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Parkinson’s disease: Pathophysiology, current treatments, and future therapeutic approaches
*Corresponding author: Jeewanjot Singh, Desh Bhagat University, Mandi Gobindgarh, Punjab, India. sandhujeewan7@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Singh J. Parkinson’s disease: Pathophysiology, current treatments, and future therapeutic approaches. RMC Glob J. 2026;2:2–8. doi: 10.25259/RMCGJ_9_2025
Abstract
Parkinson’s disease (PD) is a complex neurodegenerative disorder characterized by both motor symptoms, such as tremors, bradykinesia (slowness of movement), and rigidity, as well as non-motor symptoms. The older you get, the more likely you are to have it, specifically among people aged 60 or older. Mutations in genes such as α-synuclein (SNCA), PTEN-induced kinase 1 (PINK1), and leucine-rich repeat kinase 2 (LRRK2), as well as environmental factors, contribute to the pathogenesis of Parkinson’s disease. The disorder involves SNCA buildup in Lewy bodies and dopaminergic neuron disintegration in the substantia nigra. Present treatments primarily involve alleviating symptoms by using levodopa (L-3,4-dihydroxyphenylalanine) [L-DOPA], dopamine stimulants, and surgical interventions like deep-brain stimulation. Progress in gene therapy, stem cell research, and neuroprotective agents provides hopeful options for potential treatments that could impede the advancement of diseases. This article discusses the underlying mechanisms of PD, current treatment approaches, and possible future advancements in the research, focusing on enhancing neuroprotective and regenerative therapies for better patient results.
Keywords
Dopamine neurons
Lewy bodies
Neurodegeneration
Neuroprotective therapies
Parkinson’s disease
INTRODUCTION
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by bradykinesia, rigidity, and resting tremors. As the disease progresses, some individuals may also develop postural instability. Our information on PD is still growing, having begun with a detailed description by James Parkinson (1817) and afterward featured by Jean-Martin Charcot. Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease, with an estimated prevalence of 0.5%–1% in individuals aged 65–69 years, increasing to 1%–3% in those aged 80 years and above.1–3
The global population is projected to increase by over 30% by the year 2030,4 which will lead to a rise in the prevalence and mortality of PD. This will have an antagonistic impact on society and the economy by and large, both specifically and indirectly.
Parkinson’s disease is a neurodegenerative disorder that typically manifests later in life with resting tremors, muscular rigidity, and slowness of movement (bradykinesia). Other associated symptoms include loss of smell, cardiovascular issues, sleep disturbances, excessive salivation, tremors, and periodic involuntary limb movements, often observed in REM (rapid eye movement) sleep behavior disorder.5–7 Parkinson’s disease is estimated to affect approximately 1% of the population over the age of 60. It is associated with the loss of dopaminergic (DAergic) neurons in the substantia nigra and the presence of Lewy bodies. The majority of cases are cryptogenic; that is, around 10% of cases are hereditary, and these cases are typically seen in young people.8
ETIOLOGY
Hereditary and natural variables are two of the numerous factors that contribute to PD. The major chance figure for PD is at the normal initial age of 60 years.9 As people age, the prevalence of the disease increases, reaching 93.1 cases per 100,000 people per year in the age group of 70–79 years.10,11 Moreover, the prevalence of Parkinson’s disease varies across populations, being more common in Europe, South America, and North America than in Asian, African, and Middle Eastern countries.1
Over the last century, an increasing amount of information has become available regarding the origin of Parkinson’s disease. It has been found that the subcortical motor circuit in the substantia nigra experiences a loss of DAergic neurons, which leads to motor impairment in Parkinson’s disease.
The basal ganglia consist of several nuclei, which are affected in Parkinson’s disease. Certain brain regions send excitatory and inhibitory signals to the striatum. The primary issue is the degeneration of DAergic (dopaminergic) neurons, which leads to the symptoms. Pesticides, herbicides, and being near mechanical locales have all been connected to Parkinson’s disease.
GENETICS AND PATHOPHYSIOLOGY
Certain genes play a critical role in PD in some patients, particularly in those with mutations in key genes.12 In 1997, the α-synuclein (SNCA) quality was initially linked to familial autosomal dominant Parkinson’s disease, appearing as part of Lewy bodies, which are indeed displayed in intermittent cases. After this revelation, other thoughts appeared that the quality expansion was related to expanded levels of SNCA, recommending that it be included in the pathogenesis of PD [Figure 1].13
- Interlinked genetic and environmental triggers in Parkinsonism pathogenesis.
