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All 7 Hypotheses 1 Papers 1 Wikis 1 Gaps 1 Colliders 0 Debates 1 Bounties 0 Missions 1 Work packets 1 Genes 0 Diseases 0 Phenotypes 0 Gene ontology 0

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

30 results

Hypothesis Age-related neuroinflammation mimics early Alzheimer's disease pathology rel 2.20

Alzheimer's disease pathology starts from the claim that modulating

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Hypothesis Hippocampal-Cortical Transcriptomic Divergence Reveals Accelerated Neurodegeneration-Like Signatures rel 1.50

Alzheimer disease can redirect a disease-relevant process. The original

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Hypothesis Hippocampus ages transcriptionally faster than cerebellum, defining a regional vulnerability axis conserved across species rel 1.50

Alzheimer's disease can redirect a disease-relevant process. The original

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Hypothesis APOE and TREM2 interact to modulate age-dependent microglial dysfunction rel 1.40

Alzheimer's disease can redirect a disease-relevant process. The original

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Hypothesis ELF2-Mediated OPC Epigenetic Drift Drives Region-Dependent Myelin Dysfunction rel 1.40

Alzheimer disease can redirect a disease-relevant process. The original

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Hypothesis Hippocampal mitochondrial dysfunction accelerates with age and drives regional AD vulnerability rel 1.40

Alzheimer's disease can redirect a disease-relevant process. The original

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Hypothesis Astrocyte C3aR Signaling as Bifurcation Point for A1/A2 Fate rel 1.40

Alzheimer's disease, Parkinson's disease can redirect a disease

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Hypothesis SPP1+ DAM as Source of Autoimmunity in Neurodegeneration rel 1.40

Alzheimer's disease can redirect a disease-relevant process. The original

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Hypothesis Age-driven synaptic gene silencing precedes neuronal loss in vulnerable brain regions rel 1.40

Alzheimer's disease can redirect a disease-relevant process. The original

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Hypothesis C1q-TREM2 Competition for Phosphatidylserine as Pruning Checkpoint rel 1.40

Alzheimer's disease can redirect a disease-relevant process. The original

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Hypothesis Myelin Breakdown-Amyloid Interaction Amplifies Cortical Aging-Neurodegeneration Overlap rel 1.40

Alzheimer disease can redirect a disease-relevant process. The original

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Hypothesis TREM2-APOE4 Axis Drives Metabolic Inflexibility in DAM rel 1.40

Alzheimer's disease can redirect a disease-relevant process. The original

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Hypothesis CD8+ T-Cell Perforin Pathway as Driver of Neuronal Pyramid Loss rel 1.40

Alzheimer's disease, Parkinson's disease can redirect a disease

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Hypothesis Closed-loop transcranial focused ultrasound to restore hippocampal gamma oscillations via SST interneuron disinhibition cascades in Alzheimer's disease rel 0.90

Alzheimer's disease. While amyloid-beta oligomers directly impair PV interneuron

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Hypothesis Closed-loop transcranial focused ultrasound with gamma entrainment to restore hippocampal-cortical synchrony via PV interneuron mechanostimulation rel 0.90

Alzheimer's disease. The intervention uses closed-loop tFUS specifically

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Hypothesis Alpha-theta entrainment therapy to enhance default mode network coherence rel 0.90

Alzheimer's disease through low-frequency oscillatory modulation. Unlike gamma

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Hypothesis CYP46A1-Mediated Cholesterol Reduction Prevents eIF2α-Driven Translation Stalling in Neurodegeneration rel 0.80

This hypothesis proposes that CYP46A1 overexpression gene therapy prevents neurodegeneration

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Hypothesis CYP46A1 Small Molecule Activator Therapy rel 0.80

Alzheimer's disease through enhanced brain cholesterol metabolism. Small molecule

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Hypothesis TFEB Activation to Restore Lysosomal Biogenesis in Alzheimer's Disease Neuronal Networks rel 0.50

Alzheimer's disease, particularly amyloid-beta plaques and tau tangles

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Hypothesis LAMP2A Upregulation to Enhance Chaperone-Mediated Autophagy for Tau Clearance in Alzheimer's Disease rel 0.50

Alzheimer's disease, particularly in cortical and hippocampal neurons where

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Hypothesis ω-3 Docosahexaenoic Acid (DHA) Metabolism via 15-Lipoxygenase to Generate Specialized Pro-Resolving Mediators Against Neuroinflammation in Alzheimer's Disease rel 0.40

Alzheimer's disease rather than focusing on membrane rigidification. The mechanism

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Hypothesis TFEB Family-Wide Activation to Restore Lysosomal Networks in Early Alzheimer's Synaptic Dysfunction rel 0.30

Alzheimer's disease progression. While previous approaches have focused on individual

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Hypothesis LXRβ-Selective Agonism Enhances CYP2J2-Mediated DHA Epoxide Generation to Restore Synaptic Membrane Homeostasis in Alzheimer's Disease rel 0.30

Alzheimer's disease. LXR signaling is known to upregulate cytochrome

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Hypothesis Tau Propagation Blockade via Synaptic Ephrin-B2/ephrin-B Signaling Modulation rel 0.30

Alzheimer's disease could represent a downstream consequence of synaptic

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Hypothesis Mitochondrial Dysfunction-Mediated Neurodegeneration in Alzheimer's Disease rel 0.30

Alzheimer's disease, operating through impaired ATP synthesis and increased

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Hypothesis TFEB Family Multi-Target Activation for Synaptic Lysosomal Restoration in Alzheimer's Disease rel 0.30

Alzheimer's disease. While previous approaches focused on single-target

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Hypothesis LDLR-Mediated Neurosteroid Precursor Delivery Strategy rel 0.20

Alzheimer's disease, multiple sclerosis, and other neurodegenerative conditions where

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Hypothesis GrimAge Acceleration as a Cell-Type-Resolved CSF Biomarker Panel for Early AD Stratification rel 0.20

Alzheimer's disease from MCI and healthy aging with >85% sensitivity

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Hypothesis Closed-loop transcranial focused ultrasound with adaptive API-guided targeting to restore hippocampal gamma oscillations via PV interneuron recruitment in Alzheimer's disease rel 0.20

Alzheimer's disease through precise PV interneuron recruitment. The approach

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Hypothesis REST Complex Dysregulation as Master Epigenetic Switch rel 0.20

Alzheimer disease, making the direction of REST modulation more complex

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