Harvard Researchers Make Another Key Discovery

Throughout April and May 2017, Harvard researchers have been tackling a range of issues that influence aging. For example, ‘To age better, eat better’ — or ‘the balance in healthy aging.’

The most recent of this series, ‘probe of Alzheimer’s follows paths of infection’ — addresses one of the most problematic concerns surrounding the aging process. What they found, was both interesting and surprising, making researchers rethink the role of amyloid beta — a protein that makes up one of the hallmark signs of Alzheimer’s.

The Role of Amyloid Beta and the Development of Alzheimer’s

For years, research has focused on the protein known as amyloid beta, as it plays a critical role regarding the plaques found in the brains of Alzheimer’s patients. Although this connection is accurate, researchers are beginning to see this protein in a whole new light.

First discovered several years ago, Harvard researchers found key similarities between protein that is active in our immune system, and amyloid beta — which is believed to be a critical component during the progression of Alzheimer’s. Since then, this area of interest has continued to be investigated.

Led by a highly credible team, including, but not limited to, Robert Moir and Rudolph Tanzi, their most recent work has focused on whether or not the amyloid beta plaques are a possible response to infection. What this means, is that if proven to be correct, this could help address some of the unknowns regarding the cause of Alzheimer’s.

More specifically, if researchers were to better understand the role that amyloid beta plays within the body and brain, it’s possible that new treatment methods could be developed in order to treat the infection before plaques have an opportunity to form. This new research brings with it some new questions, such as:

  • Could Alzheimer’s be categorized alongside other autoimmune diseases, such as diabetes, where the immune system eventually turns on the body?
  • Does this contribute to the possibility that Alzheimer’s is, in fact, a form of type 3 diabetes?
  • Is amyloid beta just metabolic garbage, or is it a clue to something much greater?

Today, most researchers agree that Alzheimer’s progresses based on this protein forming in the brain, leading to damage. Of course, it’s not this ‘black and white’ — but at the basis of it all:

  • Amyloid beta begins to collect in the brain, forming what we know as plaques.
  • These plaques then lead to the development of tangles. These are made up of another protein known as tau, which collect within nerve cells.
  • Inflammation results, as the body’s natural immune system responds.
  • Connections between nerve cells die, resulting in cognitive decline.

Could Alzheimer’s Be Caused By An Infection?

Okay, so this is when things begin to get interesting.

Based on the recent work of the researchers discussed above, Alzheimer’s is beginning to relate back to a possible infection. Although you may be raising an eyebrow, this theory isn’t new. In the 70s and 80s, scientists believed that the strongest hypothesis was, in fact, that Alzheimer’s was in some way linked and even potentially caused by infection.

By 1984, amyloid beta was discovered — which altered the path of ongoing research. This initial theory was known as the pathogen hypothesis, and is now coming full circle once again.

Currently, Moir and Tanzi’s model offers a brand new perspective. They have filled in some of the gaps, connecting amyloid beta, tau, inflammation, and possible pathogens. As stated by Moir, “there is circumstantial evidence regarding the importance of amyloid beta.”

Unbelievably, if accurate, this protein may have developed 400 million years ago. Today, it is not only found within humans, but is also present in up to 60 percent of vertebrates. When looking more closely at amyloid beta, Moir noticed key similarities between key infection-fighting proteins that are found within our immune system.

After making this connection, they realized that the protein associated with Alzheimer’s, is very similar to antimicrobial peptides. These peptides are innate within our body, and without them, we would likely die from infection before reaching our 2nd birthday.

Could amyloid beta — this ‘terrible’ Alzheimer’s-associated protein actually offer antimicrobial properties?

Well, according to Moir — yes. In fact, in some cases, it offered infection-fighting abilities that were comparable to penicillin. This theory has been unraveling over the past few years, with a key finding, published last year in Science Translational Medicine. What they found was:

  • Amyloid beta protected nematode worms, lab mice, and cell cultures from human neuronal tissue against both bacterial and fungal infections.
  • Also, when mice were infected with salmonella, plaques developed 48 hours later. Those mice than lived longer than mice who did not develop any plaques.

So, what does it all mean?

Well, it appears that based on their recent work, Alzheimer’s may be caused by both genetic and infectious causes. The initial process begins with amyloid beta plaques in the brain. If caused by an infection, the direct link or culprit could be a single microbe, bacterium, fungal spore, or a virus.

In terms of genetics, a higher proportion of ‘extra-long’ amyloid beta proteins may be to blame. Researchers have discovered that there are two predominant forms of amyloid beta. One has a chain of 40 amino acids (which appears to be a beneficial solution within the body), and the other has a chain of 42 amino acids — which is predominantly the form that is seen within plaques.

Whether plaques begin to form based on these extra-long amino acid chains or an infection, the development of tau protein was described by Tanzi as being, “a bush fire.” Inflammation then fuels this potentially damaging flame, leading to damage and possible cognitive decline.

Meaning, although the cause may be based on genetics and/or an infection, the real issue here is inflammation. Researchers are now looking to the blood-brain barrier, hoping to uncover what is and what isn’t in the brain of Alzheimer’s patients. At this point, that is the next logical step.

This new research may be a sign that the human microbiome is simply out-of-whack — and if microbial factors are identified, it’s possible that specific infections could be treated early on in life — long before the initial plaques begin to form.

Each and every day new research is being uncovered, bringing us closer and closer. It’s important to stay on-top of the latest research, and at this point, simply take care of yourself. Continue to check-into our blog, as we will be covering the latest, and most significant research unraveling within the scientific community.

Further recommended reading: Your Gut Could Influence Your Risk of Alzheimer’s

Krista Hillis has a B.A.Sc degree, specializing in neuroscience and psychology. She is actively involved in the mental health and caregiving community, aiming to help others. Krista is also passionate about nutrition and the ways in which lifestyle choices affect and influence the human brain.

Comments (5)
  1. Joanne B.

    Good morning read for me, thank you! I am always trying to keep up with my knowledge on Alzheimer’s and your blog definitely helps me a lot.

  2. Rathernotsay

    I wonder if there is a strong correlation with those who suffer from phantosmia (phantom smells, particularly smoke) with brain inflammation and infection as well as leaky gut. My family history has a lot of Alzheimer’s, dementia, leaky gut and gluten intolerance. I have diabetes, high hsCRP, APOE4 gene, gut issues and episodes of phantosmia with a strong connection to consuming inflammatory foods and stress. I wouldn’t be surprised if the smoke smells were actually not phantom but something ‘on fire’ like an infection or tau protein. I would recommend adding this in questionnaires to see if there is a significant tie to inflammatory type Alzheimer’s as described in Dr Bredsen’s research.

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