In particular, transforming growth factor beta 1 (TGFB1), which has been shown to inhibit microglial inflammatory response in a rat model of PD, and matrix metallopeptidase 2 (MMP2), which has been shown to degrade α-synuclein aggregates, were found to be down-regulated in LRRK2 G2019S astrocytes.
Together, our data suggest that αSO have important effects on astrocytic functions and describe TGF-β1 as a new endogenous astrocyte-derived molecule involved in the increase in striatal glutamatergic synaptic density present in early stages of PD.
In this study, transforming growth factor-β1 (TGF-β1), a key suppressive cytokine in PD onset and development, failed to increase in the midbrain and peripheral blood of AQP4<sup>-/-</sup> mice after MPTP treatment.
These results show that an increase in TGFbeta1 levels aggravate the parkinsonian status of MPTP mice and may therefore be a risk factor for the development of PD.