The research team set out with two central questions. First, what happens clinically to patients who test positive for synuclein seeding in their spinal fluid over five years of careful observation? Second, does a patient’s baseline stage on a new biological staging system—the Neuronal Synuclein Disease Integrated Staging System, or NSD-ISS—predict how quickly they will cross meaningful clinical milestones? Both questions cut to the heart of a quiet revolution in neurology. For more than a century, Parkinson’s was classified by what patients looked like in the examination room. Now, thanks to validated biomarkers, researchers can classify it by what is happening at the molecular level, potentially years before disabling symptoms emerge.

The seed amplification assay, or SAA, is the technological engine behind this shift. The test exploits a peculiar property of misfolded alpha-synuclein: it acts as a template that recruits normal, healthy synuclein proteins and forces them to misfold as well, seeding the aggregates known as Lewy bodies that riddle the brains of Parkinson’s patients. In the laboratory, a tiny sample of cerebrospinal fluid is mixed with synthetic alpha-synuclein and monitored for hours. If pathological seeds are present, the reaction accelerates into a detectable fluorescence signal. The assay has been validated across multiple international cohorts and, critically, against postmortem brain tissue, giving neurologists a window into pathology they previously could only glimpse after death. A complementary technique—detecting phosphorylated alpha-synuclein in small skin biopsies—has added a second, less invasive line of biological evidence.

Armed with these tools, two research groups have proposed frameworks for redefining Parkinson’s disease biologically. The SynNeurGe criteria classify patients by the combined presence of pathological alpha-synuclein biomarkers, neuroimaging evidence of neurodegeneration, and disease-relevant genetic variants. The Neuronal Synuclein Disease criteria take a parallel approach, defining disease by the presence of pathological synuclein as measured by a validated biomarker, with or without evidence of dopaminergic dysfunction detected through dopamine transporter imaging. The integrated staging system then arranges these biological anchors along a seven-stage ladder: Stage 0 reserved for carriers of fully penetrant mutations in the SNCA gene; Stages 1A and 1B for people with synuclein pathology but no symptoms, depending on whether dopaminergic dysfunction is present; Stages 2A and 2B for those with subtle signs that stop short of functional impairment; and Stages 3 through 6 capturing progressively severe clinical disability.

PPMI, the international observational study launched in 2010, provided the ideal laboratory for testing whether this staging framework means anything in the real world. The researchers focused on the sporadic Parkinson’s cohort: participants diagnosed within two years of enrollment who had never taken dopaminergic medication, whose examinations showed cardinal motor features, and whose dopamine transporter scans confirmed the characteristic deficit in the striatum. Crucially, the team selected only those participants who met biological NSD criteria through a positive CSF seed amplification assay, recruited before 2020 to guarantee at least five years of follow-up. This design deliberately stripped away a longstanding source of noise in Parkinson’s research: the clinical heterogeneity that arises when a “Parkinson’s” diagnosis might actually encompass unrelated neurodegenerative processes that mimic the disease but follow entirely different biological courses.

Over the five-year observation window, participants underwent an unusually thorough annual workup. Motor and non-motor function was tracked with the Movement Disorders Society Unified Parkinson’s Disease Rating Scale across all four of its parts, alongside the Hoehn and Yahr staging scale and the Schwab and England activities of daily living score. Smell was measured with the University of Pennsylvania Smell Identification Test, autonomic function with the SCOPA-AUT, mood with the Geriatric Depression Scale, and REM sleep behavior disorder risk with a dedicated screening questionnaire. Cognition was assessed with the Montreal Cognitive Assessment and, from the study’s third year onward, formal clinician diagnoses of normal cognition, mild cognitive impairment, or dementia. Medication burden was quantified as levodopa equivalent daily dose, and dopamine transporter imaging was repeated at years one, two, and four, quantified both in the putamen—the region most affected in Parkinson’s—and across the striatum as a whole.

The broad message from the five-year trajectories is one of measurable, biologically anchored progression. Patients recruited as freshly diagnosed, biologically confirmed sporadic Parkinson’s patients showed the expected decline across motor scales and dopaminergic imaging, with the earlier PPMI analysis by Simuni and colleagues having already documented significant—though modest—correlation between worsening clinical scores and falling DAT binding over five years. What the new analysis adds is the biological filter: by restricting the cohort to synuclein-seeding-positive individuals, the study reduces the contamination from look-alike conditions that has historically muddied progression estimates. When a cohort is defined by its underlying pathology rather than its outward symptoms, the resulting disease course becomes a truer reflection of what alpha-synuclein itself does to the nervous system over time.

