• Dmitry Lim, J J Rodríguez-Arellano, Vladimir Parpura, Robert Zorec, Fares Zeidán-Chuliá, Armando A Genazzani, and Alexei Verkhratsky.
• Faculty of Life Sciences, The University of Manchester, Manchester, UK. Alexej.Verkhratsky@manchester.ac.uk.
• Curr Alzheimer Res. 2016 Jan 1; 13 (4): 359-69.

AbstractPathological remodelling of astroglia represents an important component of the pathogenesis of Alzheimer's disease (AD). In AD astrocytes undergo both atrophy and reactivity; which may be specific for different stages of the disease evolution. Astroglial reactivity represents the generic defensive mechanism, and inhibition of astrogliotic response exacerbates b-amyloid pathology associated with AD. In animal models of AD astroglial reactivity is different in different brain regions, and the deficits of reactive response observed in entorhinal and prefrontal cortices may be linked to their vulnerability to AD progression. Reactive astrogliosis is linked to astroglial Ca(2+) signalling, this latter being widely regarded as a mechanism of astroglial excitability. The AD pathology evolving in animal models as well as acute or chronic exposure to β-amyloid induce pathological remodelling of Ca(2+) signalling toolkit in astrocytes. This remodelling modifies astroglial Ca(2+) signalling and may be linked to cellular mechanisms of AD pathogenesis.

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