Endothelial and astroglial alterations in vitro and in vivo models of Alzheimer?s disease. Evidence of cell activation and autophagic induction.

CARLOS POMILIO; ROXANA GOROJOD; TODERO MARÍA FLORENCIA; ÁNGELES VINUESA; AGUSTINA ALAIMO; MÓNICA KOTLER; JUAN BEAUQUIS; FLAVIA SARAVIA

Congreso; Reunión de la Latin American and Caribbean neuroscience Societies; 2016

Alzheimer?s disease (AD) is the principal cause of dementia in the elderly. The overproduction of Amyloid-β peptides (Aβ) and their aggregation into senile plaques are recognized hallmarks in AD. Aβ is able to affect neurons and synapsis, but also it activates glial and endothelial cells -components of the neurovascular unit- altering brain homeostasis. In this study, we characterized astroglial and vascular alterations in in vitro conditions and using a mouse model of AD. Before plaque deposition, AD mice exhibited less astrocytes (p