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Mislocalized Mitochondria Sufficient for Motor Neuron Malaise
August 22, 2014
Messing with mitochondrial motility, even if the organelles functioned perfectly, was sufficient to cause neurological disease in mice, according to a paper in the August 18 Proceedings of the National Academy of Sciences online. The work, from the laboratory of Janet Shaw at the University of Utah School of Medicine in Salt Lake City, neatly separates movement of mitochondria from two of their main functions—respiration and calcium buffering...

Drug and Biomarker Candidates for C9ORF72 ALS and FTD
August 15, 2014

In the August 14 Neuron, researchers offer up a possible treatment and a potential biomarker for amyotrophic lateral sclerosis and frontotemporal dementia caused by mutations in the C9ORF72 gene. Leonard Petrucelli at the Mayo Clinic in Jacksonville, Florida, and Matthew Disney at The...

Blocking Glial Receptor Protects Motor Neurons in Culture and Mice
August 14, 2014

Neuron-supporting glial cells can rebel in amyotrophic lateral sclerosis, turning against the very motor neurons they are supposed to nurse. Blocking the microglial prostanoid receptor DP1 alleviates this toxicity, according to a paper in the August 6 Science Translational Medicine. Researchers...

C9ORF72’s Dirty Work Done by Problem Proteins
August 11, 2014

Hexanucleotide repeat expansions in the C9ORF72 gene are the leading genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis, but alas, researchers do not know whether these repeats wreak havoc by way of wonky RNA molecules or the aggregating dipeptide repeat proteins...

Yeast Chaperone Melts Protein Aggregates
August 8, 2014

Rejiggered chaperones untangle aggregates and refold mutant proteins associated with amyotrophic lateral sclerosis, frontotemporal dementia, and Parkinson’s disease, according to a paper in the July 25 Disease Models & Mechanisms online. The altered chaperones, variants of heat shock...





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