Diagnostic Potential of Alternations of Bile Acid Profiles in the Plasma of Patients with Huntington’s Disease-Reference-Cited by-同舟云学术

Diagnostic Potential of Alternations of Bile Acid Profiles in the Plasma of Patients with Huntington’s Disease

Published:2024-07-20 Issue:7 Volume:14 Page:394
ISSN:2218-1989
Container-title:Metabolites
language:en
Short-container-title:Metabolites

Author:

Chiang Ping-I¹,Chang Kuo-Hsuan²^ORCID,Tang Hsiang-Yu³^ORCID,Wu Yih-Ru²,Cheng Mei-Ling³⁴⁵^ORCID,Chen Chiung-Mei²^ORCID

Affiliation:

1. Department of Medical Education, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei 231, Taiwan

2. Department of Neurology, Chang Gung Memorial Hospital, Linkou Medical Center, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan

3. Metabolomics Core Laboratory, Healthy Aging Research Center, Chang Gung University, Taoyuan 333, Taiwan

4. Clinical Metabolomics Core Laboratory, Chang Gung Memorial Hospital, Taoyuan-333, Taiwan

5. Department of Biomedical Sciences, Chang Gung University, Taoyuan 333, Taiwan

Abstract

Huntington’s disease (HD) is characterized by progressive involuntary chorea movements and cognitive decline. Recent research indicates that metabolic disturbance may play a role in its pathogenesis. Bile acids, produced during cholesterol metabolism in the liver, have been linked to neurodegenerative conditions. This study investigated variations in plasma bile acid profiles among individuals with HD. Plasma levels of 16 primary and secondary bile acids and their conjugates were analyzed in 20 healthy controls and 33 HD patients, including 24 with symptoms (symHD) and 9 carriers in the presymptomatic stage (preHD). HD patients exhibited significantly higher levels of glycochenodeoxycholic acid (GCDCA) and glycoursodeoxycholic acid (GUDCA) compared to healthy controls. Conversely, isolithocholic acid levels were notably lower in the HD group. Neurotoxic bile acids (glycocholic acid (GCA) + glycodeoxycholic acid (GDCA) + GCDCA) were elevated in symHD patients, while levels of neuroprotective bile acids (ursodeoxycholic acid (UDCA) + GUDCA + tauroursodeoxycholic acid (TUDCA)) were higher in preHD carriers, indicating a compensatory response to early neuronal damage. These results underscore the importance of changes in plasma bile acid profiles in HD and their potential involvement in disease mechanisms. The identified bile acids (GCDCA, GUDCA, and isolithocholic acid) could potentially serve as markers to distinguish between HD stages and healthy individuals. Nonetheless, further research is warranted to fully understand the clinical implications of these findings and their potential as diagnostic or therapeutic tools for HD.

Funder

Chang Gung Medical Foundation, Taiwan

Publisher

MDPI AG

Link

https://www.mdpi.com/2218-1989/14/7/394/pdf

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