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Neurocompute

AI-driven Parkinson’s research intelligence platform exploring emerging signals, forgotten papers, and therapeutic patterns across the biomedical literature universe.

Indexed Papers
1,516
AI Scored
984
Ranked Papers
998
Coverage
1.3%
RESEARCH INTELLIGENCE BOARD

Ranked Parkinson’s Papers

1516 results
LAST INGEST 2026-05-29 06:45 PM
B
Neurosyphilis and Parkinsonism: Overlapping Pathophysiology and Emerging Therapeutic Insights.
PMID 41926293 Published: 2026-03-31 Ingested: 2026-04-28 08:58 PM Current neurovascular research
AI 76.0
Base 78.9
Rank 76.1
AI Summary

Narrative review proposing that neurosyphilis can produce Parkinsonism via shared mechanisms—BBB disruption, dopaminergic neuronal loss, TLR-driven neuroinflammation—and summarizes diagnostic approaches and potential therapeutic repurposing (β-lactams, doxycycline) and nanoparticle-based…

Why It Matters

Identifies actionable, translationally relevant mechanisms (BBB integrity, neuroinflammation, dopaminergic degeneration) and repurposing/delivery strategies that could inform PD-targeted therapeutic development and differential-diagnostic biomarker work, despite being a non-systematic review with…

B
Molecular biochemistry of soluble epoxide hydrolase in lipid mediator pathways and neuroinflammatory responses.
PMID 41956168 Published: 2026-04-08 Ingested: 2026-04-28 08:58 PM The Journal of steroid biochemistry and molecular biology
AI 82.0
Base 77.3
Rank 75.7
AI Summary

This review details how soluble epoxide hydrolase (sEH) degrades anti-inflammatory epoxy fatty acids, summarizes urea- and amide-based sEH inhibitor chemistry and PK, and presents preclinical and early clinical evidence that sEH inhibition can reduce neuroinflammation and provide neuroprotection…

Why It Matters

It identifies sEH as a druggable target with mechanistic linkage to neuroinflammation and lipid signaling and points to actionable small-molecule inhibitors and translational data that could be leveraged for Parkinson's therapeutic development.

B
Multifaceted role of CNPY2 beyond ER stress: Disease implications and therapeutic potential.
PMID 42016348 Published: 2026-01-01 Ingested: 2026-04-28 08:58 PM Cell stress
AI 83.3
Base 78.3
Rank 75.6
AI Summary

This review synthesizes evidence that CNPY2, an ER-luminal regulator of UPR, mitochondrial dynamics, oxidative stress, and apoptosis, has neuroprotective roles in Parkinson's and Huntington's disease and discusses its therapeutic potential across cancer, cardiovascular, and neurodegenerative…

Why It Matters

By linking CNPY2 to core Parkinson's-relevant mechanisms—ER stress/proteostasis, mitochondrial dysfunction, and oxidative stress—this paper highlights a tractable molecular target that could inform neuroprotective strategies and biomarker development, though primary mechanistic and in vivo…

B
Neuroprotective Role of Exercise-based Physiotherapy Combined with Pharmacological Agents in Parkinson's Disease.
PMID 41941284 Published: 2026-03-12 Ingested: 2026-04-28 08:58 PM Central nervous system agents in medicinal chemistry
AI 64.0
Base 78.3
Rank 75.6
AI Summary

Narrative review compiling preclinical and clinical evidence that combining exercise-based physiotherapy with pharmacological treatments in Parkinson's disease can enhance neuroprotection—via increased BDNF, reduced oxidative stress and inflammation, and improved motor/non-motor outcomes—while…

Why It Matters

Identifies a low-risk, clinically translatable adjunct strategy that targets neuroprotective mechanisms and warrants focused, protocolized translational or clinical trials despite currently limited actionable regimen details.

