Commentary
Cellscience Reviews Vol 5 No 1
ISSN 1742-8130


PIP2: a new key player in Alzheimer’s disease


Ottavio Arancio

Department of Pathology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, USA.

Received 20th July © Cellscience 2008


Amyloid-β peptide (Aβ) 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 Aβ 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 Aβ could explain many of the phenotypes that have been observed with oligomeric Aβ. The data open up a new target for protecting neurons from Aβ-induced synaptic impairment.
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