article · European journal of medical research
Parkinson's disease causes motor and non-motor symptoms via the degeneration of dopaminergic neurons in the substantia nigra pars compacta. Disruption of γ-aminobutyric acid (GABA) neurotransmission also plays an important role. The GABA pathway provides inhibitory tone to prevent excessive stimulation of the cerebral cortex. In Parkinson's disease, dopaminergic loss is linked to decreased GABAergic neurotransmission, which promotes oxidative stress and mitochondrial dysfunction. Dysregulation of GABAergic neurons contributes directly to both motor and non-motor symptoms. Restoring GABA activity, for example through GABA agonists, could attenuate the progression of motor symptoms and ameliorate non-motor manifestations. Improving the GABAergic pathway represents a potential novel therapeutic approach for managing Parkinson's disease symptoms.
Parkinson's disease is a debilitating condition that affects movement alongside wider neurological functions. Standard treatments predominantly focus on dopamine, which often leaves symptoms unmanaged. Establishing how the GABA pathway influences disease progression highlights an alternative neurochemical target, providing a basis for developing therapies that address both physical and non-motor symptoms while curbing underlying oxidative stress.
This work points towards potential pharmacological applications, specifically the development or repurposing of GABA agonists to manage Parkinson's disease symptoms. The primary beneficiaries would be pharmaceutical developers and neuropharmacology researchers. Because the findings outline biological mechanisms rather than experimental or clinical trials, the research sits at an early conceptual stage and remains distant from market implementation.
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Parkinson's disease (PD) is a progressive neurodegenerative disease as a result of the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The fundamental features of PD are motor and non-motor symptoms. PD symptoms develop due to the disruption of dopaminergic neurotransmitters and other neurotransmitters such as γ-aminobutyric acid (GABA). The potential role of GABA in PD neuropathology concerning the motor and non-motor symptoms of PD was not precisely discussed. Therefore, this review intended to illustrate the possible role of GABA in PD neuropathology regarding motor and non-motor symptoms. The GABA pathway is essential in regulating the inhibitory tone to prevent excessive stimulation of the cerebral cortex. Degeneration of dopaminergic neurons in PD is linked with reducing GABAergic neurotransmission. Decreasing GABA activity promotes mitochondrial dysfunction and oxidative stress, which are highly related to PD neuropathology. Hence, restoring GABA activity by GABA agonists may attenuate the progression of PD motor symptoms. Therefore, dysregulation of GABAergic neurons in the SNpc contributes to developing PD motor symptoms. Besides, PD non-motor symptoms are also related to the dysfunction of the GABAergic pathway, and amelioration of this pathway may reduce PD non-motor symptoms. In conclusion, the deregulation of the GABAergic pathway in PD might be intricate in developing motor and non-motor symptoms. Improving this pathway might be a novel, beneficial approach to control PD symptoms.
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DOI: 10.1186/s40001-024-01779-7
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