How to Avoid Amyotrophic Lateral Sclerosis

How to Avoid Amyotrophic Lateral Sclerosis

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Description

Each living cell requires energy in form of ATP for most of its processes. This energy is provided within a cell in a compartment that is termed mitochondrion. Within mitochondria, action of the mitochondrial respiratory chain generates the energy using electrons and oxygen. However and because the mitochondrial respiratory chain is so powerful, a side product of ATP is harmful ROS. During physical exercise energy demand increases, which is covered by a raised activity of the mitochondrial respiratory chain. But consequently, the risk of cellular damage inflicted by ROS also increases. To avoid damage done to cellular components, healthy individuals hold capable defense systems against ROS, notably enzymes of the GST, SOD and UCP classes. Of these, the UCP system is particularly noteworthy because of its capability to operate before ROS is generated. This UCP function is achieved by a reduction of the proton gradient across the inner mitochondrial membrane. However, because the proton gradient is coupled to ATP generation, a reduction of this gradient consequently diminishes energy production. This means that a cell has to deliberate whether ROS should be prevented at the cost of its cellular energy levels. But what happens if UCP activity is induced by external events or by exposure to specific substances that evoke a permanent energy deficit? In this book the physiological consequences of enhanced UCP activity are explained and as a result, can be connected to the origin of the neurodegenerative disease amyotrophic lateral sclerosis. Thus, potential treatment opportunities are provided that are missing so far. Further in this context, known risk factors for the initiation of ALS are discussed.show more

Product details

  • Paperback | 62 pages
  • 128.52 x 198.37 x 3.56mm | 117.93g
  • Createspace
  • United States
  • English
  • black & white illustrations
  • 1507735723
  • 9781507735725

About Dr Michael Hoffmann

Dr. Michael Hoffmann was born in 1973 in Dusseldorf, the capital city of North-Rhine-Westphalia in Germany. He studied biology and finished his Doctoral Thesis in 2004 at the Institute of Genetics, Heinrich-Heine University, Dusseldorf. For one year he taught students of medicine and pharmacy in biochemistry at the Friedrich-Wilhelms-University in Bonn. After another year as postdoc in the department of general pediatrics, he started his own projects on mitochondrial function and aging until 2013. He founded the Institute fur Wissenschaftliche Medizin in 2014 and is currently working on the theory for initiation of Amyotrophic Lateral Sclerosis (ALS). Dr. Michael Hoffmann is an expert in molecular biology, genetics, developmental biology and mitochondrial function. Selected Publications Hoffmann M, Bellance N, Rossignol R, Koopman W, Willems P, Mayatepek E, Bossinger O, Distelmaier F. C. elegans ATAD-3 Is Essential for Mitochondrial Activity and Development. PLoS One (2009). PMID: 19888333 Hoffmann M, Segbert C, Helbig, G, Bossinger O. Intestinal tube formation in Caenorhabditis elegans requires vang-1 and egl-15 signaling. Dev. Biol. (2010). PMID: 2000418 Hoffmann M, Honnen S, Mayatepek E, Watjen W, Bossinger O, Distelmaier F. MICS-1 interacts with mitochondrial ATAD-3 and modulates lifespan in C. elegans. Exp. Geront. (2012). PMID: 22245785 Hoffmann M. Enhanced Uncoupling of the Mitochondrial Respiratory Chain as a Potential Source for Amyotrophic Lateral Sclerosis. Front. Neurol. (2013). doi: 10.3389/fneur.2013.00086 Hoffmann M. Vicious Circle of Metaboreflex Dysregulation in Amyotrophic Lateral Sclerosis. AASCIT communications (2014)."show more