Bile Acid Proves Neuroprotective in Huntington's Model
A mitochondria-protecting, anti-apoptotic bile acid can reduce neurodegeneration and motor deficits in a mouse model of Huntington's disease...
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A mitochondria-protecting, anti-apoptotic bile acid can reduce neurodegeneration and motor deficits in a mouse model of Huntington's disease...
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
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