title: Fyn, a potential target for Alzheimer's disease.
abstract: Alzheimer's disease (AD) is the most common form of dementia characterized by the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles. The mechanisms leading to AD are not completely understood; however, recent evidence suggests that alterations in Fyn, a Src family kinase, might contribute to AD pathogenesis. A number of studies have demonstrated that Fyn is involved in synaptic plasticity, a cellular mechanism for learning and memory. In addition, Fyn plays a role in the regulation of Aβ production and mediates Aβ-induced synaptic deficits and neurotoxicity. Fyn also induces tyrosine phosphorylation of tau. Although many studies have implicated a role for Fyn in AD, the precise cellular and molecular mechanisms require further investigation. Novel insights into the role of Fyn in AD may help identify alternative pharmacological approaches for the treatment of AD.
authors.affiliation: Department of Physiology, University of Toronto, Toronto, ON, Canada.
authors.forename: Kai
authors.initials: K
authors.lastname: Yang
authors.forename: Jillian
authors.initials: J
authors.lastname: Belrose
authors.forename: Catherine H
authors.initials: CH
authors.lastname: Trepanier
authors.forename: Gang
authors.initials: G
authors.lastname: Lei
authors.forename: Michael F
authors.initials: MF
authors.lastname: Jackson
authors.forename: John F
authors.initials: JF
authors.lastname: MacDonald
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000201:enzymology* / Q000473:pathology; D000818:Animals; D016503:Drug Delivery Systems / Q000639:trends; D006801:Humans; D016874:Neurofibrillary Tangles / Q000201:enzymology; D010766:Phosphorylation / Q000502:physiology; D058225:Plaque, Amyloid / Q000188:drug therapy / Q000201:enzymology; D051076:Proto-Oncogene Proteins c-fyn / Q000378:metabolism* / Q000502:physiology
chemical_list: C494957:FYN protein, human; D051076:Proto-Oncogene Proteins c-fyn