neuroinflammation

Data from postmortem brain tissues adds to the evidence that inflammation is associated with autism.

In stressful conditions, specialized protein complexes in microglia induce neurotoxic activity in astrocytes that leads to the change in behavior.

Data from mouse models for mild coronavirus infections and human tissue samples offer further evidence that it doesn’t take a severe infection—or even infection of brain cells at all—to cause long-term neurological symptoms.

A study that transfused plasma from active to inactive mice suggests the protein clusterin enhances cognition.

Epidemiological research suggests that a flu diagnosis might be one factor in the eventual onset of the neurodegenerative disease, but experts say it doesn’t prove a causal relationship.

Knocking out the receptor for a lipid that causes inflammation rejuvenates macrophage metabolism and restores cognitive function in an Alzheimer’s disease model.

Overactive immune cells identified in a mouse model and in postmortem human brain tissue may offer a potential therapeutic target for cognitive delays associated with the condition, researchers report.

Functional proteomics detects elevated neuroinflammatory markers in patient plasma and cerebrospinal fluid!

An accumulation of T cells and astrocytes in postmortem brain tissue hints at possible autoimmune origins for many cases of autism.

Oligomannate, derived from a compound in seaweed, suppresses neural inflammation caused by gut bacteria in mice.

A review of several dozen hospitalized patients in Brazil finds neurological conditions, including inflammation of the brain and spinal cord, in addition to Guillain-Barre syndrome.

Just by activating these immune cells in the brain, scientists could make mice eat more and burn fewer calories.