Extensive selenium deficiency discovered in Huntington’s disease brain tissue

University of Manchester researchers conducting post mortem studies on the brains of patients with Huntington's disease (HD) found metallomic alterations—specifically widespread decreases in selenium levels throughout the brain—that may contribute to several pathogenic mechanisms, including mitochondrial dysfunction, oxidative stress, and blood-brain barrier dysfunction.

• Researchers measured the concentrations of eight essential metals (sodium, potassium, magnesium, calcium, iron, zinc, copper, and manganese) and the metalloid selenium across 11 brain regions in nine genetically confirmed, clinically manifest cases of HD and nine controls using inductively-coupled plasma mass spectrometry.
• Striking decreases in selenium levels in 11 out of 11 investigated brain regions in HD, with risk ratios and effect sizes ranging 2.3-9.0 and 0.7-1.9, respectively, were observed. 
• Increased sodium/potassium ratios were observed in every region (risk ratio = 2.5-8.0; effect size = 1.2-5.8) except the substantia nigra (risk ratio = 0.25; effect size = 0.1). 
• Multiple regions showed increased calcium and/or zinc levels, and localized decreases in iron, copper, and manganese were present in the globus pallidus, cerebellum, and substantia nigra, respectively.
• Study authors say that selenium supplementation may represent a potential therapeutic pathway for the treatment of HD that wouldn't require localized delivery in the brain due to the widespread presence of selenium deficiency in regions that show both high and low levels of neurodegeneration. 

Source:

Scholefield, M. EBioMedicine. (2023, October 6). Widespread selenium deficiency in the brain of cases with Huntington's disease presents a new potential therapeutic target. https://pubmed.ncbi.nlm.nih.gov/37806287/