10/21/2022
New Alzheimer Study Reveals Potential Good News for Patients
By
Tiar'a Literary & Illustrations
tiarapublications@gmail.com
In a recent study a potential revolutionary discovery was made that may have positive effects on those suffering from Alzheimer's disease and MS (multiple sclerosis).
Statistically, 1 in 9 American's over the age of 65 have, or will be diagnosed with a form of cognitive degeneration at some time during their lives. The reason for this, in layman terms, has to do with neurological pathways in the human brain becoming clogged by Amyloid Plaque overtime, thus impairing the electrical currents that run through the brain passing from point A to point B. Therefore, the theory posed is that if we had a way to "unclog" the Amyloid Plaque buildup from the brain's neurological pathways, that cognitive function will improve, and perhaps any form of cognitive degeneration could be reversed entirely.
According to a recent announcement published by [Medical News Today] the above theory has been proven in preliminary studies conducted on mice.
The study, which appears in the medical journal [Cell] suggests that boosting a molecule called, Spleen Tyrosine Kinase (SYK), could be an effective treatment for clearing the brain's neurological pathways (the Amyloid Plaque) which leads to the formation of Alzheimer’s and other neurodegenerative disorders.
What is Spleen Tyrosine Kinase (SYK)
SYK is formed from a fusion gene when pieces of chromosomes 9 and 22 break off and trade places. The ABL gene from chromosome 9 joins to the BCR gene on chromosome 22, to form the BCR-ABL fusion gene. Tyrosine kinase activity is crucial for the transformation of BCR-ABL.
Did you know that the human brain has cells within it capable of cleaning itself? Well, if you didn't, you do now.
Microglia are immune cells located within our central nervous system. Although the role of Microglia is not entirely clear (at present), it has been suggested through research that, as well as coordinating the neuro-inflammatory response to tissue damage, Microglia may additionally share a role in maintaining cognitive processes in the human brain.
Past studies into the role of Microglia, and Alzheimer’s disease, have been unable to identify whether the Microglia plays a beneficial, or detrimental role. This is the conundrum that requires continual research. Some, however, have discovered that Microglia acted differently depending on the stage of the Alzheimer’s disease, stating that Microglia could “Either assist with the clearance of age-related Amyloid Plaque accumulation, or Microglia can promote extensive inflammation in reaction to Amyloid or Tau, eventually causing widespread neuro-degeneration.”
Think of the Microglia as the Betta fish that cleans your fish tank. They do a great job, right? Well, what if the Betta fish did a great job cleaning, but then spat everything it just cleaned back out? The fish tank would be no better than it was before the Betta fish cleaned it. Microglia is similar to the Betta fish, except Microglia are unpredictable. Therefore, until we are able to control the Microglia from expelling what it has cleaned, we cannot be certain that its cleaning will have a lasting or positive effect. Now, if we were able to entice the Microglia to remove the Amyloid Plaque - as in the case of Alzeimer's disease - and then remove the Microglia that removed the debris from the neurological pathways that caused the disruption to begin with, these cognitive impairments would be an issue of the past. But we're not there yet.
The new study has found that, when activated, Microglia does clear away the Amyloid Plaques that impede nerve impulses and lead to symptoms such as: memory loss, confusion, language problems, and impulsive behavior.
The study was conducted using mice that had been genetically-engineered to develop Amyloid Plaques.
Using this model of Alzheimer’s disease, the researchers identified the molecule, Spleen Tyrosine Kinase (SYK), that activated the Microglia to remove the Amyloid deposits.
In mice that lacked SYK, Amyloid Plaques built up and the mice experienced memory loss. By activating SYK, the researchers triggered the Microglia to clear the Amyloid Plaques.
Results seen in mice are not always replicated in humans, as Dr. Majewska told [Medical News Today]: “Mouse models, especially for Alzheimer’s disease, cannot be easily extrapolated to humans. The authors do some comparisons to what is found in human [Alzheimer’s disease] brains but this is probably the biggest unknown and the most important future direction [for research].”
The researchers saw similar results in a mouse model of (MS) multiple sclerosis. Human nerve cells are covered by a myelin sheath that speeds up nerve impulses. In MS, the immune system damages the myelin sheath, creating lesions or plaques that build up. The accumulation of damaged myelin slows down the transmission of nerve impulses.
The researchers found that in mice without SYK, damaged myelin built up on nerve cells. They concluded that SYK was “critically involved” in removing myelin debris.
The authors of the study suggest that targeting SYK to stimulate the brain’s immune activity might offer a way to treat not only Alzheimer’s and MS, but also other neurodegenerative diseases.
They stress that further research is needed: “although our early studies suggest the SYK is a major regulator of neuroprotective Microglial responses in models of [Alzheimer’s] and MS, future studies are needed to better characterize both the upstream and downstream players that coordinate the effects of SYK on neurodegenerative disease progression.”
Dr. Griffin agreed: “While these studies add to our understanding of how immune cells in the brain can contribute to neurodegenerative disease, more research is needed before this can be applied in people. For one, SYK is expressed in several different cells in the body so we would have to think about how we specifically target the immune cells in the brain. This research suggests an avenue to boost the beneficial functions of microglia in two different neurodegenerative diseases which could be very impactful. I suspect in the end a complex disease will need a complex treatment, but this could certainly be one of the prongs of the approach if it translated to the human condition".
In summary: We have yet to discover a way to prevent or reverse Alzheimer's or other neurological impairments. However, the above research has revealed to us a link in the pathology of Alzheimer’s disease. In this case, it may be the human brain’s immune system that could act as the nucleus for potential treatments. Only time and more research will tell.