B
Distinct metabolomic and proteomic signatures in Parkinson's disease patients with REM sleep behavior disorder.
PMID 41912482 Published: 2026-03-30 Ingested: 2026-04-28 08:58 PM Signal transduction and targeted therapy
AI 84.0
Base 77.6
Rank 75.0
AI Summary

Integrated plasma metabolomics, proteomics, and gut metagenomics reveal that RBD-associated PD and idiopathic RBD show a shift from TCA toward glycolysis, dysregulated urea cycle, lipid remodeling, activation of PI3K‑Akt/IL‑17/NF‑κB/MAPK/TNF inflammatory pathways, and accumulation of gut…

Why It Matters

Provides actionable, translationally relevant evidence linking gut microbiome-driven metabolic reprogramming and inflammation to prodromal and aggressive PD subtypes, pointing to microbiome modulation, metabolic and anti‑inflammatory interventions, and biomarker development for early therapeutic…

B
HMGB1-mediated neuroinflammation: molecular mechanisms and emerging therapeutic approaches.
PMID 41964823 Published: 2026-04-11 Ingested: 2026-04-28 08:58 PM Inflammopharmacology
AI 78.0
Base 77.6
Rank 75.0
AI Summary

This review synthesizes evidence that redox- and modification-dependent extracellular HMGB1 drives neuroinflammation via TLR4/RAGE/CXCR4 and downstream NF-κB/MAPK/JAK-STAT/inflammasome pathways, links HMGB1 dysregulation to Parkinson's disease among other CNS disorders, and summarizes preclinical…

Why It Matters

It highlights HMGB1 as a mechanistically actionable inflammatory node with multiple druggable approaches and existing preclinical tools that could be leveraged for PD neuroprotection and target validation, but cautions that overcoming BBB delivery, specificity, and clinical validation is essential…

B
AI 88.0
Base 77.3
Rank 74.7
AI Summary

This review proposes that dynamic instability of neuronal lysosomal pH—driven by components such as V-ATPase, TMEM175, SLC7A11, ClC-7 and regulated by AMPK–mTORC1–TFEB—is a pathogenic mechanism in neurodegeneration and outlines strategies to restore lysosomal pH homeostatic resilience as a…

Why It Matters

It identifies concrete molecular targets and pathways linked to autophagy, mitochondria–lysosome crosstalk, and neuroinflammation and highlights translational opportunities and challenges (biomarkers, neuron-subtype specificity, brain-penetrant modulators), making it highly actionable for…

B
Vitamins as Modulators of Neurodegenerative Disease Pathways: Mechanisms and Therapeutic Perspectives.
PMID 41901170 Published: 2026-03-20 Ingested: 2026-04-28 08:58 PM Nutrients
AI 74.0
Base 77.0
Rank 74.5
AI Summary

This review synthesizes evidence that selected vitamins influence oxidative stress, inflammation, protein aggregation, neurotransmitter synthesis, and mitochondrial function—and may synergize with coenzyme Q10 to provide neuroprotective benefits across neurodegenerative diseases, including…

Why It Matters

By linking clear mechanistic pathways (oxidative stress, neuroinflammation, mitochondrial dysfunction, protein aggregation) with therapeutic dosing and safety considerations, the paper supports prioritized, hypothesis-driven evaluation of vitamin-based adjunctive strategies and potential…

B
Does ACE2 deficiency have a role in Parkinson's disease -exacerbated pulmonary fibrosis?
PMID 41903733 Published: 2026-07-01 Ingested: 2026-04-28 08:58 PM Experimental neurology
AI 84.0
Base 78.6
Rank 74.3
AI Summary

Combining MPTP mouse experiments and GEO-based bioinformatics, the paper shows ACE2 deficiency worsens dopaminergic neuron loss, α-synuclein–linked neuroinflammation and lung fibrosis via downregulated FoxO1 and upregulated TNF, JAK1-STAT3 and AGE-RAGE pathways, and it nominates diagnostic hub…

Why It Matters

The work links a clear, targetable mechanistic axis (ACE2→FoxO1/TNF/JAK1-STAT3/AGE-RAGE) to both neurodegeneration and pulmonary fibrosis, offering actionable biomarkers and drug-repurposing leads that could accelerate therapeutic strategies for PD patients with respiratory comorbidity.

