Astroglia in Alzheimer's Disease.

Alzheimer's disease is the most common cause of dementia. Cellular changes in the brains of the patients suffering from Alzheimer's disease occur well in advance of the clinical symptoms. At the cellular level, the most dramatic is a demise of neurones.

Neuroglia in Ageing.

Ageing reduces the functional capacity of all organs, so does that of the nervous system; the latter is evident in the reduction of cognitive abilities, learning and memory. While the exact mechanisms of ageing of the nervous system remain elusive, it is without doubt that morpho-functional changes in a variety of neuroglial cells contribute to this process. The age-dependent changes in neuroglia are characterised by a progressive loss of function.

Expression of familial Alzheimer disease presenilin 1 gene attenuates vesicle traffic and reduces peptide secretion in cultured astrocytes devoid of pathologic tissue environment.

In the brain, astrocytes provide metabolic and trophic support to neurones. Failure in executing astroglial homeostatic functions may contribute to the initiation and propagation of diseases, including Alzheimer disease (AD), characterized by a progressive loss of neurones over years. Here, we examined whether astrocytes from a mice model of AD isolated in the presymptomatic phase of the disease exhibit alterations in vesicle traffic, vesicular peptide release and purinergic calcium signaling.

The glutamate receptor 2 subunit controls post-synaptic density complexity and spine shape in the dentate gyrus.

In adult brain the majority of AMPA glutamate receptor (GluR) subunits contain GluR2. In knock-out (KO) mice the absence of GluR2 results in consequences for synaptic plasticity including cognitive impairments. Here the morphology of dendritic spines and their synaptic contacts was analysed via three-dimensional reconstruction of serial electron micrographs from dentate gyrus (DG) of adult wild type (WT) and GluR2 KO mice.