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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
A
The cGAS-STING-Glymphatic-gut Axis in Parkinson's disease: A proposed self-amplifying triad of Neuroinflammation and therapeutic opportunity.
PMID 41966779 Published: 2026-06-15 Ingested: 2026-04-28 08:58 PM International immunopharmacology
AI 91.0
Base 89.6
Rank 86.2
AI Summary

This review posits a testable 'vicious triad' in PD where gut-derived triggers, cGAS‑STING–driven neuroinflammation, and astrocyte/glymphatic clearance failure form a self‑amplifying loop and proposes combinatorial interventions (microbiome engineering, STING antagonists, astrocyte modulation,…

Why It Matters

By synthesizing gut-brain, innate immune (cGAS‑STING), and clearance (glymphatic/AQP4) biology into an actionable, biomarker-friendly model, the paper highlights multiple tractable targets and rational combinatorial strategies with clear translational and repurposing potential for disease‑modifying…

B
AI 91.0
Base 88.0
Rank 84.8
AI Summary

This review synthesizes evidence that immunosenescence and chronic inflammaging drive neurodegeneration by disrupting microglial and astrocyte homeostasis, mitochondrial and barrier function, and protein-aggregate clearance, and it surveys actionable therapeutic strategies—senolytics,…

Why It Matters

Directly relevant to Parkinson's therapeutic discovery because it links immune-aging mechanisms (senescent glia, systemic inflammation, BBB dysfunction) to impaired clearance of protein aggregates (e.g., α‑synuclein) and prioritizes clinically translatable interventions and delivery approaches that…

B
Flavonoids improve neurotransmitters for Parkinson's treatment: mechanism and therapeutic potential.
PMID 42038302 Published: 2026-01-01 Ingested: 2026-04-28 08:58 PM Frontiers in pharmacology
AI 88.0
Base 88.0
Rank 84.8
AI Summary

This review synthesizes preclinical evidence that diverse flavonoids (e.g., baicalein, quercetin, apigenin, luteolin, EGCG) provide multi-target neuroprotection in PD by modulating dopamine, serotonin, glutamate and acetylcholine systems and by impacting α‑synuclein pathology, mitochondrial…

Why It Matters

By naming specific flavonoid candidates, summarizing mechanisms relevant to key PD pathways and outlining translational barriers (BBB penetration, formulation, safety), the paper serves as a practical roadmap for drug-discovery teams seeking multi-target or repurposing strategies for Parkinson’s…

B
AI 78.0
Base 88.0
Rank 84.8
AI Summary

Narrative review showing that alpha‑lipoic acid and biotin converge on mitochondrial, redox, and inflammatory pathways with consistent preclinical benefit but heterogeneous and limited clinical evidence across neurodegenerative diseases.

Why It Matters

Provides a rationale for repurposing alpha‑lipoic acid (and to a lesser extent biotin) in Parkinson's disease based on mitochondrial and antioxidant mechanisms and safety profile, while highlighting the need for well‑designed PD‑specific clinical trials to establish dosing and efficacy.

B
The Gut Microbiota in Parkinson's Disease: Mechanistic Insights into Microbial-Host Interactions.
PMID 41900432 Published: 2026-03-16 Ingested: 2026-04-28 08:58 PM Microorganisms
AI 85.0
Base 87.1
Rank 84.0
AI Summary

Narrative review integrating clinical, metagenomic, metabolomic and mechanistic data that links PD-associated gut dysbiosis (reduced SCFAs, pro-inflammatory metabolic shifts, barrier dysfunction) to intestinal immune activation, α-synuclein aggregation and neuroinflammation, framing the gut…

Why It Matters

Identifies actionable upstream mechanisms—microbial metabolites, gut barrier and immune signaling—that offer paths for disease-modifying interventions, biomarkers, and translational repurposing in Parkinson's research.

B
Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes.
PMID 41947971 Published: 2026-01-01 Ingested: 2026-04-28 08:58 PM Frontiers in clinical diabetes and healthcare
AI 80.0
Base 87.1
Rank 84.0
AI Summary

Comprehensive review linking TLR2-driven chronic inflammation and metabolic dysfunction in type 2 diabetes to neuroinflammation, mitochondrial and BBB pathology, and outlining therapeutic strategies (drugs, supplements, and antidiabetic repurposing) that could mitigate diabetes-associated…

Why It Matters

TLR2 maps a mechanistic bridge between systemic metabolic inflammation and brain pathology (microglial activation, mitochondrial dysfunction, BBB disruption), offering actionable targets and repurposing opportunities relevant to Parkinson's-related neuroinflammatory and metabolic pathways despite…

B
AI 86.0
Base 87.8
Rank 83.6
AI Summary

In an acute MPTP mouse model, a GLP-2 analogue and a GLP-2/GIP dual agonist improved motor performance and reduced α‑synuclein accumulation, neuroinflammation (TNF‑α, NF‑κB) and apoptosis (↓Bax, ↑Bcl‑2), with the dual agonist showing superior effects.