Perhaps the most consequential findings concern prediction. If the NSD-ISS staging system is to earn its place in research clinics and, eventually, in therapeutic trials, it must do more than organize patients neatly on a page—it must forecast what comes next. The study analyzed whether a patient’s baseline stage predicted survival and the time required to reach clinically meaningful disease milestones: crossing thresholds on the clinical rating scales, advancing in Hoehn and Yahr stage, slipping in daily living independence, or developing cognitive impairment. The logic is straightforward and powerful. A patient sitting at Stage 2B—with confirmed synuclein pathology, dopaminergic dysfunction, and subtle signs but no functional impairment—should, in theory, march down the staging ladder at a predictable pace. Demonstrating that baseline stage genuinely stratifies risk would give trial designers a rational tool for enrichment, allowing them to recruit patients at the stage where a candidate drug is most likely to show benefit.

That trial-design implication is not academic. Across neurodegenerative disease research, therapeutic development is pivoting decisively toward biomarker-defined enrollment. The bitter lessons of Alzheimer’s trials—where anti-amyloid therapies only proved effective once trials recruited based on biological confirmation rather than syndrome alone—have not been lost on the Parkinson’s community. Drugs targeting alpha-synuclein directly, whether through immunotherapy, aggregation inhibition, or other mechanisms, are entering trials that increasingly require positive seed amplification assays or other biological confirmation as a gate for entry. A validated staging system that predicts five-year trajectory would allow sponsors to select participants early enough in the disease process for neuroprotective strategies to matter, while reserving later-stage patients for symptomatic interventions. The five-year PPMI data provide exactly the kind of naturalistic benchmark that such enrichment strategies demand.

The study also marks a conceptual milestone: the description of Parkinson’s disease under contemporary management. Patients diagnosed today are treated differently than those diagnosed twenty years ago, and their disease course may differ as a result. Describing outcomes in a biologically defined, prospectively observed cohort establishes a modern baseline against which future disease-modifying therapies can be judged. When an experimental drug claims to slow progression, the comparison will be against trajectories like those documented here—precise, biomarker-anchored, and free of the diagnostic uncertainty that plagued earlier natural history studies. In that sense, the paper functions simultaneously as a clinical report and as a foundation stone for the next generation of Parkinson’s trials.

What emerges from five years of watching synuclein-positive patients is a disease that can now be seen, staged, and tracked before it fully announces itself. The combination of CSF seed amplification assays, dopamine transporter imaging, and structured clinical assessment has converted a syndrome defined in the examination room into a biological disease measurable in the laboratory. If the staging system validated in this cohort continues to predict who declines fastest and who reaches milestones soonest, neurologists may one day tell a newly diagnosed patient not only what they have, but with unprecedented confidence what lies ahead—and researchers may finally test neuroprotective drugs in the early biological window where they stand the best chance of changing the story. For a disease that has resisted precise definition since James Parkinson first described it in 1817, that is a transformation worth watching.

Parkinson’s disease, often shrouded in clinical ambiguity until motor symptoms become overt, has long eluded early, minimally invasive diagnostic testing. Traditional methodologies rely heavily on symptomatic evaluation and imaging techniques, which seldom capture the disease in its embryonic stages. This latency fundamentally impedes timely intervention, often resulting in irreversible neuronal loss in the substantia nigra. Against this backdrop, the identification of reliable peripheral biomarkers is a strategic imperative. The researchers’ focus on lipidomics—profiling the complete spectrum of lipid molecules—embraces the hypothesis that subtle peripheral metabolic alterations mirror central neurodegeneration with sufficient fidelity to serve diagnostic and prognostic purposes.

Delving into the biochemical architecture of Parkinson’s, the study employed advanced mass spectrometry-based lipidomic profiling to scrutinize blood samples from diagnosed patients and matched controls. Red blood cells (RBCs) and plasma were chosen deliberately, offering accessible and stable sources to capture systemic metabolic disturbances associated with neurodegeneration. These biofluids, often overlooked in the search for neurodegenerative biomarkers, yielded a trove of lipid anomalies that distinguish idiopathic Parkinson’s from healthy physiology. The researchers meticulously quantified various classes of lipids including phospholipids, sphingolipids, and cholesterol derivatives to create a detailed molecular fingerprint reflective of disease status.

