Malfunctioning astrocytes have long been implicated in development and progression ALS. Work from Don Cleveland’s laboratory at the University of California, San Diego has shown that expression of mutant superoxide dismutase, one of the known genetic causes of ALS, exclusively in astrocytes leads to development of ALS-like symptoms. Other studies, led by Serge Przeborkski’s group at Columbia University, have shown the astrocytes derived from ALS patients trigger death of non-mutant motor neurons (see Feb 2014 news story). Now, investigators from David Rowitch’s laboratory at University of California, San Francisco, provide the first demonstration that astrocytes located in spatially distinct regions of the spinal cord exhibit distinct gene expression and function. In the study, published online April 28, 2014 in Nature, first author Anna Molovsky and colleagues demonstrate that a subset of astrocytes in the spinal cord secrete Semaphorin 3a, a protein necessary for survival of motor neurons of the sensorimotor circuitry controlling reflexive movements. Loss of astrocyte Semaphorin 3a leads to defects in a-motor neuron axon guidance their selective death. This work raises the long-term possibility of developing therapies targeted at astrocyte that are particularly relevant for motor circuits that degenerate in ALS. Click here to read more about these intriguing findings.
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