The pervasiveness and mortality associated with methamphetamine abuse has doubled
during the past decade suggesting a possible worldwide substance use crisis. Epitomizing the
pathophysiology and toxicology of methamphetamine abuse proclaims severe signs and
symptoms of neurotoxic and neurobehavioral manifestations in both humans and animals.
Most importantly, chronic use of this drug enhances the probability of developing
neurodegenerative diseases manifolds. Parkinson’s disease is one such neurological disorder, which significantly and evidently not only shares a number of toxic pathogenic mechanisms induced by methamphetamine exposure but is also interlinked both structurally andgenetically.
Methamphetamine-induced neurodegeneration involves altered dopamine
homeostasis that promotes the aggregation of α-synuclein protofibrils in the dopaminergic
neurons and drives these neurons to make them more vulnerable to degeneration as
recognized in Parkinson’s disease. Moreover, the pathologic mechanisms such as
mitochondrial dysfunction, oxidative stress, neuroinflammation and decreased neurogenesis
detected in methamphetamine abusers dramatically resemble to what is observed in
Parkinson’s disease cases. Therefore, the present review comprehensively cumulates a
holistic illustration of various genetic and molecular mechanisms putting across the notion of
how methamphetamine administration and intoxication might lead to Parkinson’s disease-like
pathology and Parkinsonism.