Among the most striking revelations was the dysregulation of specific sphingolipid species within the RBC membranes, revealing a potential mechanistic link to neuronal membrane integrity and signaling pathways disrupted in Parkinson’s. Sphingolipids, known for their roles in cell survival and apoptotic regulation, demonstrated perturbations that could correlate with the pathobiology of dopaminergic neuron degeneration. This observation aligns with mounting evidence implicating dysfunctional lipid metabolism in the etiology of synucleinopathies, promoting the hypothesis that pathogenic α-synuclein aggregation might be influenced or even initiated by altered membrane lipid environments.

Equally compelling were the alterations observed in plasma lipid profiles, where the researchers noted significant shifts in phosphatidylcholine and lysophosphatidylcholine concentrations. These changes not only reflect membrane remodeling but also inflammatory processes that are increasingly recognized as contributors to Parkinson’s progression. The inflammatory milieu, potentially propagated by modified lipid signaling molecules in the plasma, could exacerbate neuronal vulnerability, suggesting that these biomarkers might have dual utility in tracking both disease presence and inflammatory activity.

The technical rigor of the study was underscored by its comprehensive lipidomic workflow, incorporating ultra-high-performance liquid chromatography coupled with tandem mass spectrometry (UHPLC-MS/MS). This approach enabled unparalleled sensitivity and specificity, capturing a panoramic view of lipid perturbations. Advanced bioinformatic analyses further distilled these complex datasets into clinically actionable insights, charting lipid candidates with robust differentiation power. The multi-omics integration strategy may pave the way for holistic biomarker panels transcending the limitations of single-parameter assays.

Importantly, the study’s cohort was methodically curated to exclude confounding variables such as medication effects, comorbidities, and lifestyle factors known to influence lipid metabolism. Such stringent controls enhance the validity of the lipid biomarkers’ association with idiopathic Parkinson’s, potentially elevating them beyond mere correlates to causally informative indicators. This careful design affirms that the lipidomic alterations observed are intrinsic to Parkinson’s pathology rather than epiphenomena of secondary influences.

The implications of these discoveries stretch far beyond diagnostics. The elucidation of altered lipid metabolic pathways opens fertile new avenues for therapeutic exploration. Targeting aberrant lipid synthesis or remodeling enzymes may offer strategies to restore membrane homeostasis and disrupt pathological α-synuclein aggregation. Furthermore, plasma lipid signatures could be leveraged to monitor treatment response and disease trajectory, enabling truly personalized medicine in Parkinson’s disease management.

The prospect of blood-based lipid biomarkers transforming the Parkinson’s clinical landscape is profound. Early, accessible, and minimally invasive testing would empower neurologists and researchers alike, facilitating earlier intervention and accelerating clinical trial recruitment by identifying patients in prodromal stages. This shift could ultimately attenuate the burdensome progression of PD, improving quality of life and reducing healthcare costs.

Despite these transformative potentials, the authors prudently acknowledge certain limitations. While the lipid biomarkers demonstrated strong discriminatory power, validation in larger and ethnically diverse populations is essential to cement their clinical applicability. Additionally, longitudinal studies are necessary to ascertain the biomarkers’ predictive value over the course of disease evolution and response to therapy. The complexity of lipid pathways demands integrative systems biology approaches to unravel the causal hierarchies and interactions with genetic and environmental factors.

Moreover, this work raises tantalizing questions regarding the interplay between lipid metabolism and neurodegenerative pathways. Could lipid dysregulation be a primary driver or a downstream effect of neuronal demise? How might these lipidomic signatures intersect with other molecular hallmarks such as mitochondrial dysfunction, oxidative stress, or immune activation? Addressing these questions will undoubtedly propel the field into novel mechanistic and translational territories.

The publication of this landmark paper also reflects the surging momentum in neuro-lipidomics as an emergent discipline. As analytical technologies mature and computational methodologies expand, the capacity to decode the lipid landscape promises unprecedented insights into neurological diseases. The confluence of neurobiology, biochemistry, and systems medicine heralds a future where diseases like Parkinson’s are understood and managed with unprecedented molecular precision.

