Brain cell Alzheimers Breakthrough


A Stanford University team in America have just recently made a new discovery that could potentially unlock the secret to a cure for Alzheimer’s disease, which as western governments are well aware is becoming more prevalent as populations age. The research team involved made the breakthrough discovery.

Their conclusions suggest that when a class of brain cells known as microglia cease to function the result is the development of Alzheimer’s. The reasons this is so important is the simple fact of brain matter being made up of around 10- 15% of these cells.

As this significant brain percentage is that responsible for a two-fold combination of important jobs. Microglia act both as policemen and garbage disposal agents, seeking out and eradicating anything that might potentially harm brain tissue.

Whether this be bacteria or viruses these busy brain cells help tp preserve memory and a generally healthy brain. They are even known to search out and destroy those so-called A-Beta gummy protein deposits that medical professionals believe are one of the causes of Alzheimer’s.

The Stanford University team was led by professor of neurology and neurological sciences Dr. Katrin Andreasson. She is also  senior author of the study and commented that the research had concluded that what might be the root cause of the development of the condition is one tiny molecule.

On occasion this chemical, which makes up the protein EP2 goes wrong. Since this protein lives on microglia any misbehaviour by it triggers a cascade of misfiring signals that instruct the microglia to no longer attack A-Beta. This of course leads inevitably to plaque forming within the brain and setting off the chain-reaction that leads to Alzheimer’s disease..

She commented that in any healthy brain microglia are instrumental in constantly eradicating A-beta and ensuring that no instances of inflammation  occur. This is a vitally important aspect of brain physiology and the moment these vitally important cells lose function the cascading effect on brain construction can be devastating.

When the dreaded A-beta builds up in the brain this can also induce toxic inflammation but the simple action of blocking the effects of those EP2 molecules in the brains of mice actually reversed their Alzheimer’s. Though this research is still in the very early stages the initial results seem very promising indeed.

On going through all available information the team concluded that drugs like aspirin – if begun to be taken regularly well in advance of any symptoms showing – could possibly help keep the disease at bay. They stressed hoever that no drugs would be effective once memory loss had begun.  

NSAIDS – non-steroidal anti-inflammatory drugs – all carried health risks when used in the long-term but the team hope that a targeted drug aimed at blocking those malfunctioning EP2 molecules might possibly reverse memory loss and allow the sufferer a much better quality of life. With more people all the time being affected by this dread condition it is to be hoped that the treatment becomes generally available sooner rather than later.

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