Hypothalamic hormone linked to metabolic dysregulation in ALS

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ALS-FTD

This recent research shows that the loss of MCH+ hypothalamic neurons is linked to the metabolic problems that occur in ALS. Amyotrophic lateral sclerosis (ALS), also known as Charcot's disease, is a disease of the motor neurons (motoneurons), the nerve cells that control our muscles, and is the most common disease in adults.

The work of Matei Bolborea, a researcher in the unit, has shown that the loss of MCH+ hypothalamic neurons is linked to the metabolic problems that occur in ALS. The results have just been published in the journal Acta Neuropathologica.

The study shows that when these MCH+ neurons are no longer present in the hypothalamus, numerous metabolic problems arise, and that this neurodegeneration is coupled with TDP-43 aggregates in these same neurons.

In addition to this analysis, MCH supplementation helped to restore the metabolic deficits observed (weight loss, low food intake).

Thanks to numerous international collaborations (Ulm University, Germany; Leuven Brain Institute, Belgium; Chiba University School of Medicine, Japan), the team was able to show that the loss of MCH+ hypothalamic neurons was linked to the metabolic deficits in ALS.

This new lead opens up horizons for potential new research and therapeutic avenues. This hypothalamic neurodegeneration in ALS could explain the metabolic deficits already reported in numerous other studies.

All in all, this study shows several direct links between metabolic deficits and central neurodegeneration in ALS.

 

Source:  Bolborea M., et al.Loss of hypothalamic MCH decreases food intake in amyotrophic lateral sclerosis. Acta Neuropathol 145, 773–791 (2023). https://doi.org/10.1007/s00401-023-02569-x

Contact: Luc Dupuis, ldupuis[at]unistra.fr; Matei Bolborea mbolborea[at]unistra.fr

 

Credits: Simon J. Guillot