Synaptic Dysfunction in Alzheimer's Disease and Glaucoma: From Common Degenerative Mechanisms Toward Neuroprotection.
Synaptic Dysfunction in Alzheimer's Disease and Glaucoma: From Common Degenerative Mechanisms Toward Neuroprotection.
复制标题
DOI：
10.3389/fncel.2017.00053
复制
发表时间：
2017
影响因子：
5.3
通讯作者：
Domenici L
中科院分区：
文献类型：
--
作者：
Criscuolo C;Fabiani C;Cerri E;Domenici L
阿尔茨海默病（AD）和青光眼是两种不同的多因素神经退行性疾病，主要影响老年人。在过去的几十年里，常见的病理生理机制已经被阐明。首先，这两种疾病都是进行性的，AD会导致痴呆，青光眼会导致失明。病理上，它们都具有突触功能障碍，神经回路改变，蛋白质聚集体如β淀粉样蛋白（Aβ）和细胞内含有微管相关蛋白家族的过度磷酸化tau的微管内含物的进行性积累。在退行性变的早期阶段，这两种疾病都以突触功能障碍和丝裂原活化蛋白激酶（MAPK）的改变为特征。本文讨论了这两种疾病的共同退行性机制，以及视觉系统作为AD诊断和进展的生物标志物的潜在应用的最新结果。AD和青光眼常见的神经病理改变和机制促进了治疗策略在疾病之间的转移。特别是，我们讨论了过去和现在的证据脑源性神经营养因子（BDNF）的神经保护作用。
Alzheimer’s disease (AD) and glaucoma are two distinct multifactorial neurodegenerative diseases, primarily affecting the elderly. Common pathophysiological mechanisms have been elucidated in the past decades. First of all both diseases are progressive, with AD leading to dementia and glaucoma inducing blindness. Pathologically, they all feature synaptic dysfunction with changes of neuronal circuitry, progressive accumulation of protein aggregates such as the beta amyloid (Aβ) and intracellular microtubule inclusions containing hyperphosphorylated tau, which belongs to microtubule associated protein family. During an early phase of degeneration, both diseases are characterized by synaptic dysfunction and changes of mitogen-activated protein kinases (MAPK). Common degenerative mechanisms underlying both diseases are discussed here, along with recent results on the potential use of the visual system as a biomarker for diagnosis and progression of AD. Common neuropathological changes and mechanisms in AD and glaucoma have facilitated the transfer of therapeutic strategies between diseases. In particular, we discuss past and present evidence for neuroprotective effects of brain-derived neurotrophic factor (BDNF).