Abstract
Alterations in cytokine expression as well as deficits in synaptic activity are two features observed in early, prodromal stages of Alzheimer’s disease (AD). The cytokines TNF-α and IL-1β are not only mediators of immune responses, but are also involved in regulating synaptic activity through their effects on neuronal excitability and Hebbian plasticity. We propose that early changes occurring in the AD brain, such as increases in soluble amyloid-β oligomers, may increase the expression of certain cytokines and subsequently cause alterations in cytokine-mediated synaptic activity. A shift of focus towards the prodromal stages of AD, which incorporate the earliest detectable molecular, electrophysiological and behavioral alterations, may provide novel therapeutic targets and potential biomarkers for this currently incurable neurodegenerative disease.
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