In conclusion, the discovery of distinctive lipid biomarkers in red blood cells and plasma by Nazaar, Roberts, Horne and colleagues represents a pivotal advancement in Parkinson’s disease research. This study not only provides a viable pathway toward earlier, more accurate diagnosis but also opens innovative therapeutic horizons centered on restoring lipid homeostasis. As the global burden of Parkinson’s disease continues to escalate, such breakthroughs offer tangible hope for millions affected worldwide. The integration of lipidomics into clinical neuroscience is poised to transform the biomarker landscape, shifting paradigms from symptomatic care to proactive molecular medicine.

Subject of Research: Identification of lipid biomarkers in red blood cells and plasma for idiopathic Parkinson’s disease diagnosis and understanding of disease mechanisms.

Article Title: Discovery of lipid biomarkers for idiopathic Parkinson’s disease in red blood cells and plasma.

Article References:

Nazaar, S.M., Roberts, A.M., Horne, M. et al. Discovery of lipid biomarkers for idiopathic Parkinson’s disease in red blood cells and plasma.
npj Parkinsons Dis. (2026). https://doi.org/10.1038/s41531-026-01434-4

Image Credits: AI Generated

Parkinson’s disease, known for its hallmark motor symptoms such as tremors, rigidity, and bradykinesia, arises primarily from the progressive death of dopaminergic neurons within the substantia nigra. Despite decades of research, early diagnosis remains a formidable challenge, often relying on symptomatic evaluation that occurs well after significant neuronal loss has occurred. This research breakthrough centers around creatine-weighted imaging, marking a substantial departure from traditional structural and functional neuroimaging modalities by focusing explicitly on cerebral energy metabolism.

Creatine, a crucial molecule involved in cellular energy homeostasis, plays an essential role in buffering adenosine triphosphate (ATP) levels to meet fluctuating energetic demands. In the brain, aberrations in creatine metabolism have long been suspected to contribute to neurodegeneration, yet clinical tools to non-invasively assess these anomalies have been strikingly limited. By utilizing a refined magnetic resonance imaging (MRI) protocol tailored to detect creatine signals specifically, the authors have crafted a window into this metabolic axis, providing a rich biochemical profile of affected brain regions in vivo.

The technical innovation underpinning creatine-weighted imaging integrates advancements in MRI pulse sequences, exploiting resonant frequencies unique to creatine molecules. Enhanced sensitivity and specificity are achieved by meticulously calibrating the imaging parameters to suppress background noise and confounding signals from other metabolites. This meticulous approach enables the quantification of creatine concentration changes with remarkable spatial resolution, allowing researchers to delineate metabolic dysfunction at a cellular level within PD-affected circuitry.

Through comprehensive clinical studies involving PD patients at various disease stages, the creators of this technique have demonstrated that reduced creatine signals strongly correlate with both the severity and progression of motor symptoms. Intriguingly, alterations in creatine metabolism were detectable even in regions reportedly spared in early-stage PD, suggesting a more widespread and systemic metabolic disruption than previously recognized. These findings underscore the potential of creatine-weighted imaging not only as a diagnostic tool but also as a surrogate biomarker for disease progression and therapeutic response.

Moreover, the study reveals a compelling link between creatine metabolism and mitochondrial dysfunction, a longstanding hypothesis in PD pathogenesis. The depletion of creatine observed in affected neural structures appears to mirror compromised mitochondrial bioenergetics, implicating a cascade of metabolic failure that precedes overt neurodegeneration. These insights provide a molecular rationale for targeting creatine-related pathways as a novel therapeutic approach, rekindling interest in creatine supplementation strategies that have thus far yielded mixed clinical outcomes.

The implications extend beyond diagnostics and therapeutics, as this imaging technology could revolutionize clinical trial design by offering an objective, quantifiable measure of metabolic integrity. Traditional endpoints relying on subjective clinical scales are prone to variability; hence, incorporating creatine-weighted imaging biomarkers could sharpen the evaluation of experimental treatments, accelerating the pipeline for effective PD interventions.

Furthermore, the adoption of creatine-weighted imaging may facilitate precision medicine approaches by phenotyping PD patients based on metabolic status rather than solely clinical manifestations. This granular stratification could uncover subtypes within PD populations, guiding personalized therapy regimens and improving prognostic accuracy. Such a paradigm shift aligns with contemporary trends across neurology, where metabolomics and molecular imaging are increasingly influential.

