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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 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 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 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 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 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 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 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 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 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 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 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 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 Excessive C1q/C3/CR3 complement cascade activation initiates pre-symptomatic synaptic loss in Alzheimer's disease rel 0.80

Alzheimer's disease through a well-characterized molecular pathway. The initiation

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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 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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Mission Alzheimer's Disease rel 0.75

Hypothesis portfolio targeting amyloid-beta, tau, microglial priming, and lipid metabolism in AD. Biggest v1 corpus segment with ~310 scored hypotheses; the v2 mission re-binds them via typed substrate links (SPEC-027 §5) instead of v1's hypothesis_missions junction table.

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Hypothesis TREM2-Dependent Microglial State Transition as Therapeutic Window in Alzheimer's Disease rel 0.70

Alzheimer's Disease starts from the claim that modulating TREM2

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Hypothesis APOE4 preferentially signals through LRP1 over LDLR, altering endosomal cholesterol trafficking and causing lysosomal cholesterol sequestration that drives lysosomal dysfunction and inflammation rel 0.70

Alzheimer's disease patients, exhibits distinctive receptor binding preferences that

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Hypothesis Regional TREM2-Dependent Lipid Metabolism Determines Cortical Vulnerability in Alzheimer's Disease rel 0.70

Alzheimer's Disease starts from the claim that modulating TREM2

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Hypothesis TREM2 Agonism to Rescue APOE4-Induced Microglial Dysfunction rel 0.60

Alzheimer's disease mutations, treatment with the 4D9 TREM2 agonistic

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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 Focused Ultrasound with Microbubble Contrast Agents for Antibody CNS Delivery rel 0.50

Alzheimer's disease model harboring five familial AD mutations. In these

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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 Metabolic Inflexibility Precedes Transcriptional Reprogramming (NAD+/SIRT3 Axis) rel 0.40

Alzheimer's disease model expressing human APP and PSEN1 mutations

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Hypothesis Antisense Oligonucleotide-Mediated APOE4 Haploinsufficiency rel 0.40

Alzheimer's disease, shows marked attenuation with 60-70% reduction

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Hypothesis LRP1-Autophagy BBB Permeabilization for Antibody Transport rel 0.40

Alzheimer's pathology and BBB breakdown) as therapeutic ligand is counterintuitive

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