A Proactive Future on Parkinson's Disease

Neurodegenerative disorders such as Alzheimer’s or Parkinson’s disease are characterized by their inability to sustain active neural connections within the brain and the subsequent degeneration of these connections. Researchers are currently looking for specific reasons on the occurrence of these disorders, and some have made breakthroughs in possible causes. One such researcher, Ben Yang, came to Loyola University Chicago to talk us about neural degeneration as a response to calcium and cellular aging. His research focused on L-type Ca+ channels and their engagement in increasing sensitivity of the substantia nigra dopaminergic (SNc DA) neurons to mitochondrial toxins. This increased sensitivity is what allows the mitochondria to insufficiently perform in the electron transport chain, causing a cascade event that ultimately leads to reactive oxygen species (ROS) and free radicals interfering with oxidative processes and causing genetic mutations in neural DNA. Although researchers do know about the effects of poor mitochondrial processes on neural damage, there is still much to be discovered on other effects it may have or possibly other reasons that may contribute to neural degeneration as well.

            Just as Ben Yang researched on the possible connection of oxidative stress and its effect on calcium and subsequent effect on the SNc DA neurons, other researchers are beginning to focus more on the proactive side of Parkinson’s disorder. They are examining the effects of certain treatments in either improving Parkinson’s disease by removing these degenerated neurons or even considering ways in which the damage can be caught ahead of time before the disease can progress. One such study at the Salk Institute is examining how to remove dying neurons using immune cells in the brain that have certain receptors, TAM receptors, that usually allow microglia (a type of macrophage in the CNS) to consume dead neurons. They conducted a study on two specific TAM receptors, Axl and Mer, and noticed that in the absence of such receptors, there was a clustering of dead cells in certain areas, but more interestingly, there was an increase in newly formed neurons in the olfactory bulb. This led them to believe that not only do Axl and Mer consume dead neurons, but also consume living, but otherwise compromised, cells. They concluded that a fraction of these cells being consumed by Axl and Mer are actually living cells being cleared due to their inadequate functionality, and this process may be causing too many neurons to be eaten. In the future, these researchers hope to control these TAM receptors to target only a certain amount of degenerative neurons in diseases like Parkison’s, to ultimately improve their quality of life and possibly combat these illnesses altogether.

                                                                                                                                          

Sources:

https://www.ncbi.nlm.nih.gov/pubmed/22735187

https://www.sciencedaily.com/releases/2016/04/160406133626.htm

http://www.vilalab.org/en/research/mitochondrial.php

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917467/

Pictures:

http://www.puhuahospital.com/images/ckeditor/images/image001.jpg

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