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30 results
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amyloid targeting remains valid with better penetration, but the debate
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amyloid clearance is always beneficial and suggests complex amyloid-cognition
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amyloids can mutually influence aggregation, but the physiological relevance and mechanisms
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- Gap What mechanisms cause the diminishing effect of amyloid on tau spread beyond a critical threshold?
amyloid's potentiating effect on tau propagation diminishes at higher
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amyloid deposition, the functional connection between their platelet expression and brain
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- Gap How does amyloid mechanistically facilitate tau propagation from entorhinal cortex to neocortex?
amyloid modifies the relationship between initial tau and subsequent spread
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amyloid overproduction, but the mechanistic link between hydrolase mislocalization and amyloid
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amyloid (ρ=0.45) than tau (ρ=0.25), which is counterintuitive
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amyloid angiopathy and spontaneous hemorrhage in amyloid precursor protein transgenic
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amyloid and reduced p-tau217/p-tau181 but no correlation with
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amyloid-positive states. Understanding this mechanism could reveal how peripheral
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amyloid pathology, but the mechanistic link between cholesterol dysregulation and enhanced
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amyloid levels, contradicting the established view that pT217 is primarily
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amyloid-β pathology, contradicting the traditional amyloid cascade hypothesis. Understanding
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amyloid accumulation. The molecular basis for this differential performance compared
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amyloid accumulation but protecting from tau mislocalization and cholinergic deficits
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amyloid-β plaques, but the mechanistic connection between PKR activity
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amyloid toxicity. Gap type: unexplained_observation Source paper: Astrocytic APOE3
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amyloid plaque reduction, leaving unknown whether this pathway addresses tau tangles
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amyloids, but the precise molecular mechanisms explaining this isoform-specific
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amyloid changes to specific tau phosphorylation events remains unexplained, yet understanding
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amyloid deposition but exacerbates tau pathology, both linked to inflammatory
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amyloid angiopathy and spontaneous hemorrhage in amyloid precursor protein transgenic
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amyloid burden, APOE3Ch showed superior effects on oligomeric Aβ and plaque
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amyloid pathway have failed, creating a contradiction between the established
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amyloid oligomers and activates TREM2, but the molecular basis for this
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amyloid as a therapeutic target for preventing tau spread. Gap type
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amyloid and tau pathologies by SorLA modulation suggests independent regulatory
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amyloid assemblies trigger neurodegeneration remain largely unknown. Understanding these mechanisms
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amyloid pathology, the precise molecular pathways remain unclear. Understanding these
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