New protective mechanism against dementia discovered
Researchers from Helmholtz Munich, the Technical University of Munich and the LMU Medical Center have deciphered a mechanism that protects nerve cells from ferroptosis, a cell death program. The study shows for the first time that ferroptosis can trigger neurodegeneration in the human brain and opens up new approaches for therapies, especially in early childhood dementia.
The core of the protection is the selenoenzyme glutathione peroxidase 4 (GPX4). A mutation in the GPX4 gene can disrupt its function, causing severe dementia in children. Normally, GPX4 neutralizes harmful lipid peroxides in the cell membrane of nerve cells. A mutation (R152H), observed in three children with early childhood dementia, prevents this, triggers ferroptosis and leads to cell death.
The researchers examined cell samples from an affected child, grew nerve cells and brain organoids and transferred the mutation to a mouse model. This showed movement disorders, nerve cell loss and inflammation, similar to the children. Protein patterns in the mouse model were similar to those in Alzheimer’s, suggesting a role of ferroptosis in more common dementias as well.
Initial experiments show that ferroptosis inhibitors can slow down cell death, which enables future therapeutic approaches. The results underline the importance of long-term basic research and international cooperation for the understanding of complex diseases.
Original Paper:
A fin-loop-like structure in GPX4 underlies neuroprotection from ferroptosis: Cell
Editor: X-Press Journalistenbüro GbR
Gender Notice. The personal designations used in this text always refer equally to female, male and diverse persons. Double/triple naming and gendered designations are used for better readability. ected.
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