Targeting Higher Levels of Tau Protein in Ukrainian Patients with Wilson’s Disease
Autor: | Yevgeniya Lekomtseva, Ivan Voloshyn-Gaponov, Gorbach Tatayna |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: | |
Zdroj: | Neurology and Therapy, Vol 8, Iss 1, Pp 59-68 (2019) |
Druh dokumentu: | article |
ISSN: | 2193-8253 2193-6536 |
DOI: | 10.1007/s40120-019-0134-3 |
Popis: | Abstract Introduction Wilson’s disease (WD) is a rare genetic disorder of copper metabolism in which impaired copper homeostasis may enhance amyloid aggregation and trigger neurodegeneration. Tau protein is a highly soluble microtubule-associated phosphoprotein that plays a significant role in microtubule stabilization; it is also a critical component of neurotoxic degenerative mechanisms. Tau has been shown to be involved in neuronal degeneration and axonal damage, and impaired copper metabolism has been shown to be involved in copper intoxication and thus associated with the processes of neurodegeneration and cellular damage. We have therefore investigated tau protein as a potential marker of axonal impairment and neurodegeneration. Methods Patients with WD (n = 47; mean age ± standard deviation [SD] 30.19 ± 7.87 years; mean disease duration : 10.06 ± 3.9 years) and healthy controls (HC; n = 30; mean age 29.6 ± 4.73 years) were tested for serum tau protein levels using an enzyme-linked immunosorbent assay method. All patients were receiving a stable penicillamine dose as ongoing therapy. Results Patients with WD had a higher mean tau protein level than did the HC (221.7 ± 135.1 vs. 71.14 ± 20.56 pg/mL, p |
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