Medin And Alzheimer’s Disease
Amyloids are a family of three dozen proteins of which medin is one. In fact, medin is the most common amyloid known in humans and can be found in blood vessels of the upper body in virtually every person over 50. The reason it’s largely been ignored is because, unlike amyloid beta, there was no evidence it could become harmful or cause any disease. As a result, only a handful of research groups worldwide are investigating medin, one of which is the German Center for Neurodegenerative Diseases (DZNE). What they’re finding will no doubt inspire new studies.Medin Accumulates In Aging Mice
In 2020, DZNE researchers led by Dr. Jonas Neher, along with colleagues from other institutions, reported for the first time that medin develops in aging mice. The older the mice get, the more medin accumulates in the blood vessels of the brain. What's more, when the brain becomes active and triggers an increase in blood supply, vessels with medin deposits expand more slowly than those without it. This causes harm by preventing the brain from getting its full supply of oxygen and nutrients. Dr. Neher’s team also found that by making genetic changes that prevent medin’s development, the decline in blood vessel function thankfully stalled. The latest study followed up on this important work but focused on the role of medin specifically in the development of Alzheimer’s disease.The Link Between Medin And Alzheimer’s Disease
Previous research carried out by scientists from the U.S. and U.K. on medin in Alzheimer’s disease used samples from human donors and found that medin levels were higher in those with Alzheimer's disease or vascular dementia versus a matched sample of healthy human brain tissue. Medin levels also correlated with the amount of amyloid beta plaques, tau tangles and white matter lesions documented in the brain samples. However, it remained unclear whether increased medin came about as a response to the disease or whether it was a cause of the disease. As any good scientist would, Dr. Neher and the DZNE team wanted to learn more. In their studies, they removed tissue sections from both mice and Alzheimer's patients and stained them in such a way that medin and amyloid beta became visible and could be distinguished from one another. This revealed where they’re deposited together in the brain’s blood vessels. In the next step, the team was able to prove these two amyloids also “co-aggregate” - that is, form mixed deposits. A surprised Dr. Neher explained, saying, “Amazingly, medin interacts directly with amyloid beta and promotes its aggregation – this was completely unknown." Put simply, medin appears to cause beta amyloid proteins to accumulate in large numbers which can lead to the formation of memory-robbing brain plaques. What’s more…Medin Can Promote Blood Vessel Disease
In Alzheimer's mouse models Dr. Neher’s team found medin accumulates even more strongly in the brain’s blood vessels if amyloid beta deposits are also present. They confirmed this finding in people when they analyzed brain tissue from organ donors with Alzheimer's disease. However, when mice were genetically modified to prevent medin formation, significantly fewer amyloid beta deposits developed, and as a result, less damage to blood vessels occurred.“One Of The Causes” Of Alzheimer’s Disease
Commenting on the DZNE team’s extensive research, Dr. Neher said, “We were able to show that pathological changes in the blood vessels of Alzheimer's patients are significantly enhanced by medin. We have now been able to show through many experiments that medin actually promotes vascular pathology in Alzheimer's models. And this indicates that medin is one of the causes of the disease." The researchers concluded their paper, published in the journal Nature last November, by writing that “medin could significantly contribute to cognitive decline in Alzheimer’s disease by altering vascular function and amyloid beta deposition…we therefore propose that targeting medin might provide a novel therapeutic approach to preserving brain function during ageing and Alzheimer’s disease by improving vascular health.” While the research is still too early to reveal which natural strategies can target medin build-up in the brain specifically, a wealth of research that we’ve reported on here over the years shows that stopping rogue proteins like tau and amyloid beta begins with diet, lifestyle and the right nutritional supplements.Eat Well, Exercise, And Supplement
The science shows that omega-3 fatty acids found in fish and fish oil, such as DHA, can help reduce amyloid beta plaques and prevent the development of Alzheimer’s disease. While the brain benefits of omega-3’s are well known, there’s also the lesser-known coffee berry extract. This small red berry is rich in special antioxidant polyphenols that increase levels of brain-derived neurotrophic factor (BDNF), a memory-sharpening protein, throughout the brain. The science is why our sister company, Green Valley Natural Solutions, formulated Brain Vitality Plus. This amazing memory health supplement contains a patented form of Whole Coffee Fruit Extract called Neurofactor™, which has been shown to support your body’s production of BDNF, as well as domestically sourced and sustainable omega-3 fatty acid DHA to support attention, focus, and brain health. You can learn more about it here. Let’s not forget about your overall diet. It’s critical to eat a variety of antioxidant flavonoids found in green leafy vegetables and brightly colored fruits and vegetables. At the same time, avoid highly processed, sugar-laden foods and beverages. There’s also evidence—which we’ve reported on— that caffeine may reduce amyloid beta deposits in the brain. Coffee and certain teas—such as green tea—contain both caffeine and those memory-saving antioxidant flavonoids. By the way, if you’re wondering about coffee berry and its caffeine content, it does have a very small amount of natural caffeine that may contribute to its memory-building success. Finally, get your body moving with exercise. Studies show that people who exercise regularly and maintain a healthy weight are less likely to suffer many diseases of aging, including Alzheimer’s disease.- https://www.pnas.org/doi/10.1073/pnas.2011133117
- https://www.dzne.de/en/news/press-releases/press/new-target-for-alzheimers-therapies-found/
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9712113/
- “Amyloid” — Historical Aspects: https://www.intechopen.com/books/amyloidosis/-amyloid-historical-aspects
- The Role of Inflammation in Amyloid Diseases: https://www.intechopen.com/books/amyloid-diseases/the-role-of-inflammation-in-amyloid-diseases
- Targeting Amyloid Aggregation: An Overview of Strategies and Mechanisms: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6164555/
- Caloric restriction reduces the systemic progression of mouse AApoAII amyloidosis: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0172402
- Caloric restriction attenuates amyloid deposition in middle-aged APP/ PS1 mice: https://www.sciencedirect.com/science/article/abs/pii/S0304394009011185?via%3Dihub
- Green tea halts progression of cardiac transthyretin amyloidosis: an observational report: https://link.springer.com/article/10.1007/s00392-012-0463-z
- Caloric restriction: beneficial effects on brain aging and Alzheimer’s disease: https://link.springer.com/article/10.1007/s00335-016-9647-6
