Inclusive instructional communication in higher education: A comparative policy analysis of South Africa and Malawi.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to debilitating motor and non-motor impairments. Despite decades of intensive investigation, the precise mechanisms underlying dopaminergic neuronal degeneration remain incompletely understood. Accumulating evidence suggests that PD pathogenesis is multifactorial, involving aging, mitochondrial dysfunction, oxidative stress, neuroinflammation, impaired protein degradation, and dysregulated autophagy. Oxidative stress is considered a central contributor to PD pathophysiology. Excessive production of reactive oxygen species (ROS), excitotoxic neuronal injury, mitochondrial impairment, and inflammation-mediated cytotoxicity collectively promote oxidative damage to dopaminergic neurons within the SNc. The high metabolic demands of neurons, together with dopamine auto-oxidation and reduced antioxidant defenses, render these neurons particularly vulnerable to oxidative injury. Dopamine synthesized in the SNc plays a pivotal role in regulating motor coordination and non-motor functions. Progressive degeneration of SNc dopaminergic neurons represents the neuropathological hallmark of PD and underlies the characteristic motor symptoms, including bradykinesia, rigidity, and tremor, as well as non-motor manifestations. Neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF), are critical for synaptic plasticity, cognitive function, and dopaminergic neuron survival, and their dysregulation has been implicated in PD progression.