Why It Matters

Provides preclinical evidence that GLP-2/GIP receptor co-agonism can modulate key PD-relevant mechanisms (inflammation, α‑synuclein, apoptosis), supporting further translational work (chronic models, mechanism dissection, PK/safety) toward a potential disease-modifying therapy.

B
TNF alpha unmasks enteric malate aspartate shuttle dysfunction bridging Parkinson disease and intestinal inflammation.
PMID 41922384 Published: 2026-04-01 Ingested: 2026-04-28 08:58 PM Nature communications
AI 91.5
Base 87.6
Rank 83.5
AI Summary

TNFα promotes α-synuclein accumulation and impairs the malate–aspartate shuttle in patient iPSC-derived enteric neurons, driving a shift to glutamine oxidation, mitochondrial dysfunction that is partly rescued by Chicago-Sky-Blue 6B, and mirroring inflammation-associated metabolic and α-syn changes…

Why It Matters

The study pinpoints a druggable metabolic vulnerability (malate–aspartate shuttle dysfunction) and an inflammatory driver (TNFα) in enteric neurons, demonstrates partial pharmacologic rescue, and provides a patient-derived platform that directly supports gut‑brain–targeted PD therapeutic discovery…

B
Lipid Metabolism and Neurodegeneration: Mechanistic Insights and Therapeutic Targets.
PMID 41903861 Published: 2026-03-26 Ingested: 2026-04-28 08:58 PM Ageing research reviews
AI 82.0
Base 86.8
Rank 82.8
AI Summary

This review links disrupted lipid metabolism—altered cholesterol trafficking, sphingolipid/ceramide pathways, and phospholipid remodeling—to neuroinflammation and cell-type–specific metabolic shifts that increase neuronal vulnerability, and it outlines therapeutic approaches (ApoE modulation,…

Why It Matters

Provides actionable, translational targets and biomarker strategies tied to inflammation and membrane/lysosomal-related vulnerability that are directly relevant to Parkinson’s therapeutic discovery, despite being a review rather than new primary data.

B
Shared functional microbiome signatures in Parkinson's disease and constipation predominate irritable bowel syndrome despite taxonomic divergence.
PMID 41993915 Published: 2026-05-01 Ingested: 2026-04-28 08:58 PM Brain, behavior, & immunity - health
AI 80.0
Base 86.5
Rank 82.5
AI Summary

Shotgun metagenomics of stool from PD patients, controls, and IBS-C showed taxonomic differences but conserved functional deficits in PD—notably reduced microbial tryptophan biosynthesis, polyamine production, and B‑vitamin metabolism—while constipated PD patients trended toward higher circulating…

Why It Matters

Identifies specific microbial metabolic pathways linked to neurotransmitter production, epithelial integrity, and neuroimmune regulation that are actionable targets for microbiome‑based, dietary, or supplementation interventions in PD-related GI dysfunction and possibly…

B
Benzimidazole as a Versatile Scaffold for Developing Neurotherapeutics Against Neurodegenerative Diseases.
PMID 41945799 Published: 2026-04-14 Ingested: 2026-04-28 08:58 PM ChemMedChem
AI 74.0
Base 86.2
Rank 82.3
AI Summary

This broad review highlights benzimidazole as a versatile medicinal chemistry scaffold with preclinical MAO-B inhibitors, dopamine receptor modulators, and NMDA antagonists and reports favourable ADMET/BBB properties, but provides limited PD-specific in vivo or clinical evidence.

Why It Matters

For Parkinson’s drug discovery, benzimidazole derivatives offer actionable repurposing and multi-target opportunities (MAO-B inhibition, dopaminergic modulation, anti-excitotoxic and anti-aggregation strategies) that warrant focused in vivo PD studies and optimization toward clinical candidates.

B
Biomimicking neuromelanin reverses the gait deficits and dopaminergic neuronal loss in the Parkinson's disease.
PMID 42035500 Published: 2026-04-25 Ingested: 2026-04-28 08:58 PM Colloids and surfaces. B, Biointerfaces
AI 86.0
Base 85.6
Rank 81.8
AI Summary

This preclinical study shows polydopamine nanoparticles (synthetic neuromelanin) protect dopaminergic neurons in 6-OHDA Parkinson's models by scavenging ROS, normalizing iron metabolism, inhibiting ferroptosis, reducing microglial activation, and rescuing motor/gait deficits.

Why It Matters

Provides a mechanistically grounded, multi-target nanoparticle therapy that addresses oxidative stress, iron dysregulation and ferroptosis—key PD pathways—and demonstrates in vivo behavioral and neuroprotective efficacy, supporting translational potential.

