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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 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 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 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 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 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 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 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 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 Targeting AQP4 Sumoylation to Enhance Glymphatic Clearance as Therapeutic Strategy in Alzheimer's Disease rel 1.00

Alzheimer's Disease starts from the claim that modulating AQP4

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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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Paper Alzheimer's disease. rel 0.90

Alzheimer's disease is defined as biomarker evidence of Alzheimer

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Paper Donanemab in Early Alzheimer's Disease. rel 0.90

Alzheimer's Disease Assessment Scale (ADAS-Cog13), the Alzheimer's Disease

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Paper The Epidemiology of Alzheimer's Disease Modifiable Risk Factors and Prevention. rel 0.90

Alzheimer's disease prevention. Moreover, Alzheimer's disease is considered

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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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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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Paper CSF tau microtubule binding region identifies tau tangle and clinical stages of Alzheimer's disease. rel 0.80

Alzheimer's disease to form pathological tangles and neurites. Insoluble

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Paper A genetic link between risk for Alzheimer's disease and severe COVID-19 outcomes via the OAS1 gene. rel 0.80

Alzheimer's disease, by its enrichment in transcriptional networks expressed

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Paper Distinct microglial response against Alzheimer's amyloid and tau pathologies characterized by P2Y12 receptor. rel 0.80

Alzheimer's disease and non-Alzheimer's disease tauopathy patients

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Paper The role of innate immune genes in Alzheimer's disease. rel 0.80

Alzheimer's disease and have emerged as therapeutic targets in Alzheimer

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Paper Clonally expanded CD8 T cells patrol the cerebrospinal fluid in Alzheimer's disease. rel 0.80

Alzheimer's disease is an incurable neurodegenerative disorder in which

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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 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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