Displaying items by tag: center for neurodegeneration and experimental therapeutics
Human proteins identified that explain inter-individual differences in functional brain connectivity
This is a step toward an understanding of the brain that ultimately describes the mechanistic basis of human cognition and behavior.
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This finding suggests that therapy to remodel synapses could help memory in old age and dementia patients.
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By prohibiting the Activin A protein from functioning, researchers were able to halt the development of dyskinesia symptoms and effectively erase the brain’s “bad memory” response to L-DOPA treatments.
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Multiple system atrophy is a rare and fatal neurodegenerative disease, with no known disease modifying therapy.
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The M.D./Ph.D. student has since moved on to clinical studies, but the research into possible drugs to treat Alzheimer’s disease continues.
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TCE is a known environmental risk factor for parkinsonism. UAB researchers will evaluate whether T cell activation caused by TCE exposure leads to cognitive decline.
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In a mouse model, border-associated macrophages, not microglia, were essential for the neuroinflammation that precedes neurodegradation. Targeting this subset could be a disease-modifying therapy in neurodegenerative disease.
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Record $95 million Heersink lead gift to advance strategic growth and biomedical innovation.
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New results suggest the answer is no, implying that the role of tau in the pathogenesis of Lewy body dementias is distinct from Alzheimer’s disease.
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The University of Alabama at Birmingham’s Dr. Michelle Gray has been elected to be a member on the Scientific Board of the Hereditary Disease Foundation.
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The mechanism of widespread reorganization of DNA methylation may be a therapeutic target to prevent or reverse dyskinesia.
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Researchers have found that an interaction between a mutant gene and alpha synuclein in neurons leads to hallmark pathologies seen in Parkinson’s disease, findings that may lead to new mechanisms and targets for neuroprotection.
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An intriguing paper by Harvard researchers has everyone talking, thanks to widespread media coverage. Neuroscientist Erik Roberson, M.D., Ph.D., co-director of UAB's Center for Neurodegeneration and Experimental Therapeutics, offers his thoughts on a discovery gone viral.
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The biomarker, the protein kinase LRRK2, is a promising candidate for future exploration.
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The drug inhibits the activity of a kinase enzyme called LRRK2, and it showed no pathology in rat lungs, kidneys or livers.
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