What are the new drugs for Parkinson’s Disease?

Introduction to Parkinson’s Disease
Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects the motor system, though non-motor symptoms are increasingly recognized as equally debilitating. Characteristically, PD manifests through tremor (often a resting tremor in the hands, arms, legs, and jaw), muscular rigidity, bradykinesia (or slowness of movement), and postural instability that can greatly compromise mobility and balance. In addition to these hallmark motor symptoms, patients may experience non-motor features such as cognitive decline, depression, anxiety, sleep disturbances, autonomic dysfunction (e.g., orthostatic hypotension, constipation), and sensory abnormalities (e.g., loss of smell). These diverse symptomatic presentations reflect the multifactorial etiology of PD, which involves a gradual loss of dopaminergic neurons in the substantia nigra pars compacta as well as widespread pathology across other brain regions. Such pathology is often evidenced by the formation of Lewy bodies, abnormal aggregates of proteins (primarily alpha-synuclein), which serve as neuropathologic hallmarks of the disease. Global prevalence estimates indicate that PD affects millions worldwide and its incidence escalates with advancing age; indeed, the number of diagnoses is predicted to dramatically increase over the next few decades.

Current Treatment Landscape

Historically, treatments for PD have focused almost entirely on symptomatic relief. Levodopa, the precursor to dopamine, remains the gold standard for restoring dopaminergic signaling; however, while it offers remarkable motor improvement in the early stages, its long-term use is marred by significant complications such as motor fluctuations, dyskinesia (abnormal involuntary movements), and an overall decline in efficacy as the disease progresses. Other symptomatic agents—including dopamine agonists, monoamine oxidase-B (MAO-B) inhibitors (e.g., rasagiline, selegiline), and catechol-O-methyltransferase (COMT) inhibitors—have been introduced to both complement levodopa therapy and attempt to reduce its side effects. Despite the availability of these numerous treatments, none have convincingly shown an ability to slow, halt, or reverse the underlying neurodegeneration. This therapeutic gap is further compounded by the fact that the majority of current medications address the dopaminergic system alone, despite PD being a multi-pathway disease with complex genetic, cellular, and molecular pathology. As a result, the clinical community has become increasingly focused on developing new drugs that either improve symptomatic control with more sophisticated delivery mechanisms or—more importantly—pursue strategies aimed at modifying disease progression.

New Drug Developments for Parkinson’s Disease

Recently Approved Drugs

Recent years have witnessed the regulatory approval of new formulations and new chemical entities that target specific aspects of PD symptomatology and offer improved pharmacokinetic profiles. For instance, Amneal Pharmaceuticals’ investigational drug, IPX-203, has emerged as a promising candidate. IPX-203 is designed as an extended-release formulation of carbidopa/levodopa, and clinical trial results have shown that it provides superior “Good On” time to patients with motor fluctuations when compared to the standard immediate-release formulations, thus reducing the dosing frequency and enhancing patient adherence.

In addition, drugs that address non-motor aspects as well as complications of levodopa therapy have also advanced. Pimavanserin—approved for the treatment of Parkinson’s disease psychosis—represents a major development as it acts by inverse agonism at 5-HT2A receptors and is characterized by a favorable safety profile with no measurable activity at dopaminergic receptors, thereby not aggravating motor symptoms. Furthermore, safinamide, approved as an adjunct to dopamine replacement therapy, not only serves as a MAO-B inhibitor but also exhibits inhibitory activity on glutamate release. Clinical trials with safinamide have shown improvements in motor scores as measured by UPDRS (Unified Parkinson’s Disease Rating Scale) and support its benefit as part of combination therapy.

On another front, reformulated or newly engineered delivery systems have been patented and are in various stages of clinical testing. For example, a set of patents describe innovative drug delivery systems for both treating central nervous system (CNS) diseases and specifically PD. These novel systems focus on ensuring better bioavailability and more controlled release of therapeutic agents, such as levodopa formulations exhibiting a more constant plasma concentration, thereby leading to fewer “on-off” fluctuations. Additionally, advancements in COMT inhibitors, such as opicapone (a third-generation inhibitor), have been introduced to enhance the duration of levodopa’s action with improved tolerability profiles.

