University of Texas Health Science Center Neuro – degenerative disorders like Parkinson’s and Alzheimer’s diseases as well as amyotrophic lateral sclerosis (ALS) may now be treated, thanks to the following discovery. In a major breakthrough, researchers from The University of Texas Health Science Center San Antonio discovered that neurons lacking the substance caspase-2 are better able to withstand pesticide-induced damage to energy centers called mitochondria. The research findings can seemingly open doors to potential therapeutic target that slow changes leading to neurodegenerative disorders.

Caspase-2 is known as a master switch that can cause cell death or survival depending on the amount of cellular damage. Neurons lacking this master switch probably reveal an increase in protective activities, including the appropriate breakdown of obsolete or used proteins. This process can be purportedly termed as autophagy which delays cell death. In the current research, experts analyzed neurons from young adult mice.

It was pointed out that the absence of caspase-2 neurons possibly raises autophagy to survive. Brian Herman, Ph.D., vice president for research and professor of cellular and structural biology at the Health Science Center, senior researcher and colleagues believe that mitochondrial dysfunction is a key to neuronal death in aliments such as Parkinson’s disease, Alzheimer’s disease, ALS and Huntington’s disease. Detecting initiators in the cell death process appears important for ascertaining therapeutic approaches and offering the maximum protection of neurons during neurodegenerative conditions.

The research was published in the March 11 issue of the Journal of Biological Chemistry.