The Brain’s Immune System May Combat Alzheimer’s

A new study from the Stanford University School of Medicine concluded that Alzheimer’s disease may be prevented and symptoms may even be reversed by boosting and protecting a single cell in the brain called microglia.

The Brain's Immune System May Combat Alzheimer's

Learn more about this groundbreaking study and what it means for the future of Alzheimer’s treatment methods.

Protecting Microglia to Prevent and Reverse Alzheimer’s

Researchers from the Stanford University School of Medicine recently published a groundbreaking study that suggests Alzheimer’s can be prevented by boosting the brain’s immune system.

The study, published in the December 8, 2014 issue of The Journal of Clinical Investigation, evaluated the effects of boosting brain immunity and successfully prevented and reversed Alzheimer’s in mice.

The study focused on nerve cells called microglia, which function as garbage disposals, clearing dangerous viruses, deposits and bacteria from the brain. Dr. Katrin Andeasson, professor of neurology and neurological sciences at Stanford University School of Medicine described these nerve cells as “beat cops.”

“Microglia are the brain’s beat cops. Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”

Microglia composes 10-15% of cells in the brain and when they find anything that does not belong, they release a substance that brings other microglia to fight and destroy the foreign invader. Microglia also rids the brain of dead cells and control inflammation, constantly clearing amyloid-beta, a hallmark of Alzheimer’s.

As people age, a protein called EP2 stops the microglia from operating as efficiently as they once did. Using young mice, researchers observed that those who were genetically engineered to not have an EP2 protein did not develop Alzheimer’s, even after being injected with amyloid-beta. This would suggest that the microglia was able to rid the brain of the amyloid-beta protein on its own. For the mice who did develop Alzheimer’s, memory decline was reversed by blocking EP2.

Encouraging Results for the Future of Alzheimer’s Disease

While many are touting this finding as a “cure” for Alzheimer’s, it is important to note that there is currently no cure for the disease, and it is estimated that Alzheimer’s will reach epidemic proportions by 2050.

This groundbreaking study does provide a glimmer of hope for an effective treatment method, but much more research needs to be done before a cure is found.

The Stanford University School of Medicine hopes to next produce a compound which blocks only EP2, which would prevent unwanted and unnecessary side effects.

How do you feel about the possibility of the brain’s immune system combating Alzheimer’s? Do you think that this discovery could lead to a potential cure of the disease? Share your thoughts with us in the comments below.

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Please leave your thoughts and comments

  • Could this help other dementia such as Picks?

    • slutmonkey

      The discoveries in this paper are specific to Alzheimer’s and would not work for Pick’s since that is caused by a different protein.

      However–and I’m speculating wildly here–there may some overlap in general mechanism or a way in which this research inspires ideas about how to solve Pick’s since it’s also a problem of protein buildup. The only way to be certain would be to study Pick’s more.

  • ereilad

    Wonderful discovery but will the government ever allow such a product to be tested and marketed, even if some company is willing to manufacture the cure?

  • SSimpson

    There’s no doubt this is exciting, groundbreaking news that elicits hope in many people. One obvious, unanswered question that springs to mind is, “Why is EP2 all of a sudden a problem now at this time in history?” After all, the first Alzheimer’s patient was discovered in 1906. The Stanford researchers might have us believe EP2 became a problem shortly before this, thereby triggering the first Alzheimer’s patient. So what environmental or lifestyle changes caused this dramatic shift in EP2 production in the human body? And, what can we do to prevent or curtail EP2 production in our bodies? Answering these questions would provide a more holistic approach for those of us who prefer to prevent the disease in the first place, rather than taking drugs that may cure the disease but have their own deleterious effects.

    • Promises, promises. People live long enuf now to get Alzheimer’s.

    • slutmonkey

      First, 1906 is when the disease was first identified as its own thing rather than the patient just being called “crazy old person”. It’s almost certain that the condition existed before that. As such there is no evidence for a “dramatic shif in EP2 production” over time.

      Secondly EP2, when produced in the right quantities likely has some beneficial functions as well. Pretty much all proteins have some useful function since those that don’t face evolutionary pressure against their existence. Whatever that function is will determine the feasibility and side effects of any EP2 targeting therapies.

      Lastly as Dale pointed out, Alzheimer’s is strongly correlated with age, and the average life span was drastically shorter before the 20th century, to the point that even early AD symptoms would not have been seen before most people died of other causes.

    • Tricia2014

      S Simpson I would like to know the answer to that question as well. I’m much more likely to make the lifestyle changed as needed rather than popping a pill!!!

    • Wanda Samuelson

      The problem is processed sugar–any processed sugar. It may be the key to EP2 production. We are wired to chase sugar, the fastest energy substance to guarantee survival. Processed Sugar is plenteous now, where simple sugars were more of a seasonal commodity centuries ago. Alzheimer’s is also called Type III diabetes because there is a direct relationship to metabolic dysfunction (metabolic syndrome) and Alzheimer’s. High-fructose corn syrup is probably the biggest culprit and its consumption matches the rise of Alzheimer’s. Dr. Robert Lusing, MD, a pediatric endocrinologist at the UCSF Benioff Children’s Hospital, points out that glucose is processed in the liver, but HFCS in processed in the liver and the brain. It can be shown through MRI that ingested HFCS affects blood flow differently
      than glucose in the brain regions associated with feeding behavior,
      including the hippocampus and the striatum. This process tricks the brain–deceives it–into thinking that we are not yet full because it reaches the blood faster than simple sugars. This prevents you from triggering the body’s signals (insulin and leptin) for being full and may lead to over-consumption of total calories. Another problem with HFCS and processed sugar is their ability to punch holes in the gut, allowing “poisons” to directly enter the blood stream. Processed sugar is bad in the quanitites we consume them. The solution is to eat less and eliminate HFCS and severely reduce processed sugar, but good luck with that, because the addictive qualities of processed sugar exceed cocaine.

  • Nic

    Great news. Of course they won’t come out with a “cure” they will find some reason for only a treatment in which you will take pills for the rest of your life. At an “affordable” price I am sure.

  • NR

    Instead of working on blocking EP2 wouldn’t it be better to work on how to stop EP2 production in the body?

    • Wanda Samuelson

      Eat less, eliminate HFCS and severely reduce processed sugar. Good luck with that because their addictive qualities exceed cocaine. It has to be treated like addiction, because it is a chemically induced addiction.

      • caitlinburm

        Thank you for sharing, Wanda.

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