-amyloid (Ab) accumulates without Alzheimer's disease mutations or risk variants. However, do changes with neuronal aging potentiate Ab accumulation? We reviewed the membrane trafficking of the amyloid precursor protein in neurons and highlighted its importance in Ab production. Importantly, we reviewed the evidence supporting the impact of aging on neuronal membrane trafficking, APP processing, and consequently Ab production. Dissecting the molecular regulators of APP trafficking during neuronal aging is required to identify strategies to delay synaptic decline and protect from Alzheimer's disease.