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30 results
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amyloid β peptide, revealing a protective effect against amyloid-β and tau pathology
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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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amyloid plaques, respectively. Despite successful induction, amyloid disease-associated microglia
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amyloid-β peptide (Aβ) isoform Aβ₄₀ or Aβ₄₂ contribute
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amyloid-beta (Abeta) such that the Amyloid Cascade Hypothesis is the predominant
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amyloid reduction and slowing of clinical decline in early AD. The objective
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Amyloid Precursor Protein (APP) into Amyloid-β and Microtubule Associated
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amyloid and tau, but researchers are gradually moving away from
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amyloid accumulation followed by tau-mediated neurodegeneration. Despite advances in anti
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- Paper Accelerating rates of cognitive decline and imaging markers associated with β-amyloid pathology.
amyloid thresholds to include the range of amyloid associated with
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amyloid- and tau-PET. Amyloid-positive patients with EOAD had high
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amyloid β and tau. Interestingly, the percentage of amyloid β targeting
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amyloid stitching of myelin sheaths. Amyloid fibrils appear to be an ideal
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amyloid-β (Aβ) peptide. Donanemab, an antibody that targets a modified
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amyloid beta; AD, Alzheimer disease; APP, amyloid beta precursor protein
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amyloid β, suggesting that this pathway may remove amyloid β from
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- Paper Donanemab in Early Symptomatic Alzheimer Disease: The TRAILBLAZER-ALZ 2 Randomized Clinical Trial.
amyloid plaque. Multicenter (277 medical research centers/hospitals in 8 countries
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amyloid peptide (Aβ) is a crucial trigger for amyloid pathology
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Amyloid-Related Imaging Abnormalities (ARIA) in anti-amyloid beta therapy
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amyloid-β (Aβ) and tau imaging may be critical for tracking
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amyloid β-protein (or Aβ hypothesis, new lines of evidence
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amyloid-β induced plaques and hyperphosphorylated tau associated tangles, with
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amyloid conformations that self-propagate and are implicated in neuronal
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amyloid plaques, neurofibrillary tangles, and synaptic and neuronal loss. Recently
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amyloid beta (Aβ), α-syn seeds, and phosphorylated tau181 (p-tau181
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amyloid beta (Aβ), α-syn seeds, and phosphorylated tau181 (p-tau181
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Amyloid burden, white matter hyperintensities and local patterns of brain
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amyloid peptide (Aβ) within the brain along with hyperphosphorylated and cleaved
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amyloid plaques in AD can range from neuroprotective to neurotoxic2
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amyloid plaques and τ tangles in the brain, represents an unmet
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