Neuroimaging and if necessary, genetic testing, can help to confirm an FTD diagnosis.
Eating abnormalities in frontotemporal dementia result from a network of brain regions, rather than 1or 2 specific structures.
Addressing proteasome dysfunction may help prevent accumulation of the toxic protein.
A gene mutation behind a large amount of ALS and FTD cases may disrupt nuclear transport, destroying neurons.
The mouse model will allow researchers to effectively test therapeutic compounds.
The results support the "cognitive reserve" theory that greater mental activity promotes brain connectivity.
C9orf72 hypermethylation helps protect the brain against damage in ALS and frontotemporal degeneration.
Alzheimer's patients had 1.4 times higher concentrations of IAPP than non-Alzheimer's patients in temporal cortex.
The highest dose of intranasal oxytocin seemed to produce the best response.
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