Latest Huntingtin Stories
RICHMOND, Calif. and NEW YORK, April 5, 2011 /PRNewswire/ -- Sangamo BioSciences, Inc. (Nasdaq: SGMO) and CHDI Foundation, Inc.
This molecule, a tiny strand of nucleotides called microRNA-29 or miR-29, has already been shown to be in short supply in certain neurodegenerative illnesses such as Alzheimerâ€™s disease and Huntingtonâ€™s disease.
Lou Gehrigâ€™s disease, or amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration (FTLD) are characterized by protein clumps in brain and spinal-cord cells that include an RNA-binding protein called TDP-43.
Over expressing a transcription factor that promotes the increase in number of mitochondria greatly improves the neurological function of transgenic mice models for Huntington's disease (HD), researchers today told the American Society of Cell Biology's 50th Annual Meeting in Philadelphia.
A new study uncovers a mechanism linking a specific type of cellular stress with brain damage similar to that associated with neurodegenerative disease.
Fisetin, a naturally occurring compound found in strawberries and other fruits and vegetables, slows the onset of motor problems and delays death in three models of Huntington's disease.
Australian scientists have identified the behaviour of the mutant protein â€˜huntingtinâ€™ which leads to the fatal Huntingtonâ€™s disease providing potential targets to treat the disease.
A team of researchers, led by scientists at the University of California, San Diego, have identified a key player in the dramatic loss of neurons in mice and fly models, a discovery that could help illuminate the role of mitochondrial dysfunction in human neurodegenerative disorders, such as Parkinson's disease.
Stanford University School of Medicine researchers have identified several small molecules that mimic a key but cumbersome protein in the brain, a discovery that could open the door to new therapies for a variety of brain disorders.
In a step towards a possible treatment for Huntington's disease, scientists at Albert Einstein College of Medicine of Yeshiva University have shown for the first time that the accumulation of a mutated protein may explain damaging cellular behavior in Huntington's disease.
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