Enabling Technologies for Alzheimer Disease Research: 2003 Bar Harbor Workshop
Enabling Technologies 2003 Workshop Summary Recommendations: A Report from Bar Harbor 2003 Enabling Technologies for Alzheimer Disease Research: 2003 Bar Harbor Workshop
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Enabling Technologies 2003 Workshop Summary
The first day of Enabling Technologies 2003 focused on the natural history of Alzheimer's disease, fundamental cell biology, and mechanisms of neurodegeneration.
Recommendations: A Report from Bar Harbor 2003
Recommendations for future research from the Enabling Technologies for Alzheimer's Disease Workshop in Bar Harbor, Maine.
Does ER Stress Protein Contribute to Biopolar Disorder?
The risk of developing bipolar disorder appears to increase in people who carry a particular polymorphism of a transcription factor that aids in the clearance of "junk" protein from the endoplasmic reticulum...
Immune Effector and Calcium Sensor: Roster of Synaptic Proteins Grows by Two
Subtle changes in synaptic transmission are likely responsible for learning and memory, but the molecular cast of characters at play in this complex process is only partly known. Two papers in this week's Nature Neuroscience online introduce two new players...
MHC Polymorphisms Influence Immune Response to Amyloid β
Genetic polymorphisms in the major histocompatibility complex (MHC)—a group of proteins that help the immune system distinguish self from non-self—can profoundly influence the immune response mounted against an amyloid β vaccine...
Measuring Protein Folding One Molecule at a Time
Scientists have long puzzled over the following conundrum: If the activity of a protein solution drops by half, have half the molecules completely lost activity, or have all the proteins lost half their activity? The answer, most likely, is that...
Another Notch in the Presenilin Belt
Presenilin, the enzyme that proteolytically cleaves amyloid-β precursor protein (APP) and Notch, also processes the p75 neurotrophin receptor (p75NTR)...
Oligomers in AD: Too Much of a Bad Thing?
Neuritic plaques are classic, obvious markers of Alzheimer’s disease, but it is a puzzle why their density is a poor predictor of disease symptoms. Recently, scientists have come to suspect that soluble oligomeric, not fibrillary, β, may be the culprit in synaptic degeneration in AD...
Age-Related Changes in Brain Function—Synapses and Mitochondria Fingered
If the old saying that elephants never forget is true, then it may be because in mammals, synaptic branches laid down in early life are stable into middle age...
Learning and Neuroprotective Role Proffered for Glucagon-Derived Peptide
In this week's Nature Medicine, researchers reveal that glucagon-like peptide-1 (GLP-1), a product of proglucagon processing, may have an important role in learning and neuroprotection...
Coping with Copper—Minute Amount of Metal Plagues Rabbit Brain
This week's PNAS early online edition reports that, depending on the diet, even minor amounts of copper can lead to both amyloid plaques and a memory deficit in rabbits...
Changing Channels—Modifier Gene Renders Mutation Lethal
Some diseases, such as familial Alzheimer's disease (FAD), arise from a mutation in a single gene. In sporadic AD, however, complex interactions among multiple genes underlie the phenotype, and under these circumstances...
Repairing Damaged Tissues—Viruses Get into the Akt
Reporting in Science, Fred Gage and colleagues reveal that they can delay the progression of ALS and prolong life in mouse models by delivering appropriate growth stimuli to neurons in the central nervous system...
Linking APP with Cell Cycle Reentry and Apoptosis—One Kinase Does the Trick
Contentions that activation of the cell cycle and apoptosis at least partly underlie the neurodegeneration seen in Alzheimer's disease (AD) have slowly gained experimental support. Now, a report in the July 30 Journal of Neuroscience suggests that...
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