Year: 2017
Type: article
Abstract: Ab levels in various ways.This growing understanding of "genotypeto-phenotype" relationships in familial AD, coupled with innumerable cell culture and animal model studies of the process, have now led to specific strategies to lower brain Ab levels in order to treat and prevent AD.Although there has been a healthy debate about this 'amyloid (Ab) hypothesis', new evidence further supports the idea that an imbalance between production and clearance of Ab42 may be an initiating factor in AD.For example inheriting the apoE4 gene, which strongly predisposes to AD, impairs clearance of Ab from the brain."Oligomers" (doublets, quadruplets, etc.) of Ab isolated from AD brains can decrease synapse numbr and inhibit synapse function in animals, and injecting the oligomers into healthy adult rats impairs their memory.Ab oligomers modify the tau protein in AD-relevant ways.Human biomarker studies show that low CSF Ab42 levels and high amyloid plaque levels on PET scans precede other AD features by many years.Recent human trials of an Ab antibody (aducanumab) led to dosedependent removal of amyloid plaques from the brain, accompanied by an apparent slowing of cognitive decline.Although many other factors contribute to AD, Ab accumulation has emerged as the most extensively validated and compelling therapeutic target.
Source: Alzheimer s & Dementia
Author: Oskar Hansson
Institution: Lund University
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2766606283