Clinical Significance
Increased expression of this protein is associated with schizophrenia and is seen in a variety of human tumor cell lines. Also, aberrant release of this protein is associated with the progression of Alzheimer's disease.
Additionally, the terminal Schwann cells of ALS mice (SOD1 mutant) express Sema3A at fast-fatigable fiber neuromuscular junctions greater than wild-type mice. This expression is greatest pre-symptomatically corresponding to ALS progression in which fast-fatigable fiber denervation precedes clinical symptoms. Because Sema3A is involved in growth cone collapse and axon pruning and repulsion, it potentially holds a causal relationship to synaptic weakening and denervation that precedes motor neuron apoptosis in ALS.
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