Imagine: Stopping Cell Death – Impact on Medicine

Posted by on Oct 11, 2011 in Blog | 0 comments

Imagine: Stopping Cell Death – Impact on Medicine

Overview

Accelerated cell death or ‘apoptosis’ contributes to about half of all major medical illnesses for which adequate therapy or prevention is currently lacking. This has created an important opportunity for medical science and is creating an emerging multi-billion dollar market. Against this background of a rapidly emerging new market, a number of companies are developing several new drug classes which directly addresses apoptosis either by slowing down the process of cell death (eg. heart attacks, strokes, brain trauma, etc.) or instead, accelerating the rate of cell death where needed (eg. shrinking tumours).

R & D Pipeline

Cell death is a major concern for organs where the vital cells cannot regenerate. These include the heart, the nervous system including the brain and spinal cord.

A variety of technology platforms are being used to develop new approaches for the treatment of a large number of conditions that are caused by accelerated cell death including:

  • death of brain cells from traumatic bran injury, stroke and other brain diseases associated with memory loss.
  • heart attacks (or myocardial infarctions), one of the underlying problems of heart failure.
  • neuro-degenerative processes of the spinal cord including injury or trauma caused by accidents in automobiles, military conflict/war, civilian work life, etc.

If you would like to read more about cell death and the great potential for being able to solve this riddle for the benefit of mankind, please see the abstract (below) written by Dr. Simon Rabkin, a leading pioneers in apoptosis research. Please contact me if you would like any additional information regarding this exciting field of research.

About the author

Myron Pyzyk is the Principal Consultant and CEO of Marenon Consulting. He has over 20 years of experience in the pharmaceutical, nutraceutical & biotech industries. Mr. Pyzyk holds a B.Sc in psychology from the University of Alberta (Edmonton, Canada) and a graduate degree (M.S.) in clinical nutrition from the University of Bridgeport, Connecticut.

Scholarly Research Exchange  Volume 2009 • Article ID 979318 • doi:10.3814/2009/979318

Review Article

Apoptosis in Human AcuteMyocardial Infarction:
The Rationale for Clinical Trials of Apoptosis Inhibition in AcuteMyocardial Infarction

SimonW. Rabkin
Division of Cardiology, Department of Medicine, University of British Columbia, Vancouver, BC,
Canada V5Z 1M9
Correspondence should be addressed to SimonW. Rabkin, rabkin@interchange.ubc.ca
Received 16 October 2008; Revised 21 December 2008; Accepted 20 January 2009

The objective of the present review was to examine apoptosis in patients with acute myocardial infarction (MI) and to address (i) the prevalence of apoptosis in acute MI, (ii) techniques to determine apoptosis, (iii) time period from the onset of acute MI to the detection of apoptosis, (iv) criticisms about apoptosis in acute MI. A systematic literature search identified over 20 publications comprising over 400 patients. The prevalence of apoptosis varied from over 90% in nuclear imaging studies using annexin binding to 0.25% in an autopsy study using monoclonal antibody to single-stranded DNA. Apoptosis was present in 50–60% of infracted hearts within 24 hours of MI (detected by Bax and activated caspase-3), 26% of myocytes in patients who died within 11 days of MI (pooled mean from 5 studies using only TUNEL staining), and 12% of the myocytes of patients who died, on average, 20 days after onset of MI (pooled mean from eight studies using dual staining with caspase-3 plus TUNEL). Criticisms of the TUNEL assay appear unjustified as TUNEL is at least 85% specific using caspase-3 activation as a marker of apoptosis. Taken together, DNA fragmentation on agarose gel electrophoresis, TUNEL staining of nuclei, caspase-3 activation, bcl-2 and Bax expression, and annexin V binding overwhelming support apoptotic cell death as an important component of MI. The amount of cardiac apoptosis correlates with the presence of heart failure and fatal arrhythmias. Heart failure as a complication of MI carries a high mortality and indicates the amount of myocardium lost during the infarct. Taken together, these findings suggest the need for clinical trials in acute MI to confirm whether inhibition of apoptosis can reduce patient morbidity and mortality.



 

 

 

 

 

 

 

 

 

 

 

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