痴呆
疾病
背景(考古学)
τ蛋白
陶氏病
药物发现
神经科学
高磷酸化
阿尔茨海默病
药物开发
发病机制
医学
药品
神经退行性变
生物信息学
药理学
生物
病理
细胞生物学
磷酸化
古生物学
作者
Kendall B. E. Moore,Ta-Jung Hung,Jessica S. Fortin
标识
DOI:10.1016/j.drudis.2023.103487
摘要
Alzheimer's disease (AD) is the most common form of dementia, characterized by intracellular neurofibrillary tangles (NFTs) and extracellular β-amyloid (βA) plaques. No disease-modifying therapy is currently available to prevent the progression of, or cure, the disease. Misfolded hyperphosphorylated tau (p-tau) is considered a pivotal point in the pathogenesis of AD and other tauopathies. Compelling evidence suggests that it is a key driver of the accumulation of NFTs and can be directly correlated with the extent of dementia in patients with AD. Therefore, inhibiting tau hyperphosphorylation-induced aggregation could be a viable strategy to discover and develop therapeutics for patients with AD.
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