Professor Syed E A Haq MB BS BSc (HON) PhD DIC MRCP(UK)

Professor Syed Haq, is a Consultant Physician and Founder of The London Preventative Medicine Centre. He is the Clinical and Scientific Director of Daval International Ltd., a biopharmaceutical company developing a platform for the treatment of autoimmune (e.g., Systemic Sclerosis), neurodegenerative (e.g., Motor neuron disease, Alzheimer’s disease, Myasthenia Gravis, Multiple Sclerosis) and inflammatory (e.g., Rheumatoid arthritis) diseases using a patented polyclonal antibody/peptide composite which has recently completed two phase II clinical trials in the UK. He has worked and trained at some of the foremost institutions - Guy’s Hospital, Hammersmith and Royal Brompton Hospitals, Imperial College, Massachusetts General Hospital, Harvard Medical School, and Tufts University, New England Medical Center Hospitals Inc.

Prof. Haq has published peer-reviewed articles in several internationally renowned scientific journals including PNAS and Nature Medicine. He has been co-chairman of the Anti-ageing Conference London (2008-11), and has been an invited presenter/speaker at numerous international conferences (American Heart Association, American College of Cardiology, Anti-Ageing Medicine World Congress and the NCD National Workshop, India). Prof. Haq has received several national and international awards/fellowships from the Medical Research Council, Wellcome Trust International, American Heart Association, Astra Zeneca and the Heart Failure Society of America.

2009 - Anti Ageing medicine and molecular signalling

ß-Catenin is a transcriptional activator that regulates embryonic development as part of the Wnt/wingless pathway. The Wnt/wingless pathway plays a fundamental role in growth, ageing and cancer. ß-Catenin mediates canonical Wnt signalling by binding to and activating members of the T-cell factor (TCF) transcription factor family. The mechanisms leading to Wnt-induced stabilisation of ß-catenin has been an area of intense interest. ß-Catenin is stabilised in cells that have been exposed to growth factors and hypertrophic stimuli. The mechanism by which ß-catenin is stabilised is distinctly different from that utilised by the “traditional” Wnt signalling pathway. Although, as with Wnt signalling, inhibition of glycogen synthase kinase-3 (GSK-3) remains central, the mechanism by which this occurs involves the recruitment of activated Protein Kinase B (PKB) to the ß-catenin-degradation complex. This stabilisation occurs via a unique Wnt-independent mechanism and results in growth. Conversely, ß-catenin has been implicated as being a pivotal molecule in the defence against oxidative stress. The antagonism of Wnt signalling by several factors including oxidative stress acting via ß-catenin may be a crucial factor in elucidating the pathogenic mechanism of oxidative stress-induced ageing. This signalling cascade may be the gateway in providing greater understanding, and more specifically, ß-catenin may be the molecular switch that determines the balance between normal growth and the ageing process.