Topic: mild-cognitive-impairment

Inhibitory deficits and an excitation/inhibition(E/I) imbalance arising from loss of inhibitory synapses may predispose to subclinical-epileptiform-activity and contribute to the earliest stages of Alzheimer’s disease(AD), and progressively lead to macroscopic neuronal network dysfunction. The classical brain-criticality-hypothesis posits that neuronal-systems operate at a continuous, second-order phase-transition with E/I-balance serving as primary control parameter. However, we have recently found neuronal systems in vivo may also operate at a discontinuous, first-order phase-transition and

Alzheimer's disease (AD) is the most prevalent form of dementia, characterized by a progressive decline in cognitive function that ultimately leads to mortality. Timely detection, particularly during the early-stage of mild-cognitive-impairment (MCI) is crucial for effective intervention. Converging evidence showed that parvalbumin-interneurons (PVI) cortical microcircuitry play an important role for normal cognitive functions. PVI are highly sensitive to oxidative stress (OS) and mitochondrial impairment, conditions that are well known to increase with ageing. Therefore, there is a critical n