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Accumulation of aggregated amyloid β-protein (Aβ) in the brain is thought to be the initiating event leading to neurodegenetation and dementia in Alzheimer's disease (AD). Therefore, therapeutic strategies that clear accumulated Aβ and/or prevent Aβ production and its aggregation are predicted to be effective against AD. Immunization of AD mouse models with synthetic Aβ prevented or reduced Aβ load...
Increasing evidence supports a propensity towards inflammation in Alzheimer's disease (AD) pathogenesis. In our previous studies we observed high levels of IL-16, IL-18 and TGF-β1 mRNA expression in monocyte-macrophages of the peripheral blood of AD patients. The aim of this investigation was to determine the plasma levels of IL-12, IL-16, IL-18 and TGF-β1 in AD patients at different stages of the...
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