Collectively, these recently approved drugs and novel delivery formulations signal an important shift in the PD treatment landscape. They reflect a broader therapeutic approach that aims not only to replace the deficient neurotransmitter system but also to address the specific complications and side effects associated with long-term levodopa use. These new formulations have therefore already paved the way for improved quality-of-life for PD patients by minimizing motor complications and simplifying dosing regimens, an essential step in modern PD management.

Drugs in Clinical Trials

Beyond recently approved therapies, a robust number of candidate drugs are currently in clinical trials, representing a wide spectrum of therapeutic strategies—from symptomatic relief and improved dopaminergic stimulation to agents targeting the underlying disease process. Many of these candidates have entered Phase I–III testing and include both entirely novel chemical entities and repurposed drugs that have shown promising preclinical neuroprotective effects.

One notable category is that of extended-release levodopa formulations and novel routes of administration. In addition to IPX-203, other formulations aim to achieve steady state plasma levels while reducing peak-trough variability. For example, studies are testing subcutaneous or intestinal gel formulations that provide continuous infusion of levodopa, thereby reducing motor fluctuations associated with conventional tablet-based delivery.

Another area of active investigation is the search for drugs that modulate non-dopaminergic pathways involved in PD pathogenesis. These include agents that target molecular mechanisms such as alpha-synuclein aggregation, LRRK2 kinase activity, oxidative stress, and mitochondrial dysfunction. Recent preclinical studies and early-phase clinical trials have focused on immunotherapeutics and small molecules designed to inhibit alpha-synuclein aggregation or promote its clearance. Monoclonal antibodies and vaccine approaches targeting the misfolded forms of alpha-synuclein are being evaluated for their potential to slow disease progression.

Furthermore, LRRK2 inhibitors have generated considerable interest, especially given that mutations in the LRRK2 gene are among the most common causes of familial PD. Although early inhibitors have encountered challenges such as lung toxicity in non-human primates, ongoing efforts are directed toward refining these compounds and improving their safety profiles through better delivery systems or alternative molecular scaffolds.

Gene therapies are also making inroads into PD clinical research. Investigational approaches targeting genes involved in dopamine synthesis, such as AAV-hAADC (adenosine A-acid decarboxylase) gene therapies, have shown promise in early clinical studies by enhancing the ability of remaining neurons to produce dopamine. Additionally, cell therapies, including dopaminergic cell replacement strategies, are undergoing Phase I/II clinical trials, where the goal is to restore dopaminergic neural circuits rather than simply replacing dopamine.

Other repurposed agents are gaining attention as well—ketamine, for example, at low doses has been reviewed for its potential to ameliorate levodopa-induced dyskinesia (LID) and for its benefits in treating pain and depression in PD patients. Retrospective analyses and early phase trials have indicated that low-dose ketamine can provide an improvement in dyskinetic symptoms lasting several weeks beyond the treatment period, signifying a non-dopaminergic mechanism that might complement traditional therapies.

Recent drug repurposing strategies using data mining and bioinformatics have also identified several candidates; for instance, metformin hydrochloride has been highlighted as a potential therapeutic due to its indirect effects on oxidative stress pathways and mitochondrial function. These strategies leverage existing clinical safety data and aim to rapidly transition promising compounds into PD trials with a reduced risk profile.

In summary, the pipeline of drugs in clinical trials for Parkinson’s disease is broad and multifaceted, encompassing enhanced dopaminergic formulations, non-dopaminergic pathway modulators, immunotherapies, gene therapies, cell therapies, and repurposed drugs that target peripheral as well as central mechanisms. Together, these candidates represent a promising movement towards not only improving symptom control but also targeting the neurodegenerative process that underlies PD.

Mechanisms of Action

Pharmacodynamics and Pharmacokinetics

New drug formulations for PD are designed with a focus on improving pharmacodynamic and pharmacokinetic profiles relative to conventional treatments. Traditional immediate-release levodopa therapies are limited by their short plasma half-life of approximately 1–3 hours, leading to significant fluctuations in dopamine levels, which in turn correlate with the onset of motor complications such as dyskinesia and the “on-off” phenomenon.

Recent advances in drug design have centered on extended-release levodopa formulations that maintain more stable plasma concentrations over a longer duration. For example, IPX-203 utilizes a biphasic release mechanism that incorporates both immediate-release and sustained-release components. This dual mechanism leads to a more physiological dopaminergic stimulation, reduced dosing frequency (three doses per day compared to five for some immediate-release formulations), and improved “Good On” time. Such improvements not only enhance clinical efficacy but also reduce the incidence of side effects typically induced by peak concentrations.

