Figure 2.

Schematic summary of TGFβ1-mediated effects under physiological and pathological (PD) conditions.

Whereas TGFβ1 expression is restricted to neurons under physiological conditions and is high likely to be involved in mediating microglial quiescence as well as neuronal survival, microglia increase TGFβ1 expression under pathological conditions. In this context, TGFβ1 exerts autocrine and paracrine effects by inhibiting microglia activation and promoting neuron survival. Crosstalks between different signalling pathways (e.g., GDNF, IFNγ and TGFβ1) are high likely to have impacts on mDA neuron survival as well as microglia reactivity, however, these interactions have been only partially understood and need to be further elucidated.

GDNF: Glial cell line-derived neurotrophic factor; IFNγ: interferon-γ; iNOS: inducible nitric oxide synthase; L-DOPA: L-3,4-dihydroxyphenylalanine; mDA: midbrain dopaminergic; NO: nitric oxide; PD: Parkinson's disease; TβR: transforming growth facter beta receptor; TGFβ1: transforming growth factor β1; TNFα: tumor necrosis factor α.