Researchers are uncovering more about frontotemporal dementia (FTD), the most common type of dementia in people under 65, linked to the deterioration of the brain’s frontal and temporal lobes.
A particular interest lies in the TMEM106B gene, which has a variant that could slow the progression of FTD.
This variant seems to play a protective role, and recent insights suggest that the key to understanding its benefits might involve tiny fiber-like structures known as fibrils, produced by a part of the TMEM106B protein.
These fibrils, which sometimes form tangles in the brain, are notably piled up in most individuals with FTD. However, in those carrying the protective variant of TMEM106B, these structures are almost nonexistent.
This groundbreaking research, reported in Science Translational Medicine, opens new avenues for potential treatments.
The discovery of these thread-like structures formed by the TMEM106B protein is relatively recent. A team from the Mayo Clinic in Florida and their colleagues delved into the relationship between these structures, the protective genetic variant of TMEM106B, and FTD.
By analyzing brain tissue from deceased FTD patients who donated their brains to the Mayo Clinic Brain Bank, they found that those with the protective variant lived about three years longer than those without, suggesting a slower disease progression.
Furthermore, through the development of a specific antibody, researchers could detect and quantify these fibril structures in the brain tissue. They examined over 250 samples from the brain bank and observed a high level of these structures in most FTD patients.
However, those with the protective TMEM106B variant had significantly fewer fibrils. The presence of TMEM106B structures also correlated with levels of TDP-43, a protein strongly associated with FTD, indicating a potential link between these elements in the disease’s pathology.
Jordan Marks, an M.D.-Ph.D. student with the Mayo Clinic Graduate School of Biomedical Sciences and first author of the study, highlighted the absence of fibril buildup in individuals with the protective variant, suggesting its role in defending against FTD.
This observation opens the door for these fibrils to potentially serve as biomarkers for diagnosing FTD and assessing its severity or prognosis in the future.
The implications of these findings are significant for clinical research, emphasizing the importance of considering genetic variants of TMEM106B in patient study groups.
The study hints at possible therapeutic interventions aimed at preventing the accumulation of these tangled structures, which could potentially slow down or reduce the risk of the disease.
Further research will focus on validating these findings in more extensive patient groups and exploring the network of proteins interacting with TMEM106B to deepen understanding of how this protein’s accumulation contributes to FTD.
Additionally, a related study in Science Advances by Mayo Clinic researchers reveals novel peptides linked to TDP-43 dysfunction, also associated with amyotrophic lateral sclerosis (ALS).
This could lead to clinical tests for measuring TDP-43 pathology in living patients, offering hope for early detection and intervention in FTD and related conditions.
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The research findings can be found in Science Translational Medicine.
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