Even though the specific mechanism remains to be elucidated, our results demonstrate that the A53T-mutant α-synuclein alters the astrocyte Ca2+ signal in situ, adding up to other studies showing dysfunctional astrocyte Ca2+ signaling in various neurological disorders, including other models of PD [10], Alzheimer’s disease (AD) [20, 24, 35, 65] and Huntington’s disease [29]. This evidence concerns the gene SNCA and juvenile Huntington disease.