Oxidative stress turns a protein that normally protects healthy cells into their executioner, according to a study released today in the Proceedings of the National Academy of Sciences journal.
Researchers from Brigham and Women’s Hospital (BWH) are the first to discover that changes in monocytes (a type of white blood cell) are a biomarker for amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. This finding also brings the medical community a step closer toward a new treatment for the debilitating neurological disease that affects approximately 30,000 Americans.
Two studies published in a recent issue of Cell Medicine [2(2)] report on the therapeutic efficacy of stem cell transplantation in animal models of amyotrophic lateral sclerosis (ALS) and spinal cord injury (SCI). Cell Medicine is freely available on-line at http://www.ingentaconnect.com/content/cog/cm.
Repeated, low-dose injections of mononuclear cells derived from human umbilical cord blood (MNC hUCB, tradename: U-CORD-CELLÂ™) have been found effective in protecting motor neuron cells, delaying disease progression and increasing lifespan for mice modeling amyotrophic lateral sclerosis, or ALS, also referred to as Lou Gehrig’s disease, report University of South Florida researchers and colleagues from Saneron CCEL Therapeutics, Inc., and the Ribeirao Preto School of Medicine at the University of Sao Paulo, Brazil.
A team of researchers grafting human spinal stem cells into rats modeled with amyotrophic lateral sclerosis (ALS), also known as “Lou Gehrig’s Disease,” a degenerative, lethal, neuromuscular disease, have tested four different immunosuppressive protocols aimed at determining which regimen improved long-term therapeutic effects. Their study demonstrated that a combined, systematically delivered immunosuppression regimen of two drugs significantly improved the survival of the human spinal stem cells. Their results are published in the current issue of Cell Transplantation (20:8), now freely available on-line at http://www.ingentaconnect.com/content/cog/ct/.
Following a major Northwestern Medicine breakthrough that identified a common converging point for all forms of amyotrophic lateral sclerosis (ALS and Lou Gehrig’s disease), a new finding from the same scientists further broadens the understanding of why cells in the brain and spinal cord degenerate in the fatal disease.
Treatment with dexpramipexole Â– a novel drug believed to prevent dysfunction of mitochondria, the subcellular structures that provide most of a cell’s energy Â– appears to slow symptom progression in the neurodegenerative disease amyotrophic lateral sclerosis (ALS). Promising results of a phase 2 trial of dexpramipexole are receiving advance online publication in Nature Medicine. Some preliminary results of the study were presented at the 2009 International Symposium on ALS/MND and the 2010 American Academy of Neurology annual meeting.
Frontotemporal dementia and amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease — two fatal neurodegenerative disease with distinct symptoms — are triggered by a common mutation in many cases, according to researchers who say they have identified the mutated gene.
The ability to produce neuroprotectors, proteins that protect the human brain against neurodegenerative disorders such as Parkinson’s and ALS, is the holy grail of brain research. A technology developed at Tel Aviv University does just that, and it’s now out of the lab and in hospitals to begin clinical trials with patients suffering from amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease.
Recently published studies by a researcher in the Faculty of Medicine & Dentistry demonstrate that ALS Â– known as Lou Gehrig’s disease Â– damages neurons in parts of the brain responsible for cognition and behaviour.