Parkinson's Disease

This mitochondrial dysfunction causes the loss of dopaminergic neurons in the substantia nigra and the formation of Lewy bodies (LBs) compromising mitophagy, the process of eliminating damaged mitochondria, accelerating neurodegeneration.  Simultaneously aggregation of α-Synuclein (α-Syn) and Tau protein and its interaction increases neurotoxicity, accelerates the loss of physiological function and axonal transport dysfunction, ultimately inducing the deposition of toxic fibrils and cell death.
The Sigma-1 receptor is a protein involved in the transport of lipids and proteins between cell organelles. Sigma-1 activation reduces the release of tumor necrosis factor α (TNF-α) responsible for α-Synuclein propagation, blocks tau hyperphosphorylation and aggregation, increases dopamine and dopaminergic fiber levels, promotes the elimination of damaged mitochondria, restores motor capacity, and also regulates the expression of proteins involved in neurite formation, synaptic plasticity, and presynaptic differentiation, suggesting that it could stimulate neuronal regrowth, axon extension, and recover cognitive deficits. In Parkinson’s disease, certain neuronal cells in the brain gradually break down or die mainly due to the dysfunction of their mitochondria, membrane-bound cellular organelles that generate most of the chemical energy needed to fuel the cell.
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