Engelhardt Eliasz, Resende Elisa de Paula França, Gomes Karina Braga
Universidade Federal do Rio de Janeiro, Instituto de Neurologia Deolindo Couto, Rio de Janeiro RJ, Brazil.
Universidade Federal de Minas Gerais, Faculdade de Medicina, Belo Horizonte MG, Brazil.
Dement Neuropsychol. 2024 Dec 16;18:e2024VR01. doi: 10.1590/1980-5764-DN-2024-VR01. eCollection 2024.
The neuropathological signature of Alzheimer's disease (AD) comprises mainly amyloid plaques, and neurofibrillary tangles, resulting in synaptic and neuronal loss. These pathological structures stem from amyloid dysfunctional metabolism according to the amyloid cascade hypothesis, leading to the formation of plaques, and apparently inducing the initiation of the abnormal tau pathway, with phosphorylation and aggregation of these proteins, ultimately causing the formation of tangles. In this narrative review, the existing hypothesis related to the pathophysiology of AD were compiled, and biological pathways were highlighted in order to identify the molecules that could represent biological markers of the disease, necessary to establish early diagnosis, as well as the selection of patients for therapeutical interventional strategies.
阿尔茨海默病(AD)的神经病理学特征主要包括淀粉样斑块和神经原纤维缠结,导致突触和神经元丧失。根据淀粉样蛋白级联假说,这些病理结构源于淀粉样蛋白代谢功能障碍,导致斑块形成,并明显引发异常的tau蛋白途径启动,伴随这些蛋白质的磷酸化和聚集,最终导致缠结形成。在这篇叙述性综述中,汇总了与AD病理生理学相关的现有假说,并突出了生物学途径,以识别那些可作为疾病生物学标志物的分子,这些分子对于早期诊断以及选择治疗干预策略的患者是必要的。