B
Investigating the Neuroprotective Effects of Peripheral Nerve Microcurrent Stimulation in a Mouse Model of Parkinson's Disease.
PMID 41953799 Published: 2026-03-01 Ingested: 2026-04-28 08:58 PM Brain & NeuroRehabilitation
AI 84.0
Base 78.6
Rank 74.3
AI Summary

Peripheral microcurrent stimulation improved motor behavior and preserved substantia nigra dopaminergic neurons in MPTP-treated mice, associated with reduced α-synuclein accumulation and downregulation of TLR4, PARP, and cleaved caspase-3.

Why It Matters

This study presents a noninvasive, potentially translatable neuromodulation therapy that targets neuroinflammation and apoptotic pathways relevant to Parkinson's disease, offering a repurposable approach for neuroprotection that merits further validation in additional models and translational…

B
AI 82.0
Base 78.6
Rank 74.3
AI Summary

3-monothiopomalidomide (3MP), a novel thalidomide derivative, reduces α-synuclein aggregation, suppresses microglial inflammatory responses, preserves SNpc dopaminergic neurons, and improves motor and cognitive outcomes in cell and rat α-synuclein oligomer models, outperforming pomalidomide.

Why It Matters

By jointly targeting α-synuclein aggregation and neuroinflammation with demonstrated in vivo neuroprotection and functional benefit, 3MP is a translationally promising disease-modifying candidate for PD that directly interrupts the pathogenic α-synuclein–microglia cycle.

B
AI 82.0
Base 78.6
Rank 74.3
AI Summary

In an LPS-induced rat model of Parkinsonism, isotopically enriched 64Zn-aspartate reduced behavioral deficits and apomorphine rotations, normalized systemic inflammatory indices and CRP, shifted circulating and peritoneal phagocytes toward anti-inflammatory phenotypes, partially restored thymus…

Why It Matters

Provides strong preclinical evidence that an immunomodulatory, microbiota-stabilizing zinc compound can target neuroimmune–gut axis dysfunction in PD, making it a promising disease-modifying candidate for further mechanistic and translational studies.

B
AI 76.0
Base 78.6
Rank 74.3
AI Summary

ZPT01, a three‑herb formulation, improved motor behavior and protected dopaminergic neurons in MPTP mice and, supported by docking and cell experiments, appears to act via restoring AKT phosphorylation and suppressing COX‑2/PTGS2‑mediated neuroinflammation.

Why It Matters

This work provides preclinical evidence of a multi‑target neuroprotective and anti‑inflammatory candidate that engages translationally relevant pathways (AKT signaling and COX‑2) for PD, making it a promising starting point for further pharmacology, PK/PD, and safety studies despite the usual…

AI Summary

This in silico study uses network pharmacology, molecular docking, 100-ns MD simulations, and DFT to nominate quercetin and kaempferol from the Tianma-Gouteng herb pair as stable binders of AKT1, TP53, and STAT3, linking PI3K-AKT signaling, mitochondrial apoptosis, and neuroinflammation to…

Why It Matters

It generates disease-relevant, actionable hypotheses by prioritizing well-known flavonoids with predicted stable interactions to PD-relevant targets—making them tractable candidates for biochemical and in vivo validation—though findings are limited by being purely computational.

B
AI 72.0
Base 78.6
Rank 74.3
AI Summary

Integrative bulk and single-cell transcriptomics identified 77 shared DEGs between COVID-19 and Parkinson's disease, with enrichment of neuroinflammatory pathways and a marked increase of CHI3L1-expressing astrocytes and enhanced astrocyte–microglia/neuron signaling.

Why It Matters

Highlights CHI3L1 (YKL-40) and astrocyte-driven neuroinflammation as a candidate biomarker/mediator linking viral-induced inflammation to dopaminergic dysfunction, providing a plausible translational target for biomarker development or anti-inflammatory interventions pending functional validation.

