In a paper published in the journal Nature, scientists have identified abnormal aggregates of a protein called TAF15 in the brains of people with early-onset dementia, known as frontotemporal dementia. Frontotemporal dementia results from the degeneration of the frontal and temporal lobes of the brain, which control emotions, personality and behaviour, as well speech and understanding of words. It tends to start at a younger age than Alzheimer's disease, often being diagnosed in people aged 45 to 65, although it can also affect younger or older people. While amyloid assembly of TDP-43 or tau is the hallmark of the majority of cases of frontotemporal lobar degeneration (FTLD), the assembled protein that characterises the remaining approximately 10% of cases, was previously unknown.
New research led by scientists from the Medical Research Council (MRC) Laboratory of Molecular Biology, in Cambridge, UK, used cryogenic electron microscopy (cryo-EM) to study protein aggregates from the brains of four people who had this type of frontotemporal dementia. They found abundant TAF15 amyloid filaments in brain regions associated with motor neuron disease. Scientists are now studying whether aberrant aggregated TAF15 is present in people who have motor neurone disease in the absence of frontotemporal dementia. This study was funded by the Medical Research Council, Alzheimer's Research UK, the US National Institutes of Health, the Alzheimer's Society, the Association for Frontotemporal Degeneration, the Swiss National Science Foundation, and the Leverhulme Trust.