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30 results
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amyloid-β (Aβ) accumulation through impaired regulatory control of amyloid
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amyloid accumulation. Longitudinal analysis revealed that the rate of amyloid
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- Hypothesis H1: TREM2 Agonism to Redirect APOE4-Enhanced Microglia from Synapse Pruning to Amyloid Clearance
amyloid accumulation. Early amyloid deposition triggers microglial recruitment and activation
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amyloid precursor protein (APP) processing, generating amyloid-beta (Aβ) peptides
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- Hypothesis CLU/APOE Duality in Amyloid Clearance Determines Cell-Type-Specific Vulnerability Thresholds
amyloid precursor protein, demonstrates accelerated amyloid deposition and neuroinflammation compared
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amyloid-clearing therapies, additional monitoring for ARIA (amyloid-related imaging
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amyloid transgenic lines, even at equivalent amyloid burden. Pharmacological studies
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amyloid-β42/40 ratios (indicating reduced amyloid aggregation), elevated soluble
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amyloid plaque number and total amyloid load, accompanied by reduced
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amyloid angiopathy, and accelerated amyloid-beta accumulation without transgenic amyloid
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amyloid plaques, decreased phagocytic clearance of amyloid deposits, and altered
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amyloid pathology, have demonstrated that TREM2 overexpression reduces amyloid plaque
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amyloid status. This two-pathway model explains regional dissociation of amyloid
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amyloid clearance starts from the claim that modulating not yet specified
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amyloid-beta (Aβ) pathology. [PMID:12450488] Under this multi-target
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amyloid production, resulting in 70-80% amyloid reduction compared to 40-50% with
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amyloid burden and DAM signature expression. In mouse models, amyloid
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Amyloid Phase starts from the claim that modulating TREM2 within
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- Hypothesis Stage-Specific TREM2 Biomarker-Guided Switching — Agonist in Amyloid Phase, Antagonist in Tau Phase
amyloid-dominant early phase (Braak NFT stages I–II, amyloid
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amyloid clearance from PV interneurons in Alzheimer's disease starts
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amyloid clearance and secondary PV interneuron disinhibition in Alzheimer's disease
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- Hypothesis TREM2-APOE4 Co-targeting — Simultaneous Correction of Lipid Sensing and Clearance Deficits
amyloid clearance program in APOE4 carriers. The novelty of this
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amyloid monoclonal antibodies through reduced infusion burden, absence of amyloid
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amyloid proteins called curli fibrils, which exhibit striking structural similarities
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amyloid clearance starts from the claim that modulating not yet specified
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Amyloid-beta oligomers disrupt this machinery through multiple pathways. Soluble
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amyloid-beta (Aβ) production by disrupting the subcellular localization of β-site
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amyloid PET positivity (r = 0.6-0.7) and predicts amyloid status
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amyloid-β aggregates even without exogenous amyloid addition, and display
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Amyloid Pathology**: APOE4 protein levels inversely correlate with amyloid clearance
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