陶氏病
进行性核上麻痹
医学
τ蛋白
多巴胺能
基因亚型
神经科学
Tau病理学
病理
阿尔茨海默病
疾病
内科学
神经退行性变
多巴胺
生物
遗传学
基因
作者
Madia Lozupone,Vittorio Dibello,Antonio Daniele,Vincenzo Solfrizzi,Emanuela Resta,Francesco Panza
标识
DOI:10.1080/14656566.2024.2345734
摘要
Pharmacological therapy for PSPS may interfere with the aggregation process or promote the clearance of abnormal tau aggregates. A variety of past and ongoing disease-modifying therapies targeting tau in PSPS included genetic, microtubule-stabilizing compounds, anti-phosphorylation, and acetylation agents, antiaggregant, protein removal, antioxidant neuronal and synaptic growth promotion therapies. New pharmacological gene-based approaches may open alternative prevention pathways for the deposition of abnormal tau in PSPS such as antisense oligonucleotide (ASO)-based drugs. Moreover, kinases and ubiquitin-proteasome systems could also be viable targets.
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