Brain metal levels linked to Huntingdon’s disease

Unusual levels of various metals have been observed in human brain tissue from patients with Huntington’s disease, researchers have announced.

The post mortem tests were carried out by Dr Melissa Scholefield of the University of Manchester, UK, and colleagues in Auckland, Australia, and reported in the Lancet journal eBioMedicine.

“Its pathogenic mechanisms remain poorly understood,” they write, “and no treatment can currently slow, stop, or reverse its progression”.

Previous research has highlighted “metallomic dysfunction” in certain regions, so the team examined whether these changes may be more widespread.

In the laboratory, they tested samples from nine Huntington’s disease patients for the essential metals sodium, potassium, magnesium, calcium, iron, zinc, copper and manganese, plus selenium.

This showed “striking decreases in selenium levels in 11 out of 11 investigated brain regions”, compared with a control group with healthy brain tissue.

Furthermore, there were “Increased sodium/potassium ratios in every region except the substantia nigra”, and “multiple regions showed increased calcium and/or zinc levels”.

The team believe that these alterations “may contribute to several pathogenic mechanisms, including mitochondrial dysfunction, oxidative stress, and blood-brain barrier dysfunction as shown by previous studies in mice”.

Findings also point to selenium supplementation as a potential therapeutic pathway for Huntington’s disease treatment.

Dr Scholefield said: “This is the first known study which investigated metals simultaneously across many regions of the Huntington’s disease brain in the same cohort.

“The most striking finding is the deficiency of selenium in every part of the brain we studied.

“However, we caution that it is dangerous to self-medicate with supplements; the blood-brain barrier could mean these elements might build up in someone’s blood stream, with potentially toxic effects.”

Scholefield, M et al. Widespread selenium deficiency in the brain of cases with Huntington’s disease presents a new potential therapeutic target. eBioMedicine 6 October 2023; doi: 10.1016/j.ebiom.2023.104824


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