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Huntington disease begins to take hold early on
April 17, 2009A global analysis of brain proteins over a 10-week period in a mouse model of Huntington Disease has revealed some new insights into this complex neurodegenerative disorder. For example, profound changes (comparable to those seen in late-stage HD) actually occur well before any disease symptoms show up, and most of the changes are confined to a specific stage during disease progression. These findings should aid in determining the optimal times for therapies that aim to treat or cure this disease.
While HD (which is brought on by mutations in the gene for Huntingtin has been studied extensively at the cellular level, much of the work has been focused on late-stage disease when the various symptoms (declines in both motor coordination and cognitive ability) have already manifested. But since HD is an inherited condition, changes likely occur much earlier, and to get a better sense of disease progression, Claus Zabel and colleagues used proteomics to analyze the brains of HD mice at 2, 4, 6, 8, and 12 weeks of age, a period that covers absence of any disease-related phenotypes to the pronounced disease state.
Unexpectedly, they found a large number of protein alterations (almost 6% of the total) as early as 2 weeks of age; a significant portion of these changes contributed to an increase in glucose metabolism, which corresponds to the weight loss that occurs early during HD progression. As the disease progressed over 10 weeks, though, the affected proteins kept changing. In fact, about 70% of observed changes were confined to one of the five time points examined and no proteins were similarly altered in all 5 stages.
Therefore this study, appearing in the April issue of Molecular and Cellular Proteomics, argues against an HD model in which there is a gradual increase in the number and magnitude of protein changes and instead leans toward a more dynamic pathology. Zabel and colleagues suggest that these early changes affect late stage disease by irreversibly changing the biochemical activity in the mouse brain.
American Society for Biochemistry and Molecular Biology
Therefore this study, appearing in the April issue of Molecular and Cellular Proteomics, argues against an HD model in which there is a gradual increase in the number and magnitude of protein changes and instead leans toward a more dynamic pathology. Zabel and colleagues suggest that these early changes affect late stage disease by irreversibly changing the biochemical activity in the mouse brain.
American Society for Biochemistry and Molecular Biology
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Cognitive dysfunction reversed in mouse model of Down syndrome
A study by neuroscientist William C. Mobley, MD, PhD, chair of the Department of Neurosciences at the University of California, San Diego School of Medicine, and colleagues at Stanford University Medical School has demonstrated a possible new approach to slowing the inevitable progression of cognitive decline found in Down's syndrome.
Researchers find potential treatment for Huntington's disease
Investigators at Burnham Institute for Medical Research (Burnham), the University of British Columbia's Centre for Molecular Medicine and Therapeutics and the University of California, San Diego have found that normal synaptic activity in nerve cells (the electrical activity in the brain that allows nerve cells to communicate with one another) protects the brain from the misfolded proteins associated with Huntington's disease.
Novel mouse gene reduces major pathologies associated with Alzheimer's disease
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Mouse gene suppresses Alzheimer's plaques and tangles
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Caltech researchers show efficacy of gene therapy in mouse models of Huntington's disease
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Inhibitor of heat shock protein is a potential anticancer drug, Penn study finds
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Widely used cholesterol-lowering drug may prevent progression
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Member of NFL Hall of Fame diagnosed with degenerative brain disease
The Center for the Study of Traumatic Encephalopathy (CSTE) at Boston University School of Medicine (BUSM) announced today that a recently deceased member of the NFL Hall of Fame suffered from the degenerative brain disease Chronic Traumatic Encephalopathy (CTE) when he died, becoming the 10th former NFL player diagnosed with the disease.
Trembling hands and molecular handshakes
Fragile X tremor/ataxia syndrome (FXTAS) is a recently recognized condition, which is actually one of the most prevalent heritable neurodegenerative diseases.
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