Dysfunction in Neuronal Transport Mechanism Linked to Alzheimer's Disease
Findings confirm mutation-caused problem but also reveal a new therapeutic target
Researchers at the University of California San Diego School of Medicine have confirmed that mutation-caused dysfunction in a process cells use to transport molecules within the cell plays a previously suspected but underappreciated role in promoting the heritable form of Alzheimer’s disease (AD), but also one that might be remedied with existing therapeutic enzyme inhibitors. “Our results further illuminate the complex processes involved in the degradation and decline of neurons, which is, of course, the essential characteristic and cause of AD,” said the study’s senior author Larry Goldstein, PhD, Distinguished Professor in the departments of neuroscience and cellular and molecular medicine at UC San Diego School of Medicine and director of both the UC San Diego Stem Cell Program and Sanford Stem Cell CIinical Center at UC San Diego Health. “But beyond that, they point to a new target and therapy for a condition that currently has no proven treatment or cure.” Click here to read more.
Microsurgery Course Zurich
March 29-April 1, 2017; Zurich, Switzerland
12th World Congress on Brain Injury
March 29-April 1, 2017; New Orleans
2017 National Neuroscience Review
March 31-April 1, 2017; National Harbor, Md.
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