Other pharmacokinetic improvements include novel routes of administration such as subcutaneous injections or intestinal gels, which bypass some of the gastrointestinal absorption issues common with oral levodopa. These approaches can overcome degradation by gastrointestinal enzymes, mitigate the impact of gastric emptying variability, and achieve more predictable absorption profiles.

At the pharmacodynamic level, novel agents such as safinamide display dual modes of action. As an MAO-B inhibitor, safinamide slows the peripheral breakdown of levodopa, thereby increasing its availability in the brain. At the same time, its ability to reduce glutamate release may guard against excitotoxicity and improve motor performance without exacerbating dyskinesia. Similarly, pimavanserin exerts its effects via the serotonergic system (specifically the 5-HT2A receptor) without interfering with dopaminergic neurotransmission. This pharmacodynamic profile is particularly important for treating psychosis in PD patients, as it avoids the risk of worsening motor symptoms that is typical of dopaminergic blockade.

In addition, drugs under development targeting pathways such as alpha-synuclein aggregation or LRRK2 kinase are designed to interact with specific molecular determinants of disease progression. These drugs typically have distinct absorption, distribution, metabolism, and elimination (ADME) profiles that are optimized for central nervous system delivery (often aided by novel drug delivery systems) while minimizing systemic exposure to reduce side effects.

Thus, the new drugs for PD are not only improving upon the traditional dopaminergic replacement by better mimicking physiological dopamine release and maintaining stable plasma concentrations, but they are also broadening the therapeutic window by acting on multiple pharmacodynamic targets. Improvements in drug delivery and molecular design are key strategies that are being exploited to maximize clinical benefits while minimizing adverse effects.

Targeted Pathways

A significant advantage of the most recent therapeutic developments in PD is the broadening of target pathways beyond simple dopamine replacement. Researchers are increasingly focusing on multiple mechanistic avenues that together drive disease pathogenesis.

One major target is the abnormal aggregation of alpha-synuclein—a protein whose misfolding and accumulation are central to PD pathology, as evidenced by its presence in Lewy bodies. New therapeutic strategies include small molecules and immunotherapeutics, such as monoclonal antibodies or vaccines, explicitly aimed at reducing alpha-synuclein aggregation or enhancing its clearance through autophagic pathways. Targeting the protein–protein interactions involved in oligomerization offers an entirely novel avenue that may help slow disease progression.

Targeting oxidative stress is another promising strategy. Many of the new agents under study either directly reduce oxidative stress or stimulate endogenous antioxidant responses. For example, several repurposed agents (e.g., metformin) and natural compounds (such as ginsenosides) may exert neuroprotective effects by modulating mitochondrial function and reducing reactive oxygen species (ROS). Additionally, drugs that activate the Nrf2 pathway—or that inhibit its antagonist Bach1—are being tested because they can induce the transcription of over 250 cytoprotective genes that counteract oxidative damage, restore redox balance, and promote neuronal repair.

Another class of drugs in development aims to modulate kinases implicated in PD pathogenesis. LRRK2 inhibitors are under active investigation owing to the fact that gain-of-function mutations in the LRRK2 gene are a well-established risk factor in familial PD. Despite early setbacks related to off-target effects such as lung toxicity, improved molecular designs and delivery strategies may allow these inhibitors to safely downregulate pathological signaling pathways and potentially slow neurodegeneration.

Furthermore, novel gene therapies and cell replacement therapies are emerging with the aim not just of substituting dopamine but of restoring or protecting damaged neurons. Techniques that employ adeno-associated viruses (AAV) to deliver genes such as AADC (which encodes the enzyme aromatic L-amino acid decarboxylase) are designed to boost the endogenous production of dopamine from residual neurons. Gene therapies have the advantage of a long-term or even permanent effect, though they also face challenges related to delivery, dosing precision, and immune reactions.

Finally, novel strategies are targeting non-dopaminergic systems that can indirectly affect PD pathology. For example, low-dose ketamine has been studied as an adjuvant therapy to treat levodopa-induced dyskinesia (LID), presumably through its NMDA receptor antagonism and its potential neuroprotective effects. Such approaches provide symptomatic benefits and may also modify disease progression by reducing excitotoxicity and subsequent neuronal loss.

