Related Experiment Video
Updated: Aug 9, 2026

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
Published on: May 22, 2018
Treating Alzheimer's disease by inactivating bioactive amyloid beta peptide
1Cellular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Road, La Jolla, California 92037-1099, USA. yliu@salk.edu
Abstract:
Treating Alzheimer's disease (AD) is one of today's biggest unmet medical needs. The drugs currently available transiently relieve some symptoms but have no significant effects on the progression of the disease. Progress in the past decade suggests that the amyloidogenesis of the inactive monomeric amyloid beta peptide (Abeta) into a subset of toxic Abeta polymers is responsible for neurodegeneration in AD. Not all forms of Abeta aggregates are damaging, for there are patients whose brains accumulated large amounts of Abeta in the form of plaques, but they had no obvious neurodegeneration and symptoms of dementia. Since Abeta can polymerize into many types of polymers or aggregates, the form of Abeta that induces neurodegeneration in AD, defined here as bioactive Abeta, is not clear. Preventing the formation of bioactive Abeta or inactivating previously formed bioactive Abeta is a promising approach for treating AD. This review describes our efforts to develop a cell-based assay for detecting bioactive Abeta, to verify the concept of bioactive Abeta in an animal model of AD and in post mortem brain tissue from AD patients, and to use this assay to screen for drugs that can inactivate bioactive Abeta. These studies show the proof in principle that inactivating bioactive Abeta is a promising approach to treat AD. Several promising compounds that can inactivate bioactive Abeta species are also described.
More Related Videos
Related Concept Videos
Alzheimer's Disease: Treatment
Alzheimer's Disease: Overview
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer Disease ll: Pathophysiology
Amyloid Fibrils
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Alzheimer Disease l: Introduction

