Pittsburgh, December 5, 2014 -- A Huntington's disease research paper authored by University of Pittsburgh Department of Neurological Surgery chairman Robert Friedlander, MD, entitled "Inhibition of Mitochondrial Protein Import by Mutant Huntingtin," has been recommended by F1000Prime.com as being of special significance in its field.
The paper, published in Nature Neuroscience in June of 2014, presents evidence of a direct link between mutant Htt, mitochondrial dysfunction and neuronal pathology, with implications for mitochondrial protein import-based therapies in Huntington's disease.
F1000Prime contributor Stefano Di Donato, MD, chairman of the Department of Research, and director of the Division Biochemistry & Genetics at the Istituto Nazionale Neurologico C Besta, in Milan Italy, cited the paper “because of its broad experimental approach that recapitulates much of the previous investigation showing that Huntington disease (HD) patients and HD animal models develop several mitochondrial defects, and because it provides fresh data that offer an updated assumption on the role of mitochondria in HD pathogenesis.”
According to its website, F1000Prime identifies and recommends important articles in biology and medical research publications. Articles are selected by a peer-nominated global faculty of the world's leading scientists and clinicians who then rate them and explain their importance. Founded in 2002, the organization consists of more than 5,000 scientists and leading experts from around the world in all areas of biology and medicine.
Dr. Friedlander is director of the University of Pittsburgh’s Neuroapoptosis Laboratory. His major research interests lie in the study of the mechanistic pathways of the caspase apoptosis gene family. His work includes the evaluation of treatment strategies for neurodegenerative diseases (Huntington’s and ALS), stroke, brain trauma, and spinal cord injury through the modulation of the caspase-family apoptotic pathways.