In essence, the new drugs for Parkinson’s disease are designed to modulate several disease-relevant pathways simultaneously. While traditional therapies focused solely on replacing the lost neurotransmitter, emerging drugs address aberrant protein aggregation, oxidative stress, dysfunctional kinases, impaired neurotrophic support, and even non-dopaminergic targets. Together, these approaches promise a more holistic and effective treatment strategy.

Clinical Efficacy and Safety

Clinical Trial Outcomes

Recent clinical trial outcomes have provided encouraging data on several new drug candidates for PD. Trials of extended-release formulations, such as IPX-203, have demonstrated significant improvements in “Good On” time (the period during which patients experience optimal motor function), thereby confirming that more stable plasma dopamine levels translate into clearer clinical benefits. In studies evaluating safinamide as an adjunct treatment, both motor improvements and reductions in “off-time” have been reported, with patients showing statistically significant improvements in the UPDRS part III motor scores in the context of their regular levodopa therapy.

The promising results for pimavanserin for treating PD psychosis have also been a highlight. Clinical data indicate that pimavanserin treatment leads to a reduction in hallucinations and delusions without worsening motor symptoms—a critical advantage over other antipsychotics which often block dopamine receptors and thereby exacerbate PD motor deficits. Additionally, early clinical evidence from trials investigating low-dose ketamine suggests a sustained improvement in LID, with benefits lasting for several weeks beyond treatment—a result that, if verified in larger controlled studies, could represent a major advancement in managing levodopa-induced side effects.

Beyond these symptomatic treatments, early-phase trials of gene therapy approaches, such as AAV-hAADC, have reported improvements in dopamine synthesis and motor function, although the long-term efficacy and safety of these interventions remain under evaluation. Moreover, immunotherapy trials targeting alpha-synuclein have shown that these agents can reduce levels of pathogenic protein species in the brain, though definitive evidence of clinical benefit in terms of slowing progression is still pending.

It is important to note that while many new agents show robust improvements in specific endpoints (such as motor score improvements or “Good On” time extension), the heterogeneity in clinical trial design—ranging from trial duration to patient selection criteria—often makes direct comparison challenging. Nonetheless, these trials collectively suggest that next-generation therapy development in PD is reaching a stage where substantial symptomatic benefit, and potentially even disease-modifying effects, may be achievable.

Side Effects and Safety Profiles

Safety remains a pivotal concern in PD drug development because even highly effective treatments can be limited by intolerable side effects. The novel formulations that have reached the clinic (for example, IPX-203) appear to have a favorable safety profile largely due to their more constant plasma levels, which help to avoid the sporadic high peaks that can cause dyskinesia and other motor complications. Similarly, pimavanserin’s specific mechanism of action solely via the serotonergic system lends it a safety advantage by avoiding the motor side effects that are common with drugs impacting dopaminergic pathways.

On the other hand, early attempts at targeting non-dopaminergic mechanisms, such as LRRK2 kinase inhibitors, have faced challenges: preclinical assessments have raised concerns such as lung toxicity in primate models, meaning that such approaches require careful titration, targeted delivery, or molecular reformulation to mitigate off-target effects. Drugs that modulate alpha-synuclein, whether through immunotherapy or small molecules, are still in early-phase trials; thus, although they hold promise, their long-term safety profile, particularly regarding immune responses or unexpected toxicities, remains to be fully elucidated.

Other novel candidates, including those repurposed from other indications (e.g., low-dose ketamine), have demonstrated relatively manageable side effect profiles at doses effective for modifying dyskinesia, though caution is always advised given ketamine’s well-known psychotomimetic effects at higher doses. Gene therapy candidates and cell therapies, while conceptually attractive for their potentially long-lasting effects, also face unique safety challenges. Issues such as immune reactions to viral vectors, the risk of uncontrolled cell proliferation, or off-target gene expression remain to be comprehensively addressed in rigorous long-term safety studies.

Overall, the clinical trial outcomes thus far indicate that many of the new drugs for PD have acceptable safety profiles that enhance their potential for real-world application. Continued vigilance in monitoring adverse effects, particularly in long-term studies, is essential to ensure that the benefits of these therapies truly outweigh the risks.

