Enabling Technologies 2002 Workshop Summary
This report summarizes discussions at the second workshop on Enabling Technologies for Alzheimer's Disease (AD), held in August 2002 in Bar Harbor, Maine.
6397 RESULTS
Sort By:
This report summarizes discussions at the second workshop on Enabling Technologies for Alzheimer's Disease (AD), held in August 2002 in Bar Harbor, Maine.
A majority of investigators agree that AβPP processing, Aβgeneration, Aβ degradation, and Aβaggregation play a major role in Alzheimer's disease.
Lead discovery is hampered by the absence of good cell-based assays in which to screen libraries against AβPP secretases and other targets.
A key controversy revolved around the value of available mouse models.
Future recommendations from the Enabling Technologies for Alzheimer's Disease Workshop in Bar Harbor, Maine.
Enabling Technologies 2002 Workshop Summary Pathways and Target Discovery: Bar Harbor 2002 Lead Discovery: Bar Harbor 2002 Mouse Models: Bar Harbor 2002 Infrastructure Development: Bar Harbor 2002 Enabling Technologies for Alzheimer Disease Research: 2002
In August 2001, a diverse group of academic and industry investigators from within and outside of Alzheimer's disease research participated in this workshop in Bar Harbor, Maine.
Robert Balaban opened the discussion by observing that heart disease and AD research share certain characteristics, including a weak familial linkage, poor penetrance of some of the known risk factors, and a poor understanding of the interplay between environmental and behavioral factors with gene-gene interactions.
Tim Clark began by laying out recommendations about the information infrastructure required if many groups want to be able to do collective experimentation, to share data, and to exploit automated pattern recognition in that shared data.
Enabling Technologies 2001 Workshop Summary Summary of Scientific Discussions: Bar Harbor Summary of Technology Discussions: Bar Harbor Enabling Technologies for Alzheimer Disease Research: 2001 Bar Harbor Workshop
Neural circuits in the hippocampus defy current views about its structure and function.
Data suggest Aβ-dependent and –independent pathways combine forces to compromise cognition in otherwise healthy people.
In narrower claim, the drug is said to promote ApoE lipidation only in brain regions with extensive amyloid in mice carrying human ApoE4.
Starved for a protein that regulates lipids, neurons suffer and Aβ production soars, according to a new study.
Researchers have partnered with Google-funded Calico Life Sciences to develop a molecule that protects neurons in a variety of conditions.