We have revealed that the myophosphorylase expression is not tissue specific and consequently its functionality exceeds the skeletal muscle. This discovery has opened up new perspectives to investigate the McArdle's disease since certain comorbidities described in some patients could be explained due to an unfunctional myophosphorylase in the tissues involved. On the other hand, we are also interested in deciphering the role of the glycogen phosphorylase muscle isoform in astrocytes and microglia and to investigate how the Amyloid β-peptide (1-42)modifies the intracellular signaling mediated by glycogen phosphorylase in these two cell lineages.