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. 2024 Aug 21;21(8):1105.
doi: 10.3390/ijerph21081105.

Chronic Cocaine Use and Parkinson's Disease: An Interpretative Model

Manuel Glauco Carbone  1   2   3 , Icro Maremmani  2   3   4
Affiliations

Chronic Cocaine Use and Parkinson's Disease: An Interpretative Model

Manuel Glauco Carbone et al. Int J Environ Res Public Health. .

Abstract

Over the years, the growing "epidemic" spread of cocaine use represents a crucial public health and social problem worldwide. According to the 2023 World Drug Report, 0.4% of the world's population aged 15 to 64 report using cocaine; this number corresponds to approximately 24.6 million cocaine users worldwide and approximately 1 million subjects with cocaine use disorder (CUD). While we specifically know the short-term side effects induced by cocaine, unfortunately, we currently do not have exhaustive information about the medium/long-term side effects of the substance on the body. The scientific literature progressively highlights that the chronic use of cocaine is related to an increase in cardio- and cerebrovascular risk and probably to a greater incidence of psychomotor symptoms and neurodegenerative processes. Several studies have highlighted an increased risk of antipsychotic-induced extrapyramidal symptoms (EPSs) in patients with psychotic spectrum disorders comorbid with psychostimulant abuse. EPSs include movement dysfunction such as dystonia, akathisia, tardive dyskinesia, and characteristic symptoms of Parkinsonism such as rigidity, bradykinesia, and tremor. In the present paper, we propose a model of interpretation of the neurobiological mechanisms underlying the hypothesized increased vulnerability in chronic cocaine abusers to neurodegenerative disorders with psychomotor symptoms. Specifically, we supposed that the chronic administration of cocaine produces significant neurobiological changes, causing a complex dysregulation of various neurotransmitter systems, mainly affecting subcortical structures and the dopaminergic pathways. We believe that a better understanding of these cellular and molecular mechanisms involved in cocaine-induced neuropsychotoxicity may have helpful clinical implications and provide targets for therapeutic intervention.

Keywords: Parkinsonism; Parkinson’s disease; cocaine; cocaine addiction; extrapyramidal symptoms.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Direct and indirect pathways.
Figure 2
Figure 2
Pre-synaptic and post-synaptic effects of cocaine (from https://doi.org/10.3390/toxins14040278, (accessed on 3 May 2024) modified).
Figure 3
Figure 3
Cocaine effects on serotoninergic system (from https://doi.org/10.3390/ijms242216416, (3 May 2024) modified).
Figure 4
Figure 4
(a). Chronic cocaine use depletion of dopamine (DA), norepinephrine (NE), and serotonin (5-HT). Legend: dopamine transporter (DAT), norepinephrine transporter (NET), serotonin transporter (SERT), monoamine oxidase (MAO), reactive oxygen species (ROS), Vesicular Monoamine Transporter 2 (VMAT-2), dopamine receptor D2 (D2 receptors). (b). Chronic cocaine use neurotoxicity and neurodegeneration. Legend: myocyte enhancer factor-2 (MEF-2).
Figure 4
Figure 4
(a). Chronic cocaine use depletion of dopamine (DA), norepinephrine (NE), and serotonin (5-HT). Legend: dopamine transporter (DAT), norepinephrine transporter (NET), serotonin transporter (SERT), monoamine oxidase (MAO), reactive oxygen species (ROS), Vesicular Monoamine Transporter 2 (VMAT-2), dopamine receptor D2 (D2 receptors). (b). Chronic cocaine use neurotoxicity and neurodegeneration. Legend: myocyte enhancer factor-2 (MEF-2).
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