Abstract
Recent Advances from the Bench Toward the Bedside in Alzheimer's Disease
Highlights
Affecting approximately 30 million people worldwide, Alzheimer's disease (AD) is the most common cause of dementia and there is no cure
The overexpression of mutant amyloid precursor protein (APP) and PSEN1 leads to increased Aβ and plaque formation, yet little to no tau pathology is present in these models
Preclinical studies investigating therapeutic efficacy occurred in models lacking the full breadth of clinical disease, which could be one explanation for why these therapies fail to translate to efficacy in Phase III clinical trials
Summary
Affecting approximately 30 million people worldwide, Alzheimer's disease (AD) is the most common cause of dementia and there is no cure. 20 years ago (Scheuner et al, 1996), several mutations in the genes encoding amyloid precursor protein (APP) and presenilin (PSEN) were discovered to give rise to early-onset familial AD (FAD) through the increased production of the plaque forming peptide, Aβ. The overexpression of mutant APP and PSEN1 leads to increased Aβ and plaque formation, yet little to no tau pathology is present in these models.
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