B
AI 72.0
Base 78.6
Rank 74.3
AI Summary

In 6‑OHDA SH‑SY5Y cells and unilateral 6‑OHDA rats, Antrodia cinnamomea conjugated to citrate‑stabilized silver nanoparticles improved cell survival and motor behavior, reduced oxidative stress, inflammation, and apoptosis, increased TH/PI3K and lowered α‑synuclein and caspase‑3, with partial…

Why It Matters

This provides proof‑of‑concept for a multitarget neuroprotective strategy addressing oxidative stress, neuroinflammation, apoptosis and α‑synuclein—relevant to PD drug discovery—while translation is tempered by use of an acute toxin model and potential safety/PK issues with silver nanoparticles and…

B
miR-369-3p Modulates LRRK2-Mediated Inflammation and Autophagy in RAW264.7 Macrophages.
PMID 41977401 Published: 2026-04-02 Ingested: 2026-04-28 08:58 PM International journal of molecular sciences
AI 72.0
Base 78.6
Rank 74.3
AI Summary

In RAW264.7 macrophages, miR-369-3p directly targets and reduces LRRK2 expression, limits LPS‑induced NF-κB nuclear translocation, restores autophagy markers (LC3II/I, BECLIN-1, p62) and shifts cytokine output toward an anti-inflammatory profile.

Why It Matters

By showing a miRNA that modulates LRRK2-driven inflammation and autophagy, the study suggests a tractable therapeutic avenue relevant to PD-associated immune/gut inflammation, although results are limited to a murine macrophage line and require neuronal and in vivo validation for translational…

B
Translational advances of exosomes in neurodegeneration towards precision healthcare: From biomarkers to therapeutic frontiers.
PMID 41997082 Published: 2026-04-16 Ingested: 2026-04-28 08:58 PM Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
AI 82.0
Base 76.7
Rank 74.2
AI Summary

This review synthesizes exosome biology and translational advances across neurodegenerative diseases, emphasizing exosome-mediated propagation of misfolded proteins (including α-synuclein), disease-specific exosomal biomarkers, and engineered/ stem cell-derived exosome therapeutics for CNS delivery.

Why It Matters

For Parkinson's research it aggregates actionable leads—α-synuclein-containing exosomes as both biomarkers and pathogenic vectors, plus strategies for exosome-based CNS delivery—while clearly outlining translational barriers (scalability, PK/PD, immunogenicity) that prioritize immediate preclinical…

B
Adult Neurogenesis in Neurodegenerative Diseases: Mechanisms of Dysregulation in Alzheimer's and Parkinson's Disease.
PMID 41898603 Published: 2026-03-17 Ingested: 2026-04-28 08:58 PM International journal of molecular sciences
AI 80.0
Base 76.7
Rank 74.2
AI Summary

This review links impaired adult neurogenesis in the SGZ and SEZ to chronic inflammation, mitochondrial dysfunction, oxidative stress, and accumulation of β-amyloid, tau, and α-synuclein in AD and PD, and discusses non‑pharmacological (diet, exercise) and targeted strategies to stimulate…

Why It Matters

Identifies actionable, disease-relevant mechanisms (inflammation, mitochondria, α-synuclein) and translational interventions that could be leveraged to restore neurogenic capacity and potentially slow Parkinson's disease progression, while noting the key challenge of achieving functional…

B
Galectins as stress-integrating regulators of neuroimmune signaling and proteinopathy in the central nervous system.
PMID 42035925 Published: 2026-04-24 Ingested: 2026-04-28 08:58 PM Neurobiology of disease
AI 80.0
Base 75.7
Rank 73.3
AI Summary

A recent mechanistic review highlighting galectins (notably galectin-1/3/4/8/9) as multifunctional regulators of microglial activation, vesicle/lysosomal damage sensing, autophagy, and the aggregation/propagation of misfolded proteins including α‑synuclein across CNS disease models.

