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Consequently, inhibiting the activation of M1-type pro-inflammatory microglia has become a key strategy for promoting nerve repair [44]

The median spiny neurons of the midbrain are the primary targets of PD, but additional losses of dopaminergic neurons and accumulation of Lewy bodies in the substantia nigra pars compacta (SNpc) affect normal physiological neuronal functioning

Simultaneously, the opening of the mitochondrial permeability transition pore induces mitochondrial swelling and rupture, releasing apoptotic factors and ultimately leading to cell death [34, 35]