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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 CYP46A1-Mediated Cholesterol Reduction Prevents eIF2α-Driven Translation Stalling in Neurodegeneration rel 0.90

This hypothesis proposes that CYP46A1 overexpression gene therapy prevents neurodegeneration

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Hypothesis CYP46A1 Small Molecule Activator Therapy rel 0.90

amyloid burden by 40% and improves cognitive performance in multiple

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Hypothesis Epigenetic Age Acceleration Moderates the Amyloid-to-Tau Conversion Cascade — A "Clock Threshold" Model of AD Progression rel 0.80

amyloid cascade hypothesis predicts a long asymptomatic amyloid phase (10–20 years

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Hypothesis Alpha-theta entrainment therapy to enhance default mode network coherence rel 0.80

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

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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 0.70

amyloid-beta oligomers directly impair PV interneuron function, SST interneurons

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Hypothesis Closed-loop transcranial focused ultrasound with gamma entrainment to restore hippocampal-cortical synchrony via PV interneuron mechanostimulation rel 0.70

amyloid-beta oligomers preferentially impair PV interneurons by disrupting Nav1.1

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Hypothesis CSF p-tau217 Normalization Occurs Earlier Than Amyloid PET Negativity, Enabling Earlier Cessation Decisions rel 0.60

amyloid PET reaches cessation thresholds because p-tau217 reflects active

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Hypothesis Residual Vascular Amyloid Prevents Complete CSF p-tau217 Normalization, Requiring Composite Cessation Criteria rel 0.50

amyloid angiopathy (CAA) maintains a reservoir of vascular amyloid that

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Hypothesis LDLR-Primed LRP1 Transcytosis with pH-Responsive Escape Strategy rel 0.50

This strategy combines targeted upregulation of LDLR expression in brain

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Hypothesis LDLR-Mediated Neurosteroid Precursor Delivery Strategy rel 0.50

The LDLR-Mediated Neurosteroid Precursor Delivery Strategy proposes utilizing the

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Hypothesis J-protein substrate specificity codes enable HSP70 discrimination of β-sheet versus α-helical misfolded conformers rel 0.40

amyloid cores and polyglutamine expansions. In contrast, DNAJB2 operates through

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Hypothesis HSP90-cochaperone complexes preferentially stabilize intermediate misfolded states preceding amyloid formation rel 0.40

amyloid cores have not yet formed. HSP90's unique ATP-driven

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Hypothesis J-protein co-chaperone system mediates selective autophagy targeting of pathogenic protein aggregates rel 0.40

amyloid-like aggregates through direct interaction with LC3/GABARAP family proteins

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Hypothesis Gut-derived butyrate reprograms microglia for amyloid clearance via HDAC2 inhibition rel 0.40

amyloid plaque burden, increased microglial amyloid phagocytosis rates ex vivo

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Hypothesis Cross-Seeding: Gut Microbiome-Derived Bacterial Curli and Fungal Amyloid Synergize with Host Aβ/α-Synuclein via TLR2/TLR1 Heterodimer Signaling rel 0.40

amyloid fibers encoded by the csg operon, while Candida and Saccharomyces

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Hypothesis Gut butyrate deficiency impairs microglial amyloid clearance via HDAC2-mediated epigenetic dysregulation rel 0.40

amyloid-beta plaques. This HDAC2-mediated epigenetic silencing reduces expression

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Hypothesis APOE ε4 Drives Lipid Droplet Accumulation in a Unique Lipid-Associated Microglial Substate that Impairs Amyloid Phagocytosis rel 0.40

amyloid-beta in APOE ε4/ε4 microglia compared to ε3/ε3 controls

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Hypothesis LAMP2A Upregulation to Enhance Chaperone-Mediated Autophagy for Tau Clearance in Alzheimer's Disease rel 0.30

amyloid pathology. This hypothesis proposes that targeted upregulation of LAMP2A

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Hypothesis TFEB Activation to Restore Lysosomal Biogenesis in Alzheimer's Disease Neuronal Networks rel 0.30

amyloid-beta plaques and tau tangles that disrupt synaptic transmission

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Hypothesis APOE4-driven loss of neuronal PI(4,5)P2 bridges ganglioside-mediated amyloid nucleation and phosphoinositide-dependent synaptic failure in Alzheimer disease rel 0.30

amyloid-β42 aggregation, while disrupting phosphoinositide-dependent synaptic scaffolding (PSD-95, Homer1

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

amyloid-beta accumulation. Specifically, mutations or age-related damage to TFAM

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Hypothesis Amyloid Plaque Clearance Triggers Downstream Reduction in Tau Kinase Activity, Normalizing CSF p-tau217 rel 0.30

amyloid plaque clearance reduces microglial activation and neuronal injury, which

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Hypothesis Astrocyte Reactivity Mediated by LCN2 Promotes Synaptic Loss in Alzheimer's Disease rel 0.20

amyloid burden, offering an amyloid-independent mechanism. However, the hypothesis

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Hypothesis RAGE-Mediated Transcytotic Pump Enhancement Strategy rel 0.20

amyloid oligomers. The RAGE receptor, constitutively expressed on brain capillary

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Hypothesis TFEB Family-Wide Activation to Restore Lysosomal Networks in Early Alzheimer's Synaptic Dysfunction rel 0.20

amyloid-beta oligomers and early tau species that disrupt synaptic

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Hypothesis Ethnic and Metabolic Epigenetic Clock Divergence Explains Disparate AD Risk — Hispanic/Latino Epigenetic Resilience Paradox rel 0.20

amyloid and tau burden may trigger less neuroinflammatory amplification in this

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Hypothesis CREB-Dependent Differential Complement Regulator Positioning for Activity-Based Synaptic Vulnerability Control rel 0.20

This hypothesis proposes that the CREB-BDNF-TrkB activity-dependent

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Hypothesis Excess orexin-A worsens AD cognition through wake-driven amyloid production rel 0.20

Chronic orexin-A elevation may aggravate AD by extending wakefulness

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Hypothesis Thalamic anterior nucleus hyperconnectivity drives early-stage functional compensation that becomes pathological through adenosine-mediated metabolic vulnerability rel 0.20

amyloid-beta oligomerization at hyperconnected synapses. The transition from hyper

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Hypothesis TREM2-Deficient Microglia as Drivers of Amyloid Plaque Toxicity in Alzheimer's Disease rel 0.20

amyloid plaques, and phagocytic clearance, creating a non-cell-autonomous

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