A role for thrombospondin-1 deficits in astrocyte-mediated spine and synaptic pathology in Down's syndrome.

ABSTRACT:

Background

Down's syndrome (DS) is the most common genetic cause of mental retardation. Reduced number and aberrant architecture of dendritic spines are common features of DS neuropathology. However, the mechanisms involved in DS spine alterations are not known. In addition to a relevant role in synapse formation and maintenance, astrocytes can regulate spine dynamics by releasing soluble factors or by physical contact with neurons. We have previously shown impaired mitochondrial function in DS astrocytes leading to metabolic alterations in protein processing and secretion. In this study, we investigated whether deficits in astrocyte function contribute to DS spine pathology.

Methodology/principal findings

Using a human astrocyte/rat hippocampal neuron coculture, we found th

SUBMITTER: Garcia O 

PROVIDER: S-EPMC2996288 | biostudies-literature | 2010 Dec

REPOSITORIES: biostudies-literature