Mechanistic models of α-synuclein homeostasis for Parkinson's disease: A blueprint for therapeutic intervention

Parkinson's disease (PD) is the second most common neurodegenerative disorder worldwide, yet there no disease-modifying therapy up to this date. The biological complexity underlying PD hampers investigation of principal contributors its pathogenesis. In context, mechanistic models grounded in molecular-level knowledge provide virtual labs uncover primary events triggering onset and progression suggest promising therapeutic targets. Multiple modeling efforts research have focused on pathological role $\alpha$-synuclein ($\alpha$syn), a presynaptic protein that emerges from intricate molecular network as crucial driver neurodegeneration. Here, we collect advances mathematical $\alpha$syn homeostasis, focusing aggregation degradation pathways, discussing potential improvements possible implications strategy design.