Meanwhile, mutations in parkin RBR E3 ubiquitin protein ligase14 and PINK115 genes are known to cause autosomal recessive Parkinson’s disease, involving pathways related to mitophagy—the process responsible for the degradation of damaged mitochondria. Disability of these qualities disables mitochondrial turnover and contributes to PD by permitting inadequate mitochondria to accumulate. In expansion, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), beneath the control of PARKIN, contributes to mitochondrial biogenesis and antioxidant defense.16 Its decreased levels are seen in cases of PD.17 Meanwhile, mutations in PARKIN and mitochondrial dysfunction in Parkinson’s disease are supported by extensive studies on the effects of environmental toxins. For example, presentation to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can rapidly trigger Parkinsonian side effects by repressing mitochondrial complex I. Changes in the leucine-rich repeat kinase 2 (LRRK2) gene are related to prevailing Parkinson’s illness with variable penetrance, influencing 1%–2% of all PD disorders, rising to 5% in familial instances. It is especially predominant in a few populations, such as the Ashkenazi Jews and the Berbers of North Africa.18 These changes are related to expanded kinase movement, proposing that LRRK2 kinase inhibitors may have defensive impacts, in spite of the fact that the importance of the loss of LRRK2 movement remains under investigation [Figure 2].19
- Pathophysiological mechanisms in PD. PD: Parkinson disease.
OLD AND NEW CHALLENGES IN PARKINSON’S DISEASE THERAPEUTICS
Current clinical therapies in Parkinson’s disease
PD pharmacotherapies
The groundbreaking investigation by Carlsson and colleagues in 1957, which distinguished dopamine (DA) as a potential neurotransmitter,20 the nearby discoveries of Ehringer and Hornykiewicz in 1960 that uncovered radically diminished DA levels in the striatum of Parkinsonism (PD) patients,21 laid the foundation for the utilization of L-DOPA in clinical practice.22,23 L-DOPA has essentially changed the administration of PD’s essential engine side effects, including resting tremor, inflexibility, bradykinesia, and postural flimsiness, eventually making strides day by day in working and quality of life for patients.23 This drug has become the “gold standard” for treating Parkinson’s disease symptoms over the past few decades. In any case, drawn out L-DOPA utilization frequently leads to engine vacillations and drug-induced dyskinesias, with basic instruments not completely caught on but likely related to the pulsatile incitement of DA receptors and striatal denervation.
Apomorphine, a more seasoned non-ergot DA receptor agonist, illustrates anti-Parkinsonian adequacy comparable to L-DOPA but has truly confronted utilization challenges due to side effects, particularly emesis.24,25 Later progressions, including an injectable detailing, have made it a reasonable alternative for tending to “wearing-off” marvels in later-stage PD.25 The improvement of specialists restraining the DA digestion system, such as monoamine oxidase-B (MAO-B) inhibitors, proceeds to upgrade DA transmission and complement existing treatments. The objective of utilizing MAO-B inhibitors like selegiline and rasagiline to treat PD is to reduce the requirement for L-DOPA medications.
New drugs and surgical targets for PD
Long-term L-DOPA treatment in PD can lead to engine complications, prompting an inquiry into neuroprotective choices such as selegiline and rasagiline, along with different symptomatic medications. Current clinical trials are investigating various treatments, including novel DA agonists such as controlled-release IPX 066 and continuous duodenal infusion of carbidopa-levodopa (levodopa–carbidopa intestinal gel [LCIG]/Duodopa). Also, elective approaches are being inspected, focusing on non-DAergic neurotransmitter frameworks. Drugs under investigation include adenosine receptor antagonists (e.g., preladenant, tozadenant), serotonin receptor agonists (e.g., sarizotan), and calcium channel blockers (e.g., isradipine), among others.26–28 A few of these, such as nicotine and preladenant, may moreover offer neuroprotective benefits. Moreover, clinical trials are investigating previously unused compounds, such as deferiprone and creatine, which help reduce oxidative stress and mitochondrial damage.
Molecular therapies
As discussed recently, the prolonged use of L-DOPA is associated with undesirable side effects, such as motor fluctuations and dyskinesias.29,30 These impediments, together with noteworthy progress made in consideration of the pathobiology and patho-anatomy of Parkinsonism, have driven the development of modern pharmacologic operators and quality building approaches for the prolonged result of Parkinsonism patients.