Why It Matters

Highly relevant for Parkinson's drug discovery because galectins intersect α‑synuclein pathology, lysosomal/autophagic clearance, and neuroinflammation—making them candidate biomarkers and stage-specific therapeutic targets, though their context-dependent pro- versus anti‑inflammatory roles imply…

B
Pharmacological interventions targeting the gut-brain axis in neurological disorders: mechanisms and translational applications.
PMID 41994569 Published: 2026-01-01 Ingested: 2026-04-28 08:58 PM Frontiers in neuroscience
AI 77.0
Base 74.9
Rank 72.7
AI Summary

A mechanism-focused review summarizing pharmacological approaches that modulate the microbiota-gut-brain axis—microbiota-directed therapies, immune-inflammatory modulators, neurotransmitter-targeting agents, and barrier-restoring strategies—with an eye toward translational applications across…

Why It Matters

Highlights PD-relevant mechanisms (gut dysbiosis, neuroinflammation, BBB/intestinal barrier dysfunction) and organizes actionable intervention classes that can guide prioritization and repurposing of therapeutics for Parkinson's research and clinical translation.

B
Polyphenols and physical activity stimulate gut microbiota mediated Nrf2 signaling to combat neurodegeneration.
PMID 42033865 Published: 2026-04-20 Ingested: 2026-04-28 08:58 PM Pathology, research and practice
AI 72.0
Base 74.9
Rank 72.7
AI Summary

Review synthesizing evidence that polyphenols and exercise reshape the gut microbiota to produce metabolites (SCFAs, urolithins, indoles) that activate Nrf2 signaling and thereby support antioxidant, mitochondrial, and anti-inflammatory defenses relevant to neurodegeneration including Parkinson's…

Why It Matters

Connects a mechanistic, actionable gut microbiome→Nrf2 axis to pathways central to Parkinson's (oxidative stress, mitochondrial dysfunction, neuroinflammation), pointing to microbiome-informed dietary/exercise interventions, metabolite biomarkers, and metabolite- or Nrf2-targeted adjunct therapies…

B
AI 84.0
Base 76.6
Rank 72.6
AI Summary

This study reports zinc–tannic acid coordination nanoparticles that scavenge ROS, inhibit and disaggregate α‑synuclein fibrils, preserve mitochondrial function, and rescue motor/cognitive deficits and dopaminergic neuron loss in a PD mouse model without overt toxicity.

Why It Matters

Multimodal nanoparticle therapy targets both α‑syn aggregation and oxidative stress with in vivo efficacy and low toxicity, offering a translationally promising disease-modifying approach for Parkinson’s therapeutics.

AI Summary

The paper reports MTP150, a polyfunctionalized N-arylsulfonyl indole that ameliorates protein aggregation, neuroinflammation, oxidative stress, mitochondrial dysfunction, and DNA repair deficits, improving motor performance and neuroprotection in C. elegans, Drosophila, and cellular models of…

Why It Matters

By engaging multiple PD-relevant mechanisms (aggregation, mitochondria, inflammation, DNA repair) and showing efficacy across invertebrate and cell models, MTP150 is a promising preclinical epigenetic-based lead that merits mammalian validation and translational development.

B
ADT-OH promotes mitophagy and suppresses the cytosolic mtDNA-cGAS-STING inflammatory cascade in microglia.
PMID 41951774 Published: 2026-04-09 Ingested: 2026-04-28 08:58 PM Acta pharmacologica Sinica
AI 86.0
Base 75.8
Rank 71.9
AI Summary

ADT-OH, a slow-release H2S donor, induces SQR-dependent mitochondrial uncoupling that activates PINK1–PARKIN–mediated mitophagy in microglia, preventing mtDNA release and cGAS–STING inflammatory signaling in α-synuclein models and rescuing dopaminergic neurons and motor deficits in PD mice.

Why It Matters

This paper identifies a mechanistically actionable compound that links mitophagy induction to suppression of microglia-driven cGAS–STING inflammation and demonstrates in vivo neuroprotection, making ADT-OH a promising lead for PD therapeutic development or repurposing.

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