Role of thiamine in Huntington’s disease pathogenesis: In vitro studies

Gruber-Bzura, Beata M; Krzysztoń-Russjan, Jolanta; Bubko, Irena; Syska, Jarosław; Jaworska, Małgorzata; Zmysłowski, Adam; Rosłon, Magdalena; Drozd, Janina; Drozd, Ewa; Majorczyk, Edyta; Anuszewska, Elżbieta

doi:10.17219/acem/63091

Cited by 7 publications

(4 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, several amino acids were tested as potential biomarkers. It has been reported that plasma levels of asparagine (Asn) and Serine (Ser) were significantly decreased suggesting a potential biomarker role for these two amino acids [22].…”

Section: Metabolic Markersmentioning

confidence: 99%

Exploring Biomarkers for Huntington’s Disease

Deeb¹,

Atallah²,

Salameh³

2022

From Pathophysiology to Treatment of Huntington's Disease

View full text Add to dashboard Cite

Huntington’s disease (HD) is a progressive, non-curative, autosomal dominant neurodegenerative disease characterized by prominent psychiatric problems, as well as progressive deterioration in both cognitive function and motor control. The success of therapeutic interventions in HD patients cannot be easily examined without reliable and practical measurements by using effective biomarkers. Many clinical trials have been held to evaluate biomarkers efficacies in disease-modifying treatment before the manifestation of the disease or its severity. Biofluid (wet) biomarkers have potential advantages of direct quantification of biological processes at the molecular level, imaging biomarkers, on the other hand, can quantify related changes at a structural level in the brain. The most robust biofluid and imaging biomarkers are being investigated for their clinical use and development of future treatment and can offer complementary information, providing a more comprehensive evaluation of disease stage and progression.

show abstract

Section: Metabolic Markersmentioning

confidence: 99%

Exploring Biomarkers for Huntington’s Disease

Deeb¹,

Atallah²,

Salameh³

2022

From Pathophysiology to Treatment of Huntington's Disease

View full text Add to dashboard Cite

show abstract

“…The direct association of thiamine (VitB1) with HD is far from clear, but results have demonstrated that a deficiency in thiamine causes oxidative stress and neuroinflammation, which could contribute to the progression of HD [234][235][236]. Researchers investigated the role of supplemented thiamine in HD pathogenesis by assessing the viability of human B lymphocytes with and without the abnormal huntingtin gene [237]. Results indicated that energy metabolism is a vital step in HD pathogenesis, and thiamine deficiency caused a reduction in the cellular energy metabolism by altering the expression of various genes.…”

Section: Vitamins In Huntington's Diseasementioning

confidence: 99%

“…In the HD human B lymphocyte model, the genes affected were glyceraldehyde-3-phosphate dehydrogenase (GAPDH), isocitrate dehydrogenase gene (IDH1), and the solute carrier family 19, member 3 (SLC19A3) gene. GAPDH, IDH1, and SLC19A3 are involved in the synthetic process of ATP and other high-energy-containing molecules [237]. Thus, thiamine controls the expression of genes involved in energy metabolism and could provide effective therapy for HD.…”

Section: Vitamins In Huntington's Diseasementioning

confidence: 99%

The Role of Vitamins in Neurodegenerative Disease: An Update

et al. 2021

View full text Add to dashboard Cite

Acquiring the recommended daily allowance of vitamins is crucial for maintaining homeostatic balance in humans and other animals. A deficiency in or dysregulation of vitamins adversely affects the neuronal metabolism, which may lead to neurodegenerative diseases. In this article, we discuss how novel vitamin-based approaches aid in attenuating abnormal neuronal functioning in neurodegeneration-based brain diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Amyotrophic lateral sclerosis, and Prion disease. Vitamins show their therapeutic activity in Parkinson’s disease by antioxidative and anti-inflammatory activity. In addition, different water- and lipid-soluble vitamins have also prevented amyloid beta and tau pathology. On the other hand, some results also show no correlation between vitamin action and the prevention of neurodegenerative diseases. Some vitamins also exhibit toxic activity too. This review discusses both the beneficial and null effects of vitamin supplementation for neurological disorders. The detailed mechanism of action of both water- and lipid-soluble vitamins is addressed in the manuscript. Hormesis is also an essential factor that is very helpful to determine the effective dose of vitamins. PubMed, Google Scholar, Web of Science, and Scopus were employed to conduct the literature search of original articles, review articles, and meta-analyses.

show abstract

“…Hsp60 acts as molecular chaperone in cooperation with Hsp10 (Wyżewski et al, 2014). In addition to assisting in the protein folding, Hsp60 regulates cell apoptosis and has both pro- (Gruber et al, 2010) and anti- (Cohen-Sfady et al, 2009;Ghosh et al, 2008;Shan et al, 2003) apoptotic activities. The latter may contribute to oncogenesis by enhancing survival or growth of certain tumor cell types (Schmitt et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Functional role of Hsp60 as a positive regulator of human viral infection progression

Wyżewski¹,

Gregorczyk²,

Szczepanowska³

et al. 2018

View full text Add to dashboard Cite

Heat shock proteins (Hsps) are a family of proteins highly conserved in evolution. Members of the Hsp family are mainly responsible for proper protein folding, however they perform many other functions in living organisms. Hsp60 is a molecular chaperone that is present in mitochondria and cytosol of eukaryotic cells, as well as on their surface. It is also found in the extracellular space and in the peripheral blood. Apart from its role in assisting protein folding in cooperation with Hsp10, Hsp60 contributes to regulation of apoptosis, as well as participates in modulation of the immune system activity. Hsp60 may favor oncogenesis by promoting survival or growth of some tumor cell types. Hsp60 is a subject of medical research due to its role in pathogenesis of certain tumors and infectious diseases. In this review we discuss mechanisms by which Hsp60 promotes development and progression of infections caused by three human viruses: hepatitis B virus (HBV), human immunodeficiency virus (HIV) and influenza A virus.

show abstract

Role of thiamine in Huntington’s disease pathogenesis: In vitro studies

Abstract: Background. Oxidative stress accompanies neurodegeneration and also causes abnormalities in thiamine-dependent processes. These processes have been reported to be diminished in the brains of patients with several neurodegenerative diseases.

Cited by 7 publications

References 27 publications

Exploring Biomarkers for Huntington’s Disease

Exploring Biomarkers for Huntington’s Disease

The Role of Vitamins in Neurodegenerative Disease: An Update

Functional role of Hsp60 as a positive regulator of human viral infection progression

Contact Info

Product

Resources

About