B
AI 84.0
Base 85.0
Rank 81.2
AI Summary

This review synthesizes evidence that klotho exerts broad neuroprotective effects—reducing oxidative stress and neuroinflammation, stabilizing synapses, supporting myelination and proteostatic clearance—and outlines therapeutic approaches (recombinant protein, gene therapy, small molecules,…

Why It Matters

Klotho represents a translationally actionable neuroprotective target with multiple intervention modalities and clinical biomarker correlations relevant to slowing neurodegeneration and cognitive decline in Parkinson's disease, though PD-specific mechanistic data and blood–brain barrier delivery…

B
Flavonoid Rutin Reduces Intestinal Inflammation in an Experimental Model of Parkinson's Disease.
PMID 41903068 Published: 2026-03-28 Ingested: 2026-04-28 08:58 PM Neurotoxicity research
AI 70.0
Base 84.9
Rank 81.2
AI Summary

In a 6-OHDA rat model of Parkinson's disease, oral rutin (10 mg/kg for 14 days) reduced intestinal inflammation—decreasing intraepithelial lymphocytes, goblet cell changes, and ileal Paneth cell hyperplasia—while selected gut bacterial taxa measured by PCR were unchanged.

Why It Matters

This supports the idea that a dietary flavonoid can attenuate PD-related enteric inflammation and thus could be a candidate for gut-targeted adjunctive therapies influencing the gut-brain axis, though the study lacks central neuroprotection, behavioral outcomes, mechanistic depth, and comprehensive…

B
AI 78.0
Base 82.5
Rank 79.1
AI Summary

The study encapsulates a potent but poorly soluble MAO-B inhibitor into nanostructured lipid carriers (with luminescent carbon dots) and reports ~10-fold greater BBB permeation in an in vitro model plus retained antioxidant activity in SH-SY5Y cells with moderate cell tolerance.

Why It Matters

Improving CNS delivery of an MAO-B inhibitor addresses a Parkinson's-relevant neuroprotective mechanism and offers a translational drug-delivery approach, though the work is limited to in vitro models and needs in vivo PK, efficacy, and safety validation.

B
AI 86.0
Base 82.3
Rank 79.0
AI Summary

Comprehensive review synthesizing human and animal evidence that gut microbiota dysbiosis, altered microbial metabolites, and increased intestinal permeability contribute to α-synuclein misfolding and neuroinflammation in Parkinson’s disease, and that microbiome-targeted interventions (diet,…

Why It Matters

Identifies actionable, translational targets (microbial metabolites, gut permeability, microbiome modulation) for early biomarkers and interventions in PD while emphasizing the need for standardized, longitudinal, precision studies to validate efficacy and causality.

B
Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review.
PMID 41899406 Published: 2026-02-26 Ingested: 2026-04-28 08:58 PM Current issues in molecular biology
AI 86.0
Base 82.3
Rank 79.0
AI Summary

Narrative review that frames PD around three interconnected metabolic axes—mitochondrial and glucose/lipid dysfunction, chronic oxidative stress, and glial reprogramming—with α-synuclein as a central integrator, and advocates integrating high-quality RNA‑Seq and bioinformatics to define molecular…

Why It Matters

Synthesizes mechanistic and transcriptomic evidence to highlight actionable targets (mitochondrial metabolism, oxidative stress, glial dysregulation, α-synuclein) and proposes RNA‑Seq–driven molecular subtyping that could guide biomarker development, repurposing, and disease‑modifying therapeutic…

B
Navigating the cholesterol maze: Key insights on use of statins in neurodegenerative disorders.
PMID 42023276 Published: 2026-03-01 Ingested: 2026-04-28 08:58 PM Neuroprotection (Chichester, England)
AI 76.0
Base 82.3
Rank 79.0
AI Summary

Comprehensive review linking cholesterol dysregulation to neurodegeneration and evaluating statins' pleiotropic (cholesterol-dependent and -independent) neuroprotective mechanisms—highlighting inflammation, oxidative stress, mitochondrial dysfunction, and mixed clinical outcomes across AD, PD, HD,…

Why It Matters

For Parkinson's research, the paper surfaces actionable mechanisms (α-synuclein aggregation, mitochondrial impairment, neuroinflammation) and frames statins as a repurposing opportunity that warrants targeted, genotype- and stage-specific clinical trials to resolve heterogeneous effects and improve…

AI Summary

This computational network-pharmacology study of lavender and rose essential oils identifies 252 shared protein targets across neuropsychiatric disorders, highlights CHRM2 (muscarinic GPCR) and NR1H3 (LXR) as central hubs, and supports terpenoid binding to these targets via docking, MD, and MM/PBSA…