Future Directions in Parkinson’s Disease Treatment

Emerging Therapies

Looking ahead, the field of Parkinson’s disease therapeutics is rapidly evolving. Beyond the immediate next-generation symptomatic treatments, researchers are actively pursuing disease-modifying therapies that target the underlying neurodegenerative process. These emerging therapies include:

1. Immunotherapy and Anti-alpha-Synuclein Strategies:
Researchers continue to investigate monoclonal antibodies and vaccines that specifically target alpha-synuclein. The goal of these therapies is to either prevent the formation of toxic aggregates or promote their clearance from neurons. While early clinical trials have provided proof-of-concept data, further studies are required to confirm their long-term efficacy and safety.

2. LRRK2 Inhibitors and Kinase Modulators:
Given that mutations in the LRRK2 gene are implicated in a significant subset of familial PD and even contribute to sporadic cases, second-generation LRRK2 inhibitors that address earlier safety concerns are under active development. These agents are designed with improved selectivity and delivery systems that can limit off-target toxicity, particularly in non-neuronal tissues.

3. Gene Therapy and Cell Replacement Strategies:
Gene-based therapies, including the delivery of dopamine-synthesizing enzymes (such as AADC via AAV vectors), and cell replacement approaches using stem cell-derived dopaminergic neurons, are emerging as promising interventions. These therapies aim not only to restore dopamine levels but also to protect and regenerate neuronal circuits affected by PD.

4. Targets in Oxidative Stress and Neuroinflammation:
As oxidative stress is a major contributor to neurodegeneration in PD, agents that activate endogenous antioxidant pathways (for instance via Nrf2 activation) or that simultaneously inhibit pro-oxidant signals are under investigation. In particular, the inhibition of Bach1 (an antagonist of Nrf2) has been proposed as a synergistic approach to enhance cellular defense mechanisms and may provide broad neuroprotection across multiple pathogenic pathways.

5. Repurposing Non-Dopaminergic Agents:
Modern drug repurposing efforts are harnessing big data and artificial intelligence to identify compounds that may have been overlooked using traditional screening methods. These studies have already flagged agents such as metformin and other natural compounds (for example, ginsenoside-Rg1) that demonstrate neuroprotective and mitochondrial-stabilizing effects in experimental PD models. Additionally, there is interest in targeting the kynurenine pathway—since certain enzymes in this pathway are expressed peripherally and can modulate central nervous system inflammation and oxidative stress—thus offering a prospect for treatments less affected by the blood–brain barrier.

6. Novel Drug Delivery Approaches:
Emerging patent literature describes a range of innovative drug delivery systems designed to achieve sustained and targeted therapeutic release to the brain. Such systems make use of advanced materials and nanotechnology approaches to optimize the bioavailability of existing and new agents, reduce side effects, and enhance efficacy.

Together, these emerging therapies represent a shifting paradigm in PD treatment, moving from mere symptom alleviation to strategies that might slow, stop, or even reverse neurodegeneration.

Research and Development Trends

Future trends in Parkinson’s disease research are expected to be characterized by a more integrative and multi-targeted approach. Advances in genetics and biomarkers have already begun to enable more patient-tailored therapeutic regimens. These include:

1. Precision Medicine Approaches:
The increasing understanding of the genetic underpinnings of PD (such as mutations in LRRK2, PINK1, and SNCA) is fostering the development of precision medicine approaches where therapies can be tailored based on a patient’s genetic profile. This will allow for the stratification of patients into subgroups that are more likely to benefit from specific interventions, whether they are gene-based therapies, immunotherapies, or kinase inhibitors.

2. Multi-Modal Clinical Trials:
Given the slow progression and heterogeneity of PD, selecting the radiographic, clinical, and genetic biomarkers to track disease modification has become critical. New clinical trial designs that integrate these biomarkers with digital monitoring tools and predictive analytics (often powered by artificial intelligence) are emerging. For example, novel tools that predict the rate of disease progression based on a combination of genetics, brain imaging, and clinical assessments are being used to select patients who are likely to demonstrate progression over a shorter timeframe, thereby reducing trial duration and participant heterogeneity.

3. Combination Therapies:
Combination therapies that target multiple pathways concurrently (for instance, pairing a stable levodopa formulation with an anti-dyskinetic agent or combining a dopaminergic agent with an immunotherapeutic targeting alpha-synuclein) are likely to play a key role in future standard of care. Such regimens aim to address both motor and non-motor symptoms while delivering neuroprotective benefits. Early results from multi-arm trials are encouraging and point toward the eventual establishment of combination therapy benchmarks in PD.

