Current thinking on the mechanistic basis of Alzheimer's and implications for drug development

C Ising; M Stanley; D M Holtzman

doi:10.1002/cpt.200

Current thinking on the mechanistic basis of Alzheimer's and implications for drug development

Clin Pharmacol Ther. 2015 Nov;98(5):469-71. doi: 10.1002/cpt.200. Epub 2015 Sep 10.

Authors

C Ising¹, M Stanley¹, D M Holtzman¹

Affiliation

¹ Department of Neurology, Hope Center for Neurological Disorders, Charles F and Joanne Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, Missouri, USA.

PMID: 26250900
DOI: 10.1002/cpt.200

Abstract

Alzheimer disease (AD) is the most common cause of dementia and is characterized by the aggregation and accumulation of two proteins in the brain, amyloid-β (Aβ) and tau. Aβ and tau begin to buildup 15-20 years before the clinical onset of AD dementia. Increasing evidence suggests that preventing or decreasing the amount of aggregated forms of both Aβ and tau in the brain can serve as potential disease-modifying treatments for AD.

Publication types

Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review

MeSH terms

Alzheimer Disease / diagnosis
Alzheimer Disease / drug therapy*
Alzheimer Disease / metabolism
Amyloid beta-Peptides / antagonists & inhibitors
Amyloid beta-Peptides / metabolism
Brain / drug effects
Brain / metabolism
Brain / pathology
Drug Discovery / methods*
Humans
Immunotherapy / methods
Thinking*
tau Proteins / antagonists & inhibitors
tau Proteins / metabolism

Substances

Amyloid beta-Peptides
MAPT protein, human
tau Proteins