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.
Patients who suffer from frontotemporal dementia with extrapyramidal symptoms have brainstem atrophy and reduced metabolic activity in specific brain regions compared to those with FTD without extrapyramidal symptoms.
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.