Alzheimer's disease: The role of proteins in formation, mechanisms, and new therapeutic approaches

早老素 老年斑 载脂蛋白E 淀粉样前体蛋白 P3肽 BACE1-AS系列 淀粉样蛋白(真菌学) 阿尔茨海默病的生物化学 阿尔茨海默病 神经突 生物 神经科学 细胞生物学 疾病 医学 病理 生物化学 体外
作者
Amirreza Gholami
出处
期刊:Neuroscience Letters [Elsevier BV]
卷期号:817: 137532-137532 被引量:19
标识
DOI:10.1016/j.neulet.2023.137532
摘要

Alzheimer's disease (AD) is a progressive neurological disorder that affects the central nervous system (CNS), leading to memory and cognitive decline. In AD, the brain experiences three main structural changes: a significant decrease in the quantity of neurons, the development of neurofibrillary tangles (NFT) composed of hyperphosphorylated tau protein, and the formation of amyloid beta (Aβ) or senile plaques, which are protein deposits found outside cells and surrounded by dystrophic neurites. Genetic studies have identified four genes associated with autosomal dominant or familial early-onset AD (FAD): amyloid precursor protein (APP), presenilin 1 (PS1), presenilin 2 (PS2), and apolipoprotein E (ApoE). The formation of plaques primarily involves the accumulation of Aβ, which can be influenced by mutations in APP, PS1, PS2, or ApoE genes. Mutations in the APP and presenilin (PS) proteins can cause an increased amyloid β peptides production, especially the further form of amyloidogenic known as Aβ42. Apart from genetic factors, environmental factors such as cytokines and neurotoxins may also have a significant impact on the development and progression of AD by influencing the formation of amyloid plaques and intracellular tangles. Exploring the causes and implications of protein aggregation in the brain could lead to innovative therapeutic approaches. Some promising therapy strategies that have reached the clinical stage include using acetylcholinesterase inhibitors, estrogen, nonsteroidal anti-inflammatory drugs (NSAIDs), antioxidants, and antiapoptotic agents. The most hopeful therapeutic strategies involve inhibiting activity of secretase and preventing the β-amyloid oligomers and fibrils formation, which are associated with the β-amyloid fibrils accumulation in AD. Additionally, immunotherapy development holds promise as a progressive therapeutic approach for treatment of AD. Recently, the two primary categories of brain stimulation techniques that have been studied for the treatment of AD are invasive brain stimulation (IBS) and non-invasive brain stimulation (NIBS). In this article, the amyloid proteins that play a significant role in the AD formation, the mechanism of disease formation as well as new drugs utilized to treat of AD will be reviewed.
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