This research also challenges existing dogma by suggesting that metabolic deficiency in PD is not confined to dopaminergic neurons but involves broader brain networks implicated in motor and non-motor symptoms. By mapping the spatial distribution of creatine deficits, the technique delineates the metabolic topography of Parkinsonian pathology, which may explain the heterogeneous clinical phenotypes frequently observed among patients.

In addition to methodological robustness, the authors provide a thorough validation against established imaging techniques such as positron emission tomography (PET) and proton magnetic resonance spectroscopy (1H-MRS), demonstrating superior specificity and reproducibility. This comparative analysis bolsters confidence in creatine-weighted imaging as a viable addition to the neurodiagnostic armamentarium.

Patients and clinicians alike stand to benefit immensely from these innovations. Early and accurate diagnosis could improve patient outcomes by enabling timely intervention, while enhanced monitoring capabilities may help tailor treatment adjustments dynamically. Psychosocial impacts are not negligible, as reducing diagnostic uncertainty can alleviate patient anxiety and inform caregiving strategies.

Looking forward, the researchers anticipate integrating creatine-weighted imaging with other multimodal imaging approaches, including diffusion tensor imaging and functional MRI, to construct comprehensive neurobiological profiles of PD. Such multidimensional datasets may unravel complex disease mechanisms, fostering integrative models that better predict disease trajectory and response.

Challenges remain in scaling this technology for widespread clinical use, including standardization of imaging protocols, accessibility in diverse healthcare settings, and cost considerations. However, as MRI platforms globally evolve, the incorporation of sophisticated metabolic imaging sequences is becoming increasingly feasible, hinting at imminent translational breakthroughs.

This seminal study ultimately broadens the horizon in Parkinson’s disease research, illustrating the power of metabolic imaging to unlock concealed aspects of neurodegeneration. Creatine-weighted imaging not only enriches our understanding of PD pathophysiology but also pioneers a transformative path toward improved clinical care, embodying the convergence of technological ingenuity and medical necessity.

As the scientific community digests these findings, further research will undoubtedly probe the nuances of creatine metabolism’s role in neural health and disease. Whether this approach will extend to other neurodegenerative disorders marked by mitochondrial compromise remains an intriguing prospect worth exploration.

In sum, the introduction of creatine-weighted imaging represents a paradigm shift, offering a sensitive, non-invasive, and clinically applicable method to visualize metabolic dysfunction in Parkinson’s disease. This innovation holds promise to catalyze new diagnostic standards, therapeutic targets, and research trajectories, engraving an indelible mark on the quest to unravel and ultimately conquer Parkinson’s disease.

Subject of Research: Parkinson’s disease diagnostic imaging and metabolic biomarkers

Article Title: Creatine-weighted imaging in patients with Parkinson’s disease

Article References:
Wang, K., Yadav, N.N., Yang, Z. et al. Creatine-weighted imaging in patients with Parkinson’s disease. npj Parkinsons Dis. (2025). https://doi.org/10.1038/s41531-025-01203-9

Image Credits: AI Generated

Parkinson’s disease, long characterized primarily by its motor symptoms such as tremor, rigidity, and bradykinesia, has increasingly been recognized to encompass non-motor symptoms, including cognitive impairment. Cognitive decline in PD patients can range from mild deficits to full-blown dementia, profoundly affecting quality of life. Importantly, this new study delves into the spatial and temporal aspects of alpha-synuclein pathology, particularly its presence and seeding activity in the gastric tissues of patients recently diagnosed with Parkinson’s.

The researchers employed an advanced assay designed to detect the seeding capability of alpha-synuclein aggregates—a process by which pathological proteins induce misfolding in native alpha-synuclein molecules. This seeding amplification method is highly sensitive and specific, allowing detection even in peripheral tissues like the stomach. The assay’s application to gastric biopsy samples enabled the team to quantitatively analyze the burden of alpha-synuclein seeds in early PD patients, revealing a robust correlation with neuropsychological measures of cognitive function.

This novel approach marks a paradigm shift from relying solely on central nervous system biomarkers to interrogating peripheral tissues for insights into neurodegenerative processes. The stomach, innervated by the vagus nerve and forming a critical node in the gut-brain axis, is increasingly implicated in the early spreading of alpha-synuclein pathology. The findings reinforce the hypothesis that pathological alpha-synuclein might originate or be amplified in the gut, potentially migrating to the brain and contributing to cognitive deficits observed even at the disease’s early stages.

