According to scientists at the Medical Research Council (MRC) Laboratory of Molecular Biology in Cambridge, UK, a novel protein called TAF15 formed aggregated structures in frontotemporal dementia cases. This challenges previous assumptions about the condition and contributes to a limited set of proteins known for aggregating in neurodegenerative disorders like Alzheimer’s.
Read this article to understand this latest scientific discovery and what it means for dementia patients.
How Does The Novel Protein Contribute to Frontotemporal Dementia?
Frontotemporal dementia occurs from the deterioration of the brain’s frontal and temporal lobes, which coordinate emotions, behavior, personality, language comprehension, and speech.
This condition usually happens at an earlier age compared to Alzheimer’s disease, frequently being diagnosed in individuals between 45 and 65 years old. However, it can also present in individuals both younger and older.
In their new research, a team of scientists uncovered aggregated protein structures that could be a focal point for potential advancements in diagnostic assessments and therapies. By identifying the key protein and its structure, the researchers are now prepared to diagnose and treat this type of frontotemporal dementia.
This approach mirrors the strategies already in progress for targeting tau protein and amyloid-beta, hallmark features of Alzheimer’s disease.
How Was The Study Conducted?
The scientists utilize advanced cryo-electron microscopy (cryo-EM) techniques to examine protein aggregates at an atomic level resolution in the brains of four persons with this frontotemporal dementia type.
Until now, scientists have assumed a protein called FUS was responsible for aggregation in this dementia type, drawing parallels with other neurodegenerative disorders. Using cryo-electron microscopy (cryo-EM), the researchers determined that the responsible protein was not FUS but another protein called TAF15.
Frontotemporal Dementia and Motor Neuron Disease
Some individuals affected by frontotemporal dementia also experience motor neuron disease, a condition characterized by progressive muscle control loss. In this investigation, two individuals who had both conditions donated their brains to the study.
Researchers identified the same aggregated form of the TAF15 protein in brain regions associated with motor neuron disease. The presence of identical TAF15 aggregates in both individuals with frontotemporal dementia and signs of motor neuron disease increased the possibility that TAF15 could result in the development of both disorders.
Further Research Needed to Investigate the Impact of TAF15
The research team is currently examining whether these abnormal TAF15 aggregates are present in individuals with motor neuron disease who do not exhibit symptoms of frontotemporal dementia.
Further, identifying a TAF variant could also serve as an essential diagnostic market and a potential therapeutic target in FTLD treatment.
Conclusion
While more research is being conducted, the current findings pave the way for advanced diagnostic tools and treatments. It also raises the intriguing possibility that TAF15 could be connected to both frontotemporal dementia and motor neuron disease, shedding more light on these debilitating disorders.
