Alzheimer's disease (AD) is emerging as the most prevalent and socially disruptive illness of aging populations as more people live long enough to become affected. Although AD is placing a considerable and increasing burden on patients, caregivers and society, it represents the largest unmet medical need in neurology, because it is currently incurable. In the last few years, the amyloid hypothesis, which points to amyloid β-peptide (Aβ) as the initiating factor in AD, had a central role in the development of therapeutic strategies for AD. However, the recent clinical trials targeting Aβ have been disappointing. The need to obtain a comprehensive picture of AD pathogenesis is strong as ever. In this framework, this review focuses on Aβ effects on the synapses and on ADAM10, the enzyme able to prevent Aβ formation, analysing its function in the synapse, its contribution to AD pathology and discussing its potential as pharmacological target.
Synaptic dysfunction in Alzheimer's disease : from the role of amyloid β-peptide to the α-secretase ADAM10 / S. Musardo, E. Marcello. - In: EUROPEAN JOURNAL OF PHARMACOLOGY. - ISSN 0014-2999. - 817(2017), pp. 30-37.
|Titolo:||Synaptic dysfunction in Alzheimer's disease : from the role of amyloid β-peptide to the α-secretase ADAM10|
|Parole Chiave:||ADAM10; Alzheimer Disease; Amyloid; Synapse; Trafficking; Pharmacology|
|Settore Scientifico Disciplinare:||Settore BIO/14 - Farmacologia|
|Progetto:||Development of innovative tools for Alzheimer Disease therapy|
Validating ADAM10 as therapeutic target for dementia
Development of innovative tools for Alzheimer Disease therapy
|Data di pubblicazione:||2017|
|Digital Object Identifier (DOI):||http://dx.doi.org/10.1016/j.ejphar.2017.06.018|
|Appare nelle tipologie:||01 - Articolo su periodico|