Neurocompute scores biomedical literature, surfaces overlooked patterns, and turns Parkinson’s research into a living discovery terminal.
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View analysis →MRI study of young Metropolitan Mexico City residents links high PM2.5/ultrafine particle exposure to widespread cortical, subcortical, and cerebellar atrophy with mild cognitive impairment and prior autopsy data show accumulation of amyloid-β, p-tau, alpha-synuclein and TDP-43.
Provides epidemiologic and in vivo imaging evidence that air pollution is associated with early PD-relevant pathology (alpha-synuclein) and cognitive decline, pointing to a modifiable environmental risk and the need for biomarker development and prevention strategies despite limited direct…
Review argues that cardiovascular disease–related hypoperfusion and oxidative stress drive cytoskeletal and microtubule disintegration across neurodegenerative disorders and highlights alpha-synuclein-mediated impairment of microtubule polymerization in substantia nigra dopaminergic neurons…
Identifies a heart–brain axis and actionable mechanisms (microtubule destabilization, oxidative stress, vascular dysfunction, and proteinopathies) that point to potential therapeutic strategies and biomarkers such as microtubule stabilizers, antioxidant/vascular interventions, and cytoskeletal…
Medicinal chemistry review of the NEET protein family (mitoNEET/CISD1, CISD2, CISD3) and small‑molecule ligands that modulate their redox‑active [2Fe‑2S] clusters and roles in mitochondrial bioenergetics, mitophagy, and iron metabolism.
Because mitochondrial dysfunction, defective mitophagy, and iron dysregulation are central to Parkinson's pathogenesis, the review's focus on druggable NEET proteins and existing ligand chemistry (including pioglitazone off‑target engagement) provides a tangible translational path and repurposing…
ATP13A2 loss in astrocytes depletes cytosolic polyamines, diverting SAM into de novo polyamine synthesis which drives epigenetic reprogramming to a neuroinflammatory, neuron-toxic state; genetic and pharmacologic inhibition of SAM utilization in polyamine biosynthesis prevents this reprogramming…
Reveals a targetable metabolic–epigenetic axis (polyamine biosynthesis/SAM use) linking lysosomal dysfunction to neurotoxic inflammation with demonstrated pharmacologic rescue, creating clear translational and repurposing opportunities for Parkinson's therapeutic development.
This study shows decreased O-GlcNAcylation in PD substantia nigra and demonstrates that pharmacological elevation of O-GlcNAcylation (glucosamine or Thiamet-G) in LPS-induced mice and primary microglia preserves dopaminergic neurons, improves motor outcomes, and suppresses microglial NF-κB–driven…
Identifies O-GlcNAcylation as a druggable metabolic regulator of microglial inflammation with repurposing potential (glucosamine/OGA inhibitors) for neuroprotective, anti-inflammatory PD therapies, though validation in alpha‑synuclein models and human studies is still needed.
Comprehensive review linking Complex I/CoQ-driven ETC dysfunction and supercomplex remodeling to elevated ROS, mtDNA/mtDAMP release, and activation of NLRP3, cGAS-STING, and TLR9 inflammatory pathways, and proposing therapeutic approaches such as ETC support, supercomplex stabilization, and…
Highlights mechanistic, druggable targets and biomarker opportunities directly relevant to Parkinson’s disease—offering actionable paths for repurposing, neuroprotective interventions, and translational studies that bridge mitochondrial dysfunction and neuroinflammation.
This review surveys preclinical and mechanistic literature suggesting doxycycline’s antioxidant, anti-inflammatory, and ER-stress–modulating activities may protect dopaminergic neurons and thus could be repurposed for Parkinson’s disease.
Repurposing an FDA-approved drug with demonstrated neuroprotective effects offers a comparatively fast translational path for PD therapeutics targeting inflammation, oxidative and ER stress, but concrete molecular mechanisms and clinical efficacy data are still limited.
This systematic review/meta-analysis of 54 human studies finds both F2-isoprostanes and 8-OHdG markedly elevated in T2DM, but only 8-OHdG is moderately elevated in Parkinson's disease, indicating DNA oxidative damage rather than lipid peroxidation may better reflect oxidative stress in PD and…
Identifies 8-OHdG as a more promising biomarker for PD patient stratification and target‑engagement in trials and argues for standardized, multi-compartment and longitudinal biomarker studies to de-risk antioxidant-focused therapeutic development.
This review hypothesizes that disulfidptosis—a disulfide-stress-driven, cytoskeletal-collapse form of regulated cell death—may contribute to neurodegenerative diseases including Parkinson's, but evidence is mainly indirect and lacks direct validation in neural systems.
By linking redox imbalance, metabolism, mitochondrial dysfunction, and cytoskeletal collapse, the paper highlights a mechanistically plausible pathway that could reveal new therapeutic targets or biomarkers for Parkinson's if followed by experimental validation in relevant neuronal and glial models.
Comprehensive review mapping ubiquitination dynamics and DUB roles in PD pathogenesis, linking DUB-mediated stabilization of α-synuclein and suppression of mitophagy to therapeutic opportunities with small-molecule DUB inhibitors.