Drug treatment
Recent advancements in preclinical research for PD treatment focus on neuroprotective agents and non-DAergic options. Among these, metabotropic glutamate receptor (mGluR) agonists, especially mGluR4, have earned consideration for their potential neuroprotective impacts.31,32 mGluR4 is primarily found in presynaptic terminals and has been shown to intervene in inhibitory impacts on basal ganglia circuitry, relieving excitatory synaptic transmission connected to PD’s DAergic shortages. Studies have shown that mGluR4 agonists and positive allosteric modulators, which enhance the effects of mGluR4, can cross the blood-brain barrier and alleviate symptoms of PD, such as akinesia and drug-induced dyskinesias, in animal models.
Monosialotetrahexosylganglioside (GM1) has emerged as a potential disease-altering treatment for Parkinsonism disorder,33,34 as it plays a key role in neuronal functions such as cell surface modulation, protein phosphorylation, and synaptic activity. Research indicates that GM1 can improve neurochemical and behavioral outcomes in PD models, with a notable study in 1998 showing significant improvements in motor scores and tasks in PD patients after GM1 treatment.35
Coenzyme Q10 (CoQ10), beneficial for mitochondrial function, has also been studied as a promising therapeutic agent for Parkinsonism, yet the clinical evidence remains mixed. Some studies reported symptomatic improvements following short-term CoQ10 administration, while others did not observe benefits even with prolonged treatment. A recent phase III trial confirmed CoQ10’s safety but found no evidence supporting its efficacy in modifying disease progression, indicating a need for further research.36
N-acetyl-cysteine (NAC) is recognized for its role as a thiol antioxidant and a prodrug capable of delivering cysteine to the brain,37,38 which may counter oxidative damage in PD. Animal studies demonstrated NAC’s potential to protect DAergic neurons by enhancing mitochondrial activity and reducing reactive oxygen species.
Gene Therapy
Quality treatment for PD includes the use of viral vectors to deliver proteins with targeted expression in specific brain regions. Three fundamental approaches have been utilized in clinical trials to address PD engine side effects: administering glutamic acid decarboxylase (GAD) protein in the subthalamic nucleus (STN), administering synthetic chemicals to increase DA levels in the striatum, and infusing neurotrophic factors to protect and restore DAergic neurons. The first approach aims to modulate STN activity by delivering GAD into the STN using an adeno-associated virus vector. This strategy has shown promising results in preclinical studies and early-stage clinical trials, with significant improvements in motor function observed in patients with PD.
Cell-based therapies
Cell-based strategies have emerged as a promising approach to restore impaired DAergic neural circuits and provide prolonged relief from symptoms. These strategies are based on the premise that cell-based therapies may effectively replace DAergic neurons lost during the clinical course of PD. Each of these cell-based treatments will be thoroughly examined in this segment, covering its characteristics, preferences, and challenges.
Embryonic stem cells
These cells exhibit an exceptional proliferation rate while retaining their cellular identity even during prolonged in vitro culture.39,40 The extensive production capacity, coupled with DAergic neuronal differentiation potential, offers viable prospects for novel therapies against Parkinson’s disease using these stem cells as a workforce. Robust efficacy has been demonstrated in animal models, where ES-derived neurons facilitated functional recovery through integration, promoting motor function improvement, especially when grafted onto rats. Likewise, underlined challenges such as graft phenotypic instability and tumor formation, besides ethical issues regarding human embryonic use, along with immunorejection concerns, still threaten clinical resourcing potentials of this therapy method.
Neural stem cells (NSCs)
NSCs can differentiate into various types of central nervous system cells, including oligodendrocytes, neurons, and astrocytes.41 These cells are sourced from creating or growing central nervous system (CNS) tissue and can be refined as neurospheres with particular development variables, making them promising candidates for cell replacement treatment in Parkinson’s disease. Strikingly, as it were, midbrain-derived NSCs can separate into DAergic neurons, and transplantation frequently utilizes these cells or human fetal-derived NSCs. In any case, cell survival rates post-transplantation stay low due to reliance on developmental signals and translation components fundamental for neuronal differentiation. To address these challenges, the hereditary development of refined precursor cells may enhance the ablation of TH-positive neurons, thereby promoting the formation of functional neural connections in Parkinsonian brains.
Induced neural cells
In an endeavor to overcome the issues related to the separation and heterogeneity of inducible pluripotent stem cells (iPSCs) observed in vivo,42,43, an approach Separation is the coordinate substitution of one sort of somatic cell with another. Vierbuchen and colleagues have modified fibroblasts into functional neurons in vitro, utilizing a comparable combination technique for three transcription-independent components. The coming about of cells was called inducible neurons (iN cells).
These iN cells have shown the capacity to create DAergic neurons in vitro, maintaining a distance from the return to the pluripotent stage, subsequently lessening the chance of tumorigenesis. In any case, the capacity of these cell-derived DAergic neurons to initiate phenotypic impacts in PD creatures remains to be tested.
