The story was all over the news yesterday – Northwestern University researchers have discovered a common cause of all forms of Lou Gehrig’s disease, also known as amyotrophic lateral sclerosis (ALS). These forms include hereditary, sporadic, and ALS that targets the brain. USA Today reported the researchers “found that the basis of ALS is a malfunctioning protein recycling system in the neurons of the brain and spinal cord. Efficient recycling of the protein building blocks in the neurons are critical for optimal functioning of the neurons. They become severely damaged when they can’t repair or maintain themselves.” The hope is that this research will lead to new avenues for treatments that would regulate this protein path so it can function normally.
So why am I sharing this with you in on an Alzheimer’s site? It’s because the researchers think these new findings may support the study of other neurodegenerative diseases, such as dementia and Alzheimer’s. It’s good to hear that these breakthroughs concerning one disease may lead to the advancement of researchers’ understanding into dementia. And there are other examples of this crossover between researchers.
For instance, the Alzheimer’s Reading Room reported this spring on a study by the University of Texas Health Science Center in San Antonio (UTHSC-SA). These researchers, led by Dr. Marisa Lopez-Cruzan of the center’s cellular and structural biology department, found that neurons in young adult mice that didn’t have a substance called caspase-2 were more able to withstand pesticide-induced damage to the mitochondria, which is considered a cell’s power producer. Alzheimer’s Reading Room reported, “Caspace-2 appears to be a master switch that can trigger either cell death or survival depending on the amount of cellular damage, the team found. Neurons that lacked caspace-2 showed an increase in protective activities, including the efficient breakdown of obsolete or used proteins. This process, called autophagy, delays cell death.” The researchers believe that this evidence indicates that mitochondrial dysfunction has an important role in the death of neurons in diseases such as Alzheimer’s, ALS, Parkinson’s disease and Huntington’s disease.
And in January 2011, the Alzheimer’s Drug Discover Foundation (ADDF) awarded a grant of $195,000 to ALS Biopharma, LLC to develop therapeutics designed to clear toxic proteins that have been implicated in Alzheimer’s disease. ALS Biopharma had developed an earlier program that created small-molecule brain-penetrant inducers of heat shock protein (Hsp 70) to clear insoluble protein deposits that are found in ALS cases. The ADDF grant would support the identification and development of these inducers in order to clear two proteins – the toxic form of tau protein and beta-amyloid – that are believed to be involved in Alzheimer’s. “Small molecule therapeutics targeting Hsp70 would result in a disease-modifying therapy for Alzheimer's disease and could also be employed in related neurodegenerative diseases, such as ALS, Parkinson's and Huntington's,” said Dr. Howard Fillit, ADDF’s executive director.
Now none of this is a done deal, obviously. But it really gives me hope that scientists who are working in the trenches in the on-going battles against ALS, Alzheimer’s, Parkinson’s, Huntington’s, and other similar neurodegenerative diseases can learn from each other. And by working together they can develop potential therapies and cures that will make a difference for all of those people who suffer from these terrible diseases.
Published On: August 23, 2011