Julie G wrote:Interesting. From what I understood, cholesterol in the brain is only a problem when efflux is hampered as is often the case with E4s. Interestingly, plasmalogens appear to normalize efflux and are correlated with reduced amyloid-beta.
But wait, there's more. I just stumbled upon this tidbit today suggesting that amyloid-beta is primarily created in the liver??? https://www.newsbreak.com/news/23707915 ... Site&ss=i4
As I am just becoming familiar with much of the AD research and various interventions for prevention, this quote from the article has left me a bit confused:
In addition, dietary modifications such as lowering consumption of high-fat foods, could "potentially" slow production of these proteins [amyloid-beta] in the liver, thus reducing blood levels and preventing them from accumulating in the brain, he said.
As I understand it, one of the primary research-based strategies that has been discussed on this site to help prevent AD, is consuming a mild ketogenic diet which incorporates low carb and higher fat/protein foods. I've been eating lots of avocado, olive oil, nuts, seeds and fatty fish!!
In the mice, the researchers saw that the protein was carried in the blood by triglyceride-rich lipoproteins, which are also produced by the liver, to the brain, just as they do in humans.
Triglyceride-rich lipoproteins are also known to spread triglycerides, a type of cholesterol, from the digestive system to the bloodstream, where it travels throughout the body, potentially damaging organs such as the brain and heart.
Mice with high levels of both amyloid and triglyceride-rich lipoproteins experienced neurodegeneration -- or the loss of structure and function of brain cells -- and brain atrophy, or wasting away, according to the researchers.
Julie G wrote:Hi Sue! That struck me as well but I suspect that it's based on an outdated understanding of dietary/lipid interactions. As we know from our own N=1s and watching other members using a LCHF approach, our triglycerides tend to drop (not rise) with with higher fat as long as we concurrently reduce sugar and starchy carbs. As you'll recall from the article, amyloid was carried by triglycerides. This confirms other research suggesting that low triglycerides appear to be protective against Alzheimer's.
Because of its molecular structure and nature, RAGE [receptor for advanced glycation end products] has been under scrutiny for its potential role in mediating circulating plasma Aβ across the BBB and into the brain, where its deposition is seen in AD pathogenesis..
Increased expression of RAGE is reported to be associated with several pathological states, including Alzheimer’s disease, diabetic nephropathy, and immune/inflammatory reactions of the vessel walls
I was asking myself what happens if a high fat diet does increase the liver's output of AB while also reducing TGs. What then happens to the increased AB???
Julie G wrote:Circular wrote:I was asking myself what happens if a high fat diet does increase the liver's output of AB while also reducing TGs. What then happens to the increased AB???
Dumb question, but what evidence do you have that a high fat diet increases the liver's output of AB? … You may know of other research that backs up your assumption.
What happens if a high fat diet does increase the liver's output of AB while also reducing TGs. What then happens to the increased AB???
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