Highlights druggable deubiquitinating enzymes that can be targeted to restore proteostasis and mitochondrial quality control, providing actionable avenues for developing disease‑modifying Parkinson's therapies.
This focused review synthesizes how mitochondrial defects (bioenergetics, calcium handling, dynamics, mitophagy, ROS and mtDNA-mediated inflammation) drive neurodegeneration and evaluates mitochondria-targeted therapies—from antioxidants and mitochondrial transfer to lifestyle and…
Highly relevant to Parkinson's therapeutic discovery because it consolidates actionable mitochondrial mechanisms and intervention strategies, highlights disease-stage and patient-heterogeneity issues, and therefore serves as a practical roadmap for prioritizing target-specific interventions and…
This study demonstrates that [18F]FDG PET disease-related metabolic patterns and regional analyses can distinguish prodromal iRBD, converters, PD, and DLB and track progressive neurodegeneration across the α‑synucleinopathy continuum, with strongest performance in cognitive‑predominant…
Offers a clinically translatable biomarker for patient stratification, progression monitoring, and trial endpoints—particularly for dementia‑first synucleinopathies—enabling better selection of participants and mechanism‑linked outcome measures in therapeutic development.
A 4-week supervised home-based aerobic cycling program (3×/week at 70–80% heart rate reserve) significantly improved maximal power output, VO2peak, anaerobic threshold, and peak expiratory flow in 17 mild-to-moderate PD patients.
Shows a feasible, remotely supervised intervention that meaningfully boosts cardiopulmonary fitness and functional capacity in PD patients—valuable for symptomatic management and trial design—but provides limited mechanistic or disease-modifying therapeutic insights.
Preclinical studies indicate acupuncture exerts multi-modal neuroprotective effects in PD models—upregulating Nrf2 antioxidant defenses, modulating autophagy/alpha‑synuclein clearance, suppressing apoptosis/pyroptosis and neuroinflammation, promoting neurogenesis via BDNF/GDNF, and altering gut…
Highlights multiple disease-relevant and potentially druggable pathways (Nrf2, autophagy/lysosome, NLRP3, neurotrophic signaling, gut–brain axis) that could inform therapeutic discovery, while being limited by predominantly preventive preclinical data and heterogeneity that hinder immediate…
This review synthesizes recent advances in glial heterogeneity and plasticity—covering metabolic dysfunction, inflammatory polarization, glial-immune crosstalk, and extracellular vesicle signaling—and evaluates glia-focused interventions (reprogramming, senolytics, engineered EVs, metabolic…
By highlighting actionable glial mechanisms that drive neuroinflammation and metabolic failure and surveying translatable interventions and delivery/biomarker challenges, the paper identifies promising, though still preclinical, avenues to target glia for disease-modifying Parkinson's therapies.
Systematic review of medicinal plants and their active compounds that target autophagy in Parkinson's disease, summarizing preclinical evidence for multi-target neuroprotective effects while noting limited mechanistic validation and a lack of rigorous clinical trials.
Emphasizes autophagy modulation and related anti-inflammatory/antioxidant mechanisms as promising translational avenues and flags specific gaps—target specificity, toxicity, standardization, and need for mechanistic and clinical validation—that are critical for prioritizing plant-derived leads for…
In a paraquat-induced Drosophila PD model the authors developed an oxylipin quantification method and show that specific lipophilic plant-derived soft electrophiles (certain flavones and related phytochemicals) increase pro-resolving oxylipins in fly heads via the NF-κB orthologue relish, with sex-…
Provides a mechanistic, actionable route—dietary soft electrophiles that boost SPM/oxylipin biosynthesis—to resolve neuroinflammation linked to PD risk, making identifiable compounds and pathways ready for mammalian validation and therapeutic development.
This review synthesizes mechanisms and translational strategies for controlled blood–brain barrier modulation (e.g., receptor-mediated transcytosis, ligand-engineered nanocarriers, focused ultrasound, viral/molecular engineering) to improve delivery of neuroprotective, anti-α-synuclein, and…
By detailing clinically actionable BBB delivery platforms, safety considerations, and biomarker-directed approaches, the paper addresses a key translational bottleneck for Parkinson’s therapeutics—enabling targeted brain delivery of α-synuclein-targeting and neuroprotective agents that could…
In a small controlled study (n=28) an 8-week supervised combined aerobic-resistance program improved tremor subscore and 6-minute walk distance in people with PD while exploratory labs showed a decrease in vitamin D3 that remained significant after FDR correction.
Findings support short-term symptomatic benefit of structured exercise and suggest metabolic signals worth follow-up, but the study's small size, short duration and lack of mechanistic data limit its direct value for drug discovery or target identification.
This review synthesizes evidence that impaired brain glucose metabolism — including altered glycolysis and disrupted neuron–astrocyte metabolic coupling driven by dopamine, alpha-synuclein, and DJ-1 dysfunction — contributes to PD and evaluates strategies to restore glycolytic/energetic homeostasis.
By linking specific molecular drivers to metabolic deficits and assessing glycolysis-targeted and repurposing strategies, the paper highlights actionable therapeutic avenues with translational potential to slow Parkinson's disease progression.
