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| http://dx.doi.org/10.1186/s12879-024-09951-4 | DOI Listing |
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Background: Sleep disturbances are common in Alzheimer's disease (AD) and occur at early stages. Hyperexcitability also arises during sleep and can lead to epileptiform activity and seizures that impact memory consolidation. The underlying mechanisms of sleep disturbances and hyperexcitability in AD pathology remain unclear but are likely associated with changes in brain networks and altered functional connectivity (FC).
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Background: Synaptic dysfunction plays an important role in Alzheimer's disease (AD) and cognitive decline. We investigated the association between cerebrospinal fluid (CSF) synaptic protein levels and quantitative EEG (qEEG) measures, two modalities to measure synaptic dysfunction in AD pathology. We assessed combined and independent prognostic value of both modalities for cognitive decline along the AD continuum.
View Article and Find Full Text PDFBackground: Plasma glial fibrillary acidic protein (GFAP) is associated with amyloid-β (Aβ) and tau, but their causal relationships remain unclear. We used Mendelian randomization (MR; using genetic causal anchors to avoid reverse causation) to clarify the causal relationship between plasma/brain GFAP, Aβ, and tau.
Methods: Study participants are from two independent datasets: the Harvard Aging Brain Study (HABS) and the Religious Orders Study/the Rush Memory and Aging Project (ROSMAP) (Table 1).
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Alzheimers Dement
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Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA.
Background: Autophagy-lysosomal pathway (ALP) dysfunction emerges early in Alzheimer's disease(AD). In mouse AD models, lysosomal acidification deficits impair ALP in neurons, in some inducing massive autolysosome accumulations, intraneuronal amyloid plaque, and early neuronal death yielding an extracellular amyloid plaque. This distinctive neurodegenerative pattern (PANTHOS) emerges in early-stage AD and is recapitulated in human late-onset AD (accompanying poster).
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