Brain folds that form during fetal development may have an impact on the age at which symptoms of frontotemporal dementia occur.
Amyloid fibrils in those with frontotemporal lobar degeneration (FTLD) contain a little-known protein called TMEM106B. Researchers speculate TMEM106B could be found to be the cause of FTLD.
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.
PolyP, an inorganic polyphosphate released by astrocytes in people with ALS and frontotemporal dementia contributes to the signature motor neuron death associated with the disease pathologies.
Damage to the multiple demand network, a brain network associated with general intelligence, causes people with dementia to struggle to adapt to changes in their environment
Mislocalization of the TDP-43 protein alters the genetic instructions for UNC13A. The findings provide a potential new therapeutic target for the treatment of ALS and frontotemporal dementia.
Researchers recreated the damage seen in frontotemporal dementia in brain organoid models. The study reveals an experimental drug designed to treat Crohn's disease may help prevent neuron death associated with FTD.
Researchers report Alzheimer's disease and other neurodegenerative disorders can be confirmed in living patients by specific biomarkers in cerebrospinal fluid.
Study links anhedonia, or the loss of pleasure, to the early onset of frontotemporal dementia. Neuroimaging revealed symptoms of anhedonia were marked by atrophy in the frontal and striatal brain areas of those with FTD.
Study reveals those with frontotemporal dementia have greater white matter hyperintensity than those with other forms of dementia. The amount of white matter hyperintensity was associated with the severity of FTD symptoms.
c9ASO, an investigational ASO drug, targets the TDP-43 protein, reducing its buildup and decreasing neurological decline associated with ALS and FTD.
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.