4. Advanced Drug Delivery Systems:
The development of novel drug delivery platforms—such as implantable devices, nanocarriers, and advanced formulations that allow for pulsatile or continuous drug release—is a trend that is expected to further improve the pharmacokinetics and patient adherence of future treatments. These systems are designed to bypass physiological obstacles like the gastrointestinal tract and blood–brain barrier, thus ensuring that therapeutic agents reach their target more effectively.

5. Collaborative and Open Science Models:
The challenges inherent in PD drug discovery have spurred a collaborative approach across academia, industry, and government. Open science contests and international collaborations are increasingly common, as demonstrated in initiatives like the CACHE (Critical Assessment of Computational Hit-Finding Experiments) program, which leverages artificial intelligence to identify novel therapeutic hits for PD. Such collaborative models are expected to accelerate the pace of discovery and reduce the traditional barriers of high cost and prolonged development timelines.

6. Translational Research Focus:
With an emphasis on bridging the gap between preclinical success and clinical efficacy, significant resources are now devoted to better preclinical models that more accurately recapitulate the slow progression and multifaceted pathology of PD. Novel models based on endogenous neurotoxins (e.g., aminochrome) and improved animal models are contributing to a more realistic evaluation of therapeutic candidates.

These trends indicate that the field is moving toward a more holistic understanding and treatment of Parkinson’s disease, reflecting an interplay between advanced molecular insights and novel drug development strategies.

Conclusion

In summary, new drugs for Parkinson’s disease are emerging on multiple fronts as researchers strive to overcome the shortcomings of conventional dopaminergic therapies. Beginning with a disease that is characterized by progressive motor dysfunction, non-motor deficits, and complex underlying pathology, the current therapeutic landscape has expanded beyond mere symptomatic replacement therapy. Recently approved drugs such as extended-release formulations (e.g., IPX-203) and agents like pimavanserin and safinamide have already begun to refine treatment paradigms by improving both efficacy and safety profiles.

In clinical trials, the pipeline is rich and diverse. Novel agents encompass repurposed drugs (e.g., low-dose ketamine for dyskinesia and metformin for mitochondrial protection), immunotherapeutics aimed at halting alpha-synuclein aggregation, kinase inhibitors (such as next-generation LRRK2 inhibitors), gene therapies that aim to boost dopamine synthesis, and even cell replacement strategies. Advances in pharmacodynamic and pharmacokinetic engineering—through novel delivery systems and extended-release formulations—are addressing previous issues with inconsistent plasma drug levels and troublesome side effects.

Mechanistically, these new drugs are targeting a broad array of pathways. Apart from traditional dopaminergic replacement, there is an increasing focus on reducing oxidative stress, modulating neuroinflammation, correcting dysfunctional protein handling (notably alpha-synuclein aggregation), and normalizing disrupted kinase signaling groups. By improving receptor targeting, optimizing absorption, and tailoring drugs to engage multiple molecular targets, researchers hope to slow—and eventually modify—the disease progression rather than simply manage symptoms.

Clinical trial outcomes so far are promising, with improvements noted in key outcome measures such as “Good On” time, reduction in off-time, and amelioration of levodopa-induced dyskinesia, alongside early signals from neuroprotective and gene-based approaches. Safety profiles vary among these drugs: while novel formulations of levodopa and selective serotonin receptor modifiers such as pimavanserin appear to offer favorable tolerability, other more innovative candidates (such as early LRRK2 kinase inhibitors) must overcome potential off-target effects like lung toxicity. Clearly, while efficacy and safety are both critical, focus must be placed on long-term outcome data as more drugs become approved for extended use.

Looking to the future, emerging therapies continue to broaden the treatment landscape. Innovations include the use of precision medicine approaches that customize therapy based on genetic and phenotypic profiles, the development of advanced drug delivery systems that ensure consistent central nervous system access, and an increasing utilization of collaborative research models and AI-driven drug repurposing strategies. As both academic and industrial stakeholders collaborate more closely, the next two decades promise to deliver not only improved symptomatic therapies but also interventions that might modify or even reverse the neurodegenerative trajectory of Parkinson’s disease.

In conclusion, the new drugs for Parkinson’s disease represent a remarkable shift in therapeutic strategy.

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