Using neurons created from iPS cells derived from people with ALS, researchers develop a new drug which appears to halt the impact of the genetic mutations in some forms of ALS and dementia.
A new study investigates the link between frontotemporal dementia and abnormal eating behaviors.
A new study points to a potential new target to treat neurodegenerative diseases.
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.
Study reveals why some people with ALS are prone to developing autoimmune diseases. A genetic mutation that decreases the expression of C9orf72 causes the stimulation of interferon genes (STING) protein to become hyperactive. The hyperactivity leads to increased production of interferons. This can lead to systemic inflammation and the development of autoimmune diseases.
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.
A new study reports on a link between coprophagia and certain neurodegenerative diseases and dementias.
Chemically activating neurons and placing mice in stimulating environments reverses alterations and restores some neural connectivity in frontotemporal dementia. If translated into humans, the findings could help develop new treatments for fighting the effects of dementia in the elderly.
Researchers report retinal degeneration could be one of the earliest signs of FTD in people who have a genetic risk for the disorder.
Researchers have identified a common mechanism in both frontotemporal dementia and neuronal ceroid lipofuscinosis.