Embryonic motor neuron programming factors reactivate immature gene expression and suppress ALS pathologies in postnatal motor neurons.

Emily R Lowry, Tulsi Patel, Jonathon A Costa, Elizabeth Chang, Shahroz Tariq, Hranush Melikyan, Ian Davis, Siaresh Aziz, Georgia Ntermentzaki, Francesco Lotti, Hynek Wichterle

Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY, USA. [email protected]. · pubmed

Paper

Abstract

Aging is a major risk factor in amyotrophic lateral sclerosis (ALS) and other adult-onset neurodegenerative disorders. Whereas young neurons are capable of buffering disease-causing stresses, mature neurons lose this ability and degenerate over time. We hypothesized that the resilience of young motor neurons could be restored by reexpression of the embryonic motor neuron selector transcription factors ISL1 and LHX3. We found that viral reexpression of ISL1 and LHX3 selectively in postnatal motor neurons reactivates aspects of their youthful gene expression program and alleviates key disease-relevant phenotypes in the SOD1

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Research summary

The paper claims that reexpression of embryonic motor neuron factors ISL1 and LHX3 in postnatal motor neurons can reactivate youthful gene expression and alleviate ALS symptoms. This research is relevant as it explores mechanisms to restore youthful characteristics in neurons, potentially addressing the underlying causes of neurodegeneration associated with aging.

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