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Fryad Majeed RAHMAN
PhD in Human Molecular Genetics

NORT, UMR Inserm U1062, INRA 1260
Faculty of Medicine - Timone Campus
University of  Aix-Marseille - France

MSc in Genomics and Health

EA 4263, Therapy of Genetic Disorders
Faculty of Medicine - Timone Campus
University of the Mediterranean - France

MSc in Biotechnology

Department of Biology / Faculty of Science
University of Babylon - Iraq

BSc in Biology - Microbiology

Department of Biology / Faculty of Science
University of Salahaddin - Kurdistan


Publications: 1 Book Chapter + 5 Jour. Articles + 1 Conf. paper

e-mail: fryad.rahman@univsul.edu.iq 
Mobile: +964 (0) 770 1411903
        +964 (0) 750 1469802
Area of My Research

Ascorbic acid has been considered, for a long time, only as an antioxidant. Since a few years, growing evidences, from literature, demonstrate that this molecule has other function. This is why different groups tried to find new targets for ascorbic acid (AA), not only to prevent scurvy, but also as a drug. In this line of evidence, we report that high doses of AA partially correct the phenotype of a Charcot–Marie- Tooth type 1A model, created in the lab. Charcot-Marie-Tooth disease (CMT) is the most common hereditary peripheral neuropathy, affecting 1 in 2,500 people, the most frequent form of the disease, CMT-1A, involves abnormal myelination of the peripheral nerves. AA resulted in substantial amelioration of the CMT-1A phenotype and and reduced the expression of PMP22 to a level below what is necessary to induce the disease phenotype. As AA has already been approved by the FDA for other clinical indications, it offers an immediate therapeutic possibility for patients with the disease. Based on this result, several clinical trials have been undertaken. 
Moreover, AA is a competitive inhibitor of adenylate cyclase, acting as aglobal regulator of intracellular cyclic adenosine monophosphate (cAMP) levels. My hypothesis is that AA could be a signaling molecule during embryogenesis and adult cell differentiation?