期刊
EXPERT REVIEW OF NEUROTHERAPEUTICS
卷 9, 期 11, 页码 1635-1645出版社
TAYLOR & FRANCIS LTD
DOI: 10.1586/ERN.09.107
关键词
Alzheimer's disease; beta-amyloid; mitogen-activated protein kinase; receptor for advanced glycation end products; synaptic dysfunction
资金
- National Institute of Aging [PO1 AG17490]
- American Health Assistance Foundation (AHAF grant) [A2008-335]
Genetic and biological studies provide strong support for the hypothesis that accumulation of beta amyloid peptide (A beta) contributes to the etiology of Alzheimer's disease (AD). Growing evidence indicates that oligomeric soluble A beta plays an important role in the development of synaptic dysfunction and the impairment of cognitive function in AD. The receptor for advanced glycation end products (RAGE), a multiligand receptor in the immunoglobulin superfamily, acts as a cell surface binding site for A beta and mediates alternations in the phosphorylation state of mitogen-activated protein kinase (MAPKs). Recent results have shown that MAPKs are involved in neurodegenerative processes. In particular, changes in the phosphorylation state of various MAPKs by A beta lead to synaptic dysfunction and cognitive decline, as well as development of inflammatory responses in AD. The present review summarizes the evidence justifying a novel therapeutic approach focused on inhibition of RAGE signaling in order to arrest or halt the development of neuronal dysfunction in AD.
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