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.
In the brains of adult mice, astrocytes coupling contributes to neural functioning in the hippocampus, an area of the brain associated with spatial memory and learning.
Astrocytes may play a significant role in information processing and memory, a new study reports.
In patients with ALS, astrocytes within the brain become pro-inflammatory and tend to lose their protective function, resulting in changes in the ability to uptake glutamate.
A new study reveals the mechanisms by which neurons and astrocytes work together to form synapses.
Stem cell study reveals astrocytes carrying the Alzheimer's associated APOE4 gene release more cholesterol than those carrying the APOE3 gene. Findings shed light on how different versions of the APOE gene in astrocytes influence amyloid-beta production and how the oversupply of cholesterol associated with APOE4 astrocytes may promote amyloid-beta formation in Alzheimer's patients.
Cholesterol produced by astrocytes in the brain is required for the production of amyloid-beta. The findings shed light on how and why amyloid-beta forms, and may explain why genes associated with cholesterol have been implicated as risk factors for Alzheimer's disease.
