PIP2: a new key player in Alzheimer's disease.

Cellscience Pub Date : 2008-07-27
Ottavio Arancio
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引用次数: 0

Abstract

Amyloid-beta peptide (Abeta) oligomers are likely to underlie the earliest amnesic changes in Alzheimer's disease through impairment of synaptic function. A recent work from the laboratories of Tae-Wan Kim and Gilbert Di Paolo and colleagues implicates the phosphoinositide signaling pathway in synaptic changes due to elevation of Abeta oligomers. Given that phosphatidylinositol 4,5-bisphosphate (PIP2) is central to many essential processes in neurons including neuronal and synaptic function, reduction in the levels of PIP2 in response to oligomeric Abeta could explain many of the phenotypes that have been observed with oligomeric Abeta. The data open up a new target for protecting neurons from Abeta-induced synaptic impairment.

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PIP2:阿尔茨海默病的新关键参与者
淀粉样蛋白- β肽(Abeta)寡聚物可能通过突触功能损伤导致阿尔茨海默病早期失忆症的改变。Tae-Wan Kim和Gilbert Di Paolo及其同事的实验室最近的一项研究表明,由于β寡聚物的升高,磷酸肌苷信号通路在突触变化中起作用。考虑到磷脂酰肌醇4,5-二磷酸(PIP2)在包括神经元和突触功能在内的许多神经元基本过程中起着核心作用,PIP2水平的降低对低聚Abeta的反应可以解释低聚Abeta所观察到的许多表型。这些数据为保护神经元免受β诱导的突触损伤开辟了一个新的目标。
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