In all three types of frontotemporal dementia, researchers found the more the inflammation in each part of the brain, the more harmful the build-up of junk proteins.
The protein beta-arrestin-2 increases tau tangle accumulation in Alzheimer's disease and frontotemporal dementia but interfering with the removal of excess tau from the brain.
Gentamicin and G418, two aminoglycoside antibiotics, were effective at correcting genetic mutations associated with a specific form of frontotemporal dementia. The findings are promising for the treatment of frontotemporal dementia.
Those with a genetic predisposition to frontotemporal dementia (FTD) can become resilient to the neurodegenerative disease by remaining physically and mentally active.
Reducing activity in the anterior cingulate decreases empathetic responses in rats. The data suggests an observer shares the emotions of others as it enables them to prepare for danger.
The NLPR3 inflammasome and the inflammatory response it triggers play a critical role in the emergence of tau pathology.
Researchers discovered increased inflammatory activity in a subgroup of patients with frontotemporal dementia. The increased inflammation was indicated by elevated levels of cytokines known to increase inflammatory response and decreased levels of IL-10, which reduces inflammation. The inflammation was associated with Parkinsonism's symptoms and rapid cognitive and functional decline. The study also revealed patients with FTD are less likely to develop cancer.
Researchers have identified the location of dysfunctional brain networks that lead to impaired sentence production and word-finding in primary progressive aphasia (PPA). PPA can occur in those with neurodegenerative diseases, such as frontotemporal dementia and Alzheimer's disease. Mapping the networks allows clinicians to apply non-invasive brain stimulation to potentially improve speech in those with PPA.
A microscopy study revealed tau controls Fyn clustering in dendrites. The findings shed new light on how certain forms of dementia may occur.
Researchers have engineered a vaccine using virus-like particles that target Tau tangles in mouse models of Alzheimer's disease. Following the administration of the vaccine, the mice developed antibodies that cleared tau proteins, with the response lasting for a month. The mice also showed improvements in memory based tests and had less brain shrinkage than their peers who did not receive the vaccine. This suggests the vaccine prevented apoptosis. Researchers hope to move the vaccine to human clinical trials in the future.