| Literature DB >> 28494972 |
Stefania Forner1, David Baglietto-Vargas1, Alessandra C Martini1, Laura Trujillo-Estrada1, Frank M LaFerla2.
Abstract
Alzheimer's disease (AD) is characterized by memory loss, cognitive decline, and devastating neurodegeneration, not only as a result of the extracellular accumulation of beta-amyloid peptide (Aβ) and intracellular accumulation of tau, but also as a consequence of the dysfunction and loss of synapses. Although significant advances have been made in our understanding of the relationship of the pathological role of Aβ and tau in synapse dysfunction, several questions remain as to how Aβ and tau interdependently cause impairments in synaptic function in AD. Overall, more insight into these questions should enable researchers in this field to develop novel therapeutic targets to mitigate or delay the cognitive deficits associated with this devastating disease.Entities:
Keywords: Alzheimer’s disease; beta-amyloid; synaptic impairment; tau
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Year: 2017 PMID: 28494972 DOI: 10.1016/j.tins.2017.04.002
Source DB: PubMed Journal: Trends Neurosci ISSN: 0166-2236 Impact factor: 13.837