PGC1-α in MS
Research type
Research Study
Full title
Downregulation of PGC-1α as the mediator of mitochondrial dysfunction, oxygen/energy cost of walking and fatigability in multiple sclerosis.
IRAS ID
363394
Contact name
Don Mahad
Contact email
Sponsor organisation
University of Edinburgh
Duration of Study in the UK
1 years, 0 months, 0 days
Research summary
Multiple sclerosis (MS) is a chronic neurological disorder that affects the function of immune cells, central nervous system (brain, eyes and spinal cord) and muscle. A number of studies have suggested the decrease in function of energy producing parts of cells or powerhouses called mitochondria in the disease process of MS. The exact cause of energy deficient state in MS is not known. Consistent findings from animal models indicate a molecular pathway relating to the main regulator of metabolism in cells called peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) as a possible cause of energy failure in MS. In this study we aim to determine whether this regulator (PGC-1α) plays a role in the underlying disease processes of MS. We will increase the amount of this regulator using a drug called Pioglitazone and measure a number of parameters in 12 people with MS (pwMS) who exercise regularly. These include mitochondria in immune cells derived from blood, proteins in the tears derived from pwMS, structure and function of a muscle in the legs, oxygen/energy measurement in relation to walking, walking and balance before and after exercise as well as cognitive function. Pioglitazone will be prescribed for six months and the above measurements will be taken at the beginning, middle (12 weeks) and end of the study (24 weeks). The assessments may identify the regulator (PGC-1α) as an important part of the disease process in MS. The study will be conducted at the Anne Rowling Regenerative Neurology Clinic (ARRNC), University of Edinburgh.
REC name
South Central - Berkshire B Research Ethics Committee
REC reference
25/SC/0356
Date of REC Opinion
20 Nov 2025
REC opinion
Further Information Favourable Opinion