Glial and vascular morphology in mouse model of Ataxia telangiectasia

Ataxia telangiectasia mutated (Atm) protein kinase is one of the most important master regulators of the DNA damage response, as it takes part in DNA double strand break repair. Loss of Atm activity causes ataxia telangiectasia (A-T). A-T is characterized by cerebellar degeneration and telangiectasia, formation of small dilated blood vessels. Such vascular alterations contribute to brain homeostasis imbalance. As the brain depends on a constant blood supply for proper function, vascular alterations cause changes in blood flow and lead to cellular dysfunction. Here, we established vascular morphology and pericytes distribution in the cerebella of A-T mouse models, using high throughput histology. Our data show that pericytes play a crucial role in vascular abnormalities in Atm-/- mice.