IgA cells that originate in the gut play a role appear to have neuroprotective properties against diseases associated with neuroinflammation, such as meningitis.
Myeloid cells can suppress the immune response, allowing breast cancer cells to metastasize in the brain and form secondary tumor sites.
A new intranasal delivery system shows promise in reducing neuroinflammation and slowing the progression of multiple sclerosis.
Parkinson's patients carrying mutations in PINK1 and Parkin genes have increased levels of circulating interleukin 6 and mitochondrial DNA. The findings strengthen a link between genetic risk factors from Parkinson's disease and inflammation.
Researchers have identified a bio-chemical circuit that supports neuron-microglia communication. When neurons are active, they release ATP. Microglia sense extracellular ATP and the compound draws the immune cell toward the neuron.
IFITM3, a protein that plays a role in the immune response to pathogens, also plays a key role in the accumulation of amyloid-beta plaques. As IFITM3 directly affects plaque formation, researchers suggest both viral and bacterial infections could increase the risk of Alzheimer's development.
DHA treatment reduced the size of the damaged brain area and initiated a repair mechanism in animal models of stroke. DHA affected the levels of MANF and TREM2, two proteins critical for communication between brain cells.
Coronavirus infection can lead to an array of neurological complications, including delirium, stroke, and a rare, often fatal neuroinflammatory condition called ADEM. The neurological complications did not always correlate with the severity of respiratory symptoms. In some patients, brain inflammation was likely caused by an immune response to COVID-19, suggesting the neurological damage may be a result of immune system activation rather than the virus itself.
From losing the sense of taste or smell to developing an increased risk of stroke, researchers investigate both the known and potential long-term implications of COVID-19 infection in the brain.
A 3D human tissue culture model demonstrated a possible causal relationship between Alzheimer's disease and herpes simplex virus 1 (HSV-1) infection. 40 Alzheimer's associated genes were over-expressed in the HSV-1 infected brain tissue, including genes associated with the production of amyloid-beta.
Reducing neuroinflammation in the brain before cognitive impairment becomes apparent can help slow the progression of Alzheimer's disease.
A new method called Tox-seq found only one sub-group of microglia caused oxidative stress. The gene expression signatures of this sub-group from a mouse model matched patterns observed in cells suspected of causing damage in progressive multiple sclerosis patients. The pattern of gene expression associated with oxidative stress in mouse cells included genes involved in coagulation.
