Throughout April and May 2017, Harvard researchers have been tackling a range of issues that influence aging. For example, ‘To age better, eat better’ \u2014 or ‘the balance in healthy aging.’<\/p>\n
The most recent of this series, ‘probe of Alzheimer’s follows paths of infection’ \u2014 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 \u2014 a protein that makes up one of the hallmark signs of Alzheimer’s.<\/p>\n
The Role of Amyloid Beta and the Development of Alzheimer’s<\/b><\/span><\/p>\n 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.<\/p>\n First discovered several years ago, Harvard researchers found key similarities between protein that is active in our immune system, and amyloid beta \u2014 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.<\/p>\n Led by a highly credible team, including, but not limited to, Robert Moir<\/a> and Rudolph Tanzi<\/a>, 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.<\/p>\n 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:<\/p>\n 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’ \u2014 but at the basis of it all:<\/p>\n Could Alzheimer’s Be Caused By An Infection?<\/b><\/span><\/p>\n Okay, so this is when things begin to get interesting.<\/span><\/p>\n 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. <\/span><\/p>\n By 1984, amyloid beta was discovered \u2014 which altered the path of ongoing research. This initial theory was known as the pathogen hypothesis<\/i>, and is now coming full circle once again. <\/span><\/p>\n 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<\/a>, \u201cthere is circumstantial evidence regarding the importance of amyloid beta.\u201d <\/span><\/p>\n 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. <\/span><\/p>\n 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<\/sup> birthday. <\/span><\/p>\n Could amyloid beta \u2014 this ‘terrible’ Alzheimer’s-associated protein actually offer antimicrobial properties? <\/span><\/p>\n\n
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