Findings point to microglial TREM2 as a potential target for the treatment of ALS.
A drug currently being tested in cancer clinical trials appears to prevent dysfunction in an immune cell signaling pathway associated with Alzheimer's disease. Blocking the pathway could prevent Alzheimer's from developing and slow the progression of symptoms for those who already have the disease.
Testing for specific inflammatory proteins in cerebrospinal fluid can help doctors to diagnose the early onset of Alzheimer's disease and track the progression of the disease in patients.
A two-week course of CBD helps normalize and restore the function of two proteins associated with reducing amyloid-beta accumulation in mouse models of familial Alzheimer's disease. CBD also reduces levels of IL-6, an immune protein associated with inflammation in Alzheimer's patients.
PLCG2-P522R, a genetic variant that protects against Alzheimer's disease, enhances key functions of immune cells.
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.
Stimulating activation of microglia may help eliminate Alzheimer's associated plaques, thus helping to prevent the progression of the neurodegenerative disease.
Findings could help in the development of treatments to prevent brain inflammation associated with Alzheimer's disease.
Study in mice and humans reveals reinforcing the activity of microglia could slow, or potentially halt, the proliferation of Tau tangles in Alzheimer's disease.
Changes in gene expression help researchers identify ALS associated pathways and establish the key drivers of motor neuron degeneration in the disease.
Two rare genetic variants on the NOTCH3 and TREM2 genes have been identified in some Alzheimer's patients.
Researchers report therapeutic activation of the TREM2 gene during the early stages of Alzheimer's disease may help to counteract the formation of amyloid beta protein aggregates.
