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✓ Hypotheses 1 + Papers 1 + Wikis 1 + Gaps 1 + Colliders 0 + Debates 0 + Bounties 0 ✓ Missions 1 + Work packets 1 + Genes 0 + Diseases 0 + Phenotypes 0 + Gene ontology 0

19 results

Mission Parkinson's Disease rel 0.75

Hypothesis portfolio for alpha-synuclein, LRRK2, GBA, and mitochondrial dysfunction in PD. v1 has 252 scored PD hypotheses; v2 retains them as bound artifacts and adds the Mission Index Score's top-quartile component (SPEC-027 §4.2) to surface the upper tail v1's AVG hides.

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Hypothesis TFEB Activation to Restore Lysosomal Function in Parkinson's Disease Alpha-Synuclein Clearance rel 0.60

Parkinson's disease is characterized by the accumulation of misfolded

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Hypothesis TFEB Activation to Restore Lysosomal Biogenesis in Parkinson's Disease Dopaminergic Networks rel 0.40

Parkinson's disease, particularly alpha-synuclein oligomers and Lewy bodies

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Hypothesis H6-V1: Aberrant eIF2α Phosphorylation Drives Mitochondrial Translation Dysfunction rel 0.20

The eukaryotic initiation factor 2α (eIF2α) phosphorylation pathway critically regulates

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Hypothesis TFEB-mediated Autophagy Enhancement to Clear Protein Aggregates in Neurodegeneration rel 0.20

Parkinson's, and Huntington's disease, the accumulation of misfolded

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Hypothesis CYP46A1-Mediated Cholesterol Reduction Prevents eIF2α-Driven Translation Stalling in Neurodegeneration rel 0.10

This hypothesis proposes that CYP46A1 overexpression gene therapy prevents neurodegeneration

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Hypothesis J-protein co-chaperone system mediates selective autophagy targeting of pathogenic protein aggregates rel 0.10

**Molecular Mechanism and Rationale** The J-protein co-chaperone system

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Hypothesis Enhancement of Astrocytic Ketone Body Production via HMGCS2 Overexpression rel 0.10

Parkinson's disease, and other neurodegenerative conditions where neuronal glucose

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Hypothesis Dasatinib plus Quercetin Senolytic Clearance of p16Ink4a-High Neurons in Alzheimer's and Parkinson's Disease Models rel 0.10

The dasatinib (D)+quercetin (Q) senolytic combination exploits differential dependencies

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Hypothesis PINK1/Parkin–TREM2 Axis: Convergent Mitophagy Failure Unifies PD (SNCA/αSyn) and AD (tau/Abeta) Pathology rel 0.10

Parkinson's disease (PD) and Alzheimer's disease (AD) pathophysiology

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Hypothesis LDLR-Mediated Lipid Carrier Neurotherapeutic Delivery rel 0.10

Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis.

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Hypothesis Synaptic Vesicle Cycle Hijacking: Shared Convergent Mechanism for α-Synuclein (PD) and Tau (AD) Trans-synaptic Propagation rel 0.10

Parkinson's disease and tau (MAPT) in Alzheimer's disease

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Hypothesis LDLR-Mediated Neuroinflammation Modulation Strategy rel 0.10

Parkinson's disease, and multiple sclerosis, where chronic neuroinflammation and lipid

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Hypothesis CYP46A1 Small Molecule Activator Therapy rel 0.10

This approach employs pharmacological activation of endogenous CYP46A1 rather than

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Hypothesis H2S/butyrate imbalance drives enteric alpha-synuclein pathology via TLR4 signaling rel 0.10

Parkinson's disease, elevated H2S-producing Desulfovibrio species and depleted

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Hypothesis CYP46A1 Inhibition Therapy for Neurodegeneration rel 0.10

Parkinson's disease, where preserving synaptic cholesterol content might outweigh

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Hypothesis Exosomal α-Synuclein as an Interneuronal Propagation Vector in Parkinson's Disease rel 0.10

Misfolded α-synuclein aggregates are transmitted via exosomes from donor

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Hypothesis Mitophagy Induction as Neuroprotective Strategy in Sporadic Parkinson's Disease rel 0.10

PINK1/PARKIN-mediated mitophagy is impaired in sporadic PD due to upstream

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Hypothesis Alpha-theta entrainment therapy to enhance default mode network coherence rel 0.10

Alpha-theta entrainment therapy targets somatostatin (SST) interneurons to restore

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