Why It Matters

Modulation of a druggable GPCR (CHRM2) and a lipid/inflammation regulator (NR1H3) offers plausible, actionable leads for influencing cholinergic dysfunction and neuroinflammation relevant to Parkinson's disease, but the findings are purely in silico and require biochemical and in vivo validation…

B
Models of neuroprotection in Parkinson's disease: Exploring cellular, molecular, and microenvironmental targets.
PMID 41967563 Published: 2026-04-11 Ingested: 2026-04-28 08:58 PM Experimental neurology
AI 78.0
Base 80.4
Rank 77.3
AI Summary

A broad review summarizing neuroprotective strategies for PD—gene therapy, exosomes, microbiome modulation, vagus nerve stimulation, anti-inflammatory approaches, and sex-hormone factors—focused on underlying molecular mechanisms and combined therapies.

Why It Matters

By integrating multiple translationally relevant targets and intervention modalities, the review helps prioritize therapeutic avenues and combination strategies that could slow or stop dopaminergic neuron loss in PD.

B
Hyaluronic acid: emerging roles and biomaterial innovations in Alzheimer's and Parkinson's disease therapy.
PMID 41948730 Published: 2026-01-01 Ingested: 2026-04-28 08:58 PM Frontiers in pharmacology
AI 75.2
Base 80.4
Rank 77.3
AI Summary

This review compiles preclinical evidence that hyaluronic acid (HA)–based biomaterials modulate neuroinflammation, autophagic flux, α‑synuclein propagation, and ECM remodeling while enabling targeted drug/gene delivery and scaffolded cell transplantation in Alzheimer's and Parkinson's disease.

Why It Matters

Highlights HA as a multimodal, translationally relevant platform for neuroprotection and targeted delivery in PD (autophagy/α‑synuclein modulation, mitochondrial/dopamine targeting, and cell-supporting hydrogels) but underscores formulation variability and scarce clinical validation, pointing to…

B
AI 75.0
Base 79.5
Rank 76.6
AI Summary

Review synthesizing PD molecular mechanisms—α-synuclein, mitochondrial dysfunction, neuroinflammation, impaired autophagy, sirtuins and insulin/incretin signaling—and evaluating phytochemicals (resveratrol, curcumin, quercetin, baicalein, berberine, EGCG) and incretin mimetics as multi-target…

Why It Matters

Provides a translationally relevant synthesis that highlights actionable targets and repurposing opportunities (GLP-1/GIP agonists, sirtuin modulators, phytomolecules) to prioritize preclinical and early clinical work, though it is a review without novel experimental data.

B
Lipid droplets in neurodegenerative diseases: pathological drivers and therapeutic vulnerabilities.
PMID 41956992 Published: 2026-04-09 Ingested: 2026-04-28 08:58 PM Cell death discovery
AI 82.0
Base 79.2
Rank 76.3
AI Summary

This review summarizes evidence that lipid droplets modulate neuronal lipid metabolism, oxidative stress, inflammation, and interact with α-synuclein, and proposes targeting LD dynamics (e.g., lipophagy or LD-associated proteins) as therapeutic strategies for neurodegenerative diseases including…

Why It Matters

It highlights actionable, translational targets (lipophagy pathways and LD-associated proteins) linked to α-synuclein pathology and neuroinflammation, making LD metabolism a promising and tractable avenue for PD drug discovery and repurposing efforts.

B
AI 74.0
Base 79.2
Rank 76.3
AI Summary

Narrative review synthesizing preclinical and clinical evidence that gut microbiota perturbations alter brain function through neural (vagus), immune (cytokine/neuroinflammation), and metabolic (SCFAs, TMAO, tryptophan derivatives) pathways and noting associations between dysbiosis and…

Why It Matters

Identifies plausible, targetable BGMA mechanisms and putative microbial biomarkers that could be translated into PD therapeutic strategies or biomarker studies, although it lacks primary causal human data and direct interventional evidence.

B
Long non-coding RNAs in neurodegenerative diseases - Molecular mechanisms, liquid biopsy biomarkers, and therapeutic targets: A review.
PMID 41919473 Published: 2026-03-31 Ingested: 2026-04-28 08:58 PM Biomolecules & biomedicine
AI 84.0
Base 78.9
Rank 76.1
AI Summary

Comprehensive review detailing how long non-coding RNAs regulate key neurodegenerative processes (protein aggregation, neuroinflammation, mitochondrial dysfunction, LLPS, exosome signaling), their detectability as liquid-biopsy biomarkers, and therapeutic targeting strategies (ASOs, gene editing,…

Why It Matters

Provides actionable, translationally relevant insights linking lncRNA-mediated mechanisms to PD-relevant pathways and outlines biomarker and ASO/gene-therapy opportunities while clearly noting challenges in specificity, validation, and blood–brain barrier delivery.

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