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:
Pictures:
http://www.puhuahospital.com/images/ckeditor/images/image001.jpg
https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=&url=https%3A%2F%2Fwww.uab.edu%2Fnews%2Flatest%2Fitem%2F2689-uab-studies-find-deep-brain-stimulation-changes-rhythms-to-treat-parkinsons-disease-and-tremor&psig=AFQjCNEWY8NlyXPJa8oT3d1a-zH9igQ55g&ust=1476995860403678
It is true that this disease is really necessary to get proper treatment but there are some people or professionals who are really working hard to prevent and cure this disease. I know an amazing parkinson's disease treatment and it is really effective.
ReplyDelete