The Path to Cell Destruction

This week my classmates and I dissected an article pertaining to the MAPK signaling cascade and its role in neurodegenerative diseases. Diseases such as Parkinson’s, Alzheimer’s and Lou Gehrig’s disease (also known as ALS) are characterized by progressive motor cell death impairing motor function. We always ask ourselves what the underlying cause of such ailments are, and thanks to the evolution of research in neuroscience such causes can be illuminated and eventually comprehended.
Inside of a cell there is a nucleus and it is composed of proteins that encode specific functions for the cell. The MAPK pathway is a series of chemical messengers that are activated by stimuli outside of the cell. This pathway is important for carrying out essential function such as making new/different cells and the act of executing certain cells. The MAPK pathway has many branches that activate other pathways on other organelles in the body such as the mitochondria and endoplasmic reticulum. These organelles are important for energy and making other proteins essential to the body. When mutations in the MAPK pathway occur, activity happening downstream causes a multitude of problems. Mutations in certain enzymes and proteins in the cell causes cellular function to alter and affect the functions of other organelles. The presence of free radicals cause stress on cells and the changes ensue. Constant stressing of cells and the changes that are caused by them cause components of the MAPK pathway to take a route towards cell death.
So how is the MAPK pathway associated with Parkinson, Alzheimer’s and ALS? The direct cause is not completely clear yet, but there are a lot of indications and research that supports that the MAPK pathway plays a role in these neurodegenerative diseases. In ALS, a mutation in the SOD1 gene causes oxidative stress to neurons. This mutation in the SOD1 gene makes it so a neuron cell called an astrocyte unable to clear away an area of highly concentrated neurotoxins. The high concentration of neurotoxicity causes the cell to undergo a programmed cell death. Similar activity is seen in Parkinson’s and Alzheimer’s where neurons undergo programmed cell death. The problem with these diseases is that motor function is being compromised because of neurotoxicity. Aging shows strong correlation with the onset of these diseases but are being seen as early as 20-30 year old individuals. The Concordia Cobbers are using neuroscience in collaboration with neurochemistry to study such topics so that one day we will be the pioneers of present and new research.

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