Importantly, the study details that patients exhibiting higher gastric alpha-synuclein seeding activity scored worse on cognitive assessments, notably in domains related to executive function, attention, and memory. The authors propose that such peripheral measures could serve as biomarkers predicting not just motor symptom severity but also cognitive trajectories in PD, potentially pinpointing individuals at risk for more rapid cognitive decline.

From a methodological standpoint, the rigorous inclusion criteria and sophisticated analytical protocols lend heft to the study’s conclusions. Patients were carefully selected to represent a typical early PD population, and matched controls were included to validate the specificity of the assay. Gastric biopsies were obtained endoscopically, underscoring the clinical feasibility of deploying such tests in routine diagnostic workflows.

The implications of these results are substantial. If confirmed in larger cohorts, gastric alpha-synuclein seeding assays could transform early PD diagnosis by incorporating cognitive risk assessment, thus enabling stratified patient management. Furthermore, the gut-centric nature of alpha-synuclein pathology invites exploration of therapies targeting peripheral alpha-synuclein aggregation, offering a potentially less invasive and more accessible intervention point compared to central nervous system-directed approaches.

The study also sparks compelling questions regarding the pathophysiological sequence of events. Does gastric alpha-synuclein aggregation precede central nervous system involvement, or is it merely a peripheral reflection of systemic pathology? Understanding this chronological order is vital for developing preventive strategies that could intercept disease progression at its nascent stage.

Moreover, the investigation aligns with emerging evidence from epidemiological and experimental models suggesting that gastrointestinal dysfunction and altered microbiota composition are intimately linked with Parkinson’s disease pathogenesis. Alpha-synuclein aggregation in enteric nervous system structures could be not only a marker but also a mediator of disease progression, contributing to the multifaceted symptomatology characteristic of PD.

The integration of seeding assays with cognitive evaluations also paves the way for future research aiming to dissect molecular underpinnings of neurodegeneration beyond motor impairment. Since cognitive dysfunction imposes a significant burden on patients and caregivers, elucidating its early biological correlates is paramount for devising therapeutic interventions tailored to preserve cognitive health.

Challenges remain to be addressed, including standardizing seeding assay protocols across centers, determining optimal biopsy sites, and validating findings across diverse populations. Additionally, longitudinal studies are needed to track changes over time, establishing whether gastric alpha-synuclein seeding activity predicts cognitive decline or responds to treatment modifications.

This research contributes to a growing body of work positioning Parkinson’s disease as a systemic rather than purely neurological disorder. Such systemic perspectives are catalyzing a shift towards multidisciplinary paradigms in diagnosis and treatment, emphasizing the interplay among neural, immune, and gastrointestinal systems.

As we deepen our comprehension of the gut-brain axis in neurodegeneration, the opportunity emerges to reframe clinical management strategies by incorporating peripheral biomarkers and targeting early-stage pathological processes. This may ultimately lead to more precise, personalized medicine approaches in Parkinson’s disease, enhancing outcomes and extending quality of life.

In conclusion, the insightful analysis correlating gastric alpha-synuclein seeding activity with cognitive impairment offers a transformative addition to Parkinson’s disease research. By bridging peripheral pathology with central nervous system outcomes, this study lays critical groundwork for early diagnostic innovations and therapeutic development. The findings underscore the importance of considering extraneural tissues in neurodegenerative disease frameworks and highlight the value of sensitive molecular assays in unraveling complex disease mechanisms.

As the field advances, leveraging such biomarker-driven insights will be key to overcoming current clinical challenges surrounding early diagnosis and heterogenous disease manifestations. This study not only provides a roadmap for future investigations but also invites renewed optimism for tackling one of the most burdensome neurodegenerative diseases via novel conceptual and technical approaches.

Subject of Research:
Parkinson’s disease, alpha-synuclein pathology, cognitive decline, gut-brain axis, gastric biopsy biomarkers.

Article Title:
Cognitive function correlates with gastric alpha-synuclein seeding activity in early Parkinson’s disease

Article References:
Shin, C., Im, J.P., Han, JY. et al. Cognitive function correlates with gastric alpha-synuclein seeding activity in early Parkinson’s disease. npj Parkinsons Dis. 11, 311 (2025). https://doi.org/10.1038/s41531-025-01152-3

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41531-025-01152-3