B grade · PMID 41948730
View analysis →Finding therapies hidden in 1,516 Parkinson’s papers.
Neurocompute scores biomedical literature, surfaces overlooked patterns, and turns Parkinson’s research into a living discovery terminal.
Ranked discovery teasers
B grade · PMID 41971071
View analysis →B grade · PMID 41956992
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View analysis →B grade · PMID 41919473
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View analysis →B grade · PMID 41956168
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All ranked Parkinson’s papers
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.
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…
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…
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.
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…
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.
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…
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.
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,…
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.
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…
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…
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…
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.
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…
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…
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…
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.
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…
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…
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…
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…
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…
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…
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…
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…
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…
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.
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.
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…
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.
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.
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…
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.
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.
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…
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…
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.
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.
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.