The development of new therapeutics for Alzheimer's disease.
Existing treatments for Alzheimer's disease (AD) fail to address the underlying pathology of the disease; they merely provide short-lived symptomatic relief. Consequently, the progression of AD is unrelenting, leading to a continual decrease in cognitive abilities. Recent advances in understanding the genetic factors that predispose to AD, as well as in biomarker development, have brought with them the promise of earlier and more reliable diagnosis of this disease. As improvements continue to be made in these areas, the shortcomings of current AD treatments appear all the more acute because opportunities for early intervention are hindered by a lack of "curative" or even disease-modifying drugs. This State of the Art report reviews existing AD therapeutics and highlights recent progress made in the design and development of drugs that are aimed at disrupting AD disease progression by inhibition of the protein misfolding of β-amyloid (Aβ) into neurotoxic oligomeric aggregates.
Carter
M D
MD
Department of Chemistry, Dalhousie University, Halifax, Nova Scotia, Canada.
Simms
G A
GA
Weaver
D F
DF
D000367:Age Factors; D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism; D053829:Amyloid Precursor Protein Secretases / Q000037:antagonists & inhibitors; D016229:Amyloid beta-Peptides / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D002986:Clinical Trials as Topic; D018450:Disease Progression; D016503:Drug Delivery Systems; D038362:Glycogen Synthase Kinase 3 / Q000037:antagonists & inhibitors; D006801:Humans; D016874:Neurofibrillary Tangles / Q000378:metabolism; D016875:tau Proteins / Q000819:agonists / Q000037:antagonists & inhibitors
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D016875:tau Proteins; D038362:Glycogen Synthase Kinase 3; D053829:Amyloid Precursor Protein Secretases