Topic: β-amyloid oligomers

Alzheimer’s disease (AD) represents an urgent yet unmet challenge for modern society, calling for exploration of innovative targets and therapeutic approaches. Astrocytes, considering their crucial functions in the CNS, represent promising cell-target.Our aim was to investigate if deletion of the regulatory CaNB1 subunit of calcineurin in astrocytes could mitigate AD-related memory deficits, neuropathology and neuroinflammation.We have generated two, acute and chronic, AD mouse models with astrocytic CaNB1 deletion (ACN-KO). In the acute one we evaluated the ability of β-amyloid oligomers (AβO

Cholinergic transmission is fundamental in memory mechanisms. Accordingly, the early degeneration of cholinergic fibers characterizing Alzheimer’s disease (AD) contributes to cognitive impairment, and mice lacking functional α7 nicotinic acetylcholine receptors (A7KO) develop an age-dependent AD-like phenotype, featuring increased levels of β-amyloid and phospho-tau, hippocampal plasticity deficits, neuronal loss and astrogliosis. Astrocytes, recognized partners of neurons in brain function, are characterized by a signaling system based on variations in intracellular Ca2+ concentration. Experi