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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 Myelin Breakdown-Amyloid Interaction Amplifies Cortical Aging-Neurodegeneration Overlap rel 2.30

amyloid status. This two-pathway model explains regional dissociation of amyloid

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Hypothesis TREM2 Agonism to Rescue APOE4-Induced Microglial Dysfunction rel 2.10

amyloid production, resulting in 70-80% amyloid reduction compared to 40-50% with

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Hypothesis Pharmacologically Boost AQP4X Readthrough to Restore Perivascular Clearance rel 1.40

amyloid-β peptides, tau aggregates, and other neurotoxic species. The loss

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Hypothesis TREM2-Dependent Microglial State Transition as Therapeutic Window in Alzheimer's Disease rel 1.30

amyloid plaques. Enhancing TREM2 signaling may restore neuroprotective microglial functions

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Hypothesis Stage-Dependent Biphasic SPP1 Targeting: Early Enhancement Followed by Late Inhibition rel 1.20

amyloid phagocytosis, but sustained SPP1 signaling induces complement-mediated synaptic

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Paper Cerebral β-Amyloidosis in Mice Investigated by Ultramicroscopy. rel 1.20

amyloid plaques, the β-amyloid load (volume percent) and the amyloid

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Hypothesis Focused Ultrasound with Microbubble Contrast Agents for Antibody CNS Delivery rel 1.00

amyloid-β antibodies achieved remarkable therapeutic efficacy, with quantitative analysis

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Hypothesis C1Q-Triggered NLRP3 Inflammasome Assembly in Plaque Macrophages rel 1.00

amyloid combination strategies leverage the pathway's role in amyloid

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Paper Distinct characteristics of amyloid deposits in early- and late-onset transthyretin Val30Met familial amyloid polyneuropathy. rel 1.00

amyloid polyneuropathy (FAP ATTR Val30Met) cases unrelated to endemic foci

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Hypothesis Bacterial Curli Amyloid → Nucleation of α-Synuclein Misfolding in Enteric Neurons rel 0.90

amyloid proteins may interact with tau, amyloid-β, and huntingtin

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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 TREM2 Agonism Has Narrow Early-Window at DAM1→DAM2 Transition Checkpoint rel 0.90

amyloid pathology, single-cell RNA sequencing has revealed distinct microglial

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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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Paper Genetic variation in Aquaporin-4 moderates the relationship between sleep and brain Aβ-amyloid burden. rel 0.90

amyloid clearance and to be most effective during sleep. Ablation

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Paper Aqp4 stop codon readthrough facilitates amyloid-β clearance from the brain. rel 0.90

amyloid-β. Immunotherapeutics aimed at reducing amyloid beta are in clinical

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Paper Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. rel 0.90

amyloid precursor protein (APP) and presenilins (PS1, PS2) increase production

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Paper Recent Advances from the Bench Toward the Bedside in Alzheimer's Disease rel 0.90

amyloid hypothesis (Hardy and Selkoe, 2002Hardy J. Selkoe D.J. The amyloid

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Hypothesis TREM2 Super-Agonist Induction of DAM Program rel 0.80

amyloid pathology confirmed by PET imaging or CSF amyloid-β42

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Hypothesis αvβ3 Integrin-FAK-SYK-CARD9/NF-κB Pathway rel 0.80

amyloid plaques compared to wild-type controls, with corresponding increases

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Hypothesis LRP1/NLRP3/IL-1β Cascade Links Aβ Endocytosis to Inflammasome Activation and SPP1 Induction rel 0.80

amyloid-beta (Aβ) oligomer clearance and neuroinflammatory responses in neurodegenerative

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Hypothesis P2RY12-mediated autophagy inhibition in cerebral VSMCs impairs CAA clearance rel 0.80

amyloid PET scans, confirming amyloid pathology presence. Safety considerations center

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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 LRP1-Mediated Transcytosis for CNS Antibody Delivery rel 0.80

amyloid-β (Aβ), tissue plasminogen activator (tPA), and lactoferrin. The transcytotic

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

amyloid (positive amyloid PET scans) but preserved cognitive function or mild

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Hypothesis TREM2-Mediated Astroglial Reactivity in Neurodegeneration rel 0.80

amyloid-β oligomers—TREM2 undergoes conformational changes that facilitate TYROBP

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Hypothesis Aβ42 oligomers drive TDP-43 phosphorylation at s409/410 through CDK5/p25 activation specifically in AD, generating a phospho-signature distinct from ALS/FTLD rel 0.80

amyloid-β42 (Aβ42) oligomer accumulation to pathological TDP-43 phosphorylation

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Paper The AβA2V paradigm: From molecular insights to therapeutic strategies in Alzheimer's disease and primary tauopathies. rel 0.80

amyloid β peptide, revealing a protective effect against amyloid-β and tau pathology

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Hypothesis TFEB-Dependent Lysosome Biogenesis rel 0.70

amyloid-β, tau, α-synuclein, and TDP-43. TFEB-mediated

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Hypothesis TFEB-mediated transcriptional upregulation of lysosomal genes as a therapeutic strategy for AD rel 0.70

amyloid-β (Aβ) peptides and hyperphosphorylated tau proteins overwhelms the cellular

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