SARS_CoV_2, the virus responsible for COVID-19 infects and replicates in astrocytes, reducing neural viability.
A new method that targets the astrocytes surrounding glioblastoma brain cancer eradicates tumor cells and extends lifespan in animal models.
Study reveals how a molecule produced by astrocytes interferes with normal neuron development in a range of neurodevelopmental disorders.
Astrocytes enhance healing following a brain hemorrhage by transferring their mitochondria to damaged neurons.
Microglia that express the Alzheimer's associated APOE4 genetic variant are unable to effectively metabolize lipids. This causes lipids to build up, promoting inflammation and preventing effective neurotransmission.
Targeting the GAT3 protein in the thalamus could help block and prevent long-term damage following brain injury.
Study reveals the role of the urea cycle in the brain and explores the dual nature of astrocytes in the brains of those with Alzheimer's pathology.
Neuroimaging technology allowed researchers to capture the activity of microglia and astrocytes in the brain. The researchers were able to quantify alterations in the morphology of different cell populations implicated in neuroinflammation.
The release of potassium ions from neurons charges the electrical activity of astrocytes, allowing for the control of neurotransmission. The astrocyte-neuron crosstalk raises questions as to how the interaction works in brain pathology and the implications for memory and learning.
Abnormalities in astrocytes may play a critical role in some of the behavioral symptoms experienced by those with autism.
Alpha2-NKA, a protein that drives toxicity in astrocytes, was discovered in higher levels of brain samples from people who died of PSP, Alzheimer's and other tau-related neurodegenerative disorders. Treatment with an FDA-approved drug called digoxin may suppress the inflamed astrocytes and halt disease progression for those with tauopathy disorders.
PolyP, an inorganic polyphosphate released by astrocytes in people with ALS and frontotemporal dementia contributes to the signature motor neuron death associated with the disease pathologies.