Mesenchymal stem cells
The term “mesenchymal stem cells” was coined the same year by Kaplan’s group, indicating their capacity and ability to differentiate into different lineages, especially adipocytes, osteoblasts, and chondroblasts.44 Marrow-derived stem cells (MSCs) have shown up to ensure in treating neurodegenerative diseases, particularly for securing and reestablishing DA neurons in PD. Explore illustrates that though they may update motor work, they may not have partitioned to create neurons in vivo, suggesting that their accommodating impacts might be independent of neuronal partition. MSCs can migrate to injury sites and promote cellular recovery by releasing growth factors (GFs), anti-inflammatory cytokines, and microvesicles/exosomes, exerting various protective effects that enhance neuroprotection and neurogenesis. Bone marrow-derived stem cells (BMSCs) have shown up as basic cautious qualities for DAergic neurons, particularly through factors like brain-derived neurotrophic factor (BDNF) glial cell line-derived neurotrophic factor (GDNF). Conditioned media derived from bone marrow–derived mesenchymal stem cells (BMSCs) have been shown to enhance the survival of dopaminergic (DAergic) neurons both in vitro and in vivo, particularly in PD models.
Future perspectives
Current medicines for PD, such as L-DOPA and different DA agonists and inhibitors, essentially point to reestablishing DA levels in the brain but do not address the fundamental neurodegeneration of DA neurons.45 Whereas successful in easing indications, these treatments fall flat in securing existing neurons from harm or reestablishing those as of now misplaced. Moreover, PD movement includes other variables like mitochondrial damage, oxidative stress, and neuroinflammation.46 This raises important questions about potential alternative strategies to L-DOPA and ways to enhance its efficacy and reduce side effects through combination therapies. Safinamide, a recently endorsed sedative by the European Drugs Office, presents as a promising expansion to PD treatment regimens. It acts as an MAO-B inhibitor and squares certain glutamate receptors and calcium channels, upgrading DAergic transmission with fewer side effects compared to L-DOPA.47,48 Safinamide appears to have neuroprotective impacts by reducing oxidative stress and excitotoxicity, which may offer assistance in protecting DA neurons. Opicapone is a recently endorsed, once-daily, strong third-generation catechol-O-methyltransferase (COMT) antagonist utilized as an adjunctive treatment to L-DOPA in adults with PD who have experienced using it.49 Dose-limited engine changes of this hydrophilic 1,2,4-oxadiazole analog increment L-DOPA bioavailability without critical cytotoxic impacts. Previous studies have shown that opicapone prolongs peripheral COMT inhibition and increases sensitivity to L-DOPA without exhibiting toxicity. Clinical studies have illustrated the capacity of opicapone to decrease COMT action and increase engine response to fake treatment, predominant to the activities of other COMT inhibitors such as entacapone. It also appeared that a single day-by-day dosage of opicapone may disentangle treatment regimens, reducing the accumulation of everyday L-DOPA measurements and drawing out dosage intervals, in this way possibly improving patient quality of life. The secretome derived from human mesenchymal stem cells has emerged as a potential alternative therapeutic strategy for PD, focusing on enhancing the survival of DAergic neurons. This approach mitigates challenges posed by coordinate cell transplantation, such as the required cell amounts and the complexities of conveyance. iPSCs are proposed as a reasonable source for producing MSC-like cells (iMSCs) in larger amounts, advertising a steadier and more powerful source of secretome production. The life span and practicality of iPSCs may increase their therapeutic potential compared to developed MSCs. In expansion, iPSCs can serve as an advanced in vitro model to consider the complexities of PD and may uncover unused helpful targets and methodologies to decrease DAergic neuron degeneration.50
CONCLUSION
Parkinson’s disease remains a significant medical challenge due to its progressive nature and the limitations of current treatments that primarily focus on symptomatic relief. Although L-DOPA and other DA-based therapies offer temporary improvements, they do not address the underlying neurodegeneration. Emerging research in genetic therapies, stem cells, and neuroprotective drugs holds promise for altering disease progression. However, these approaches still face challenges related to safety, efficacy, and ethical considerations. Future studies should prioritize the development of therapies that target the root causes of PD, such as mitochondrial dysfunction and SNCA aggregation, to provide more comprehensive and lasting treatments for patients.
Acknowledgment:
I sincerely thank my friend and guide for their unwavering support and encouragement.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient’s consent not required as there are no patients in this study.
Financial support and sponsorship:
Nil.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The author confirms that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
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