How Alzheimer's mutates the immune system
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- เผยแพร่เมื่อ 29 ก.ย. 2024
- David Gate studies how neurodegenerative disease changes the immune system
And for people with Alzheimer's disease, some of the changes he and his colleagues have identified are at the genetic level - with one modification to T cells potentially leading to an abnormal inflammatory response in the brain. Now he thinks that understanding and targeting these changes could be a route to treating the disease.
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Sound quality is not very great! Especially the sound of David Gate.
That was the alzheimers. Alzheimers make your voice sound like that
@@colintheil1508 Perhaps the video should have pointed that out if this was the case!
People need to stop using AirPods Mics for professional interviews, they're terrible sound quality.
This is no fault of nature, nor the production company, it's just the AirPods mic recording is terrible on calls and video interviews like this.
Who wants to do dural taps on 83 y.o. yaaaaay. Eep. Yes let's fund David's proper wall faux finish and liquid encouragement (ginger juice!?) APOE4 is a thing!!! Canny!
Awesome stuff
Amazing discovery!! 👏🏽👏🏽👏🏽
Cool
This could also explain the mechanism behind an already observed connection. Exercise training has been linked to brain health and exercise training has a powerful anti-inflammatory effect on the body. This effect on the immune system could also possibly explain the link between exercise and brain health, including in older adults.
Very interesting!
Amazing
Coolmuch one 👀ツ
Dang that’s amazing! ❤
Interesting. CXCR3 is apparently an X-linked gene, and according to one report, it can escape X-inactivation (Lyonization) during infection. ~ Does thiamine deficiency affect CXCR3 expression?
Excuse my curiosity, but what would be the link beetween thiamine deficiency, x inactivation and cxcr3? I understand that vitamin B1 deficiency can lead to dementia but would the comparison go further?
@@MrSupremeYann No need to excuse curiosity! 😺 Low B1 status is associated with Alzheimer disease, women are more prone to AD, and women are more vulnerable to the effects of B1 deficiency. Interestingly, APOE4 increases AD risk, but APOE4 is common in Nigeria, and yet AD rates are lower in Nigeria*, at least in people who eat a traditional diet - this is called the Nigerian Paradox. Also in Nigeria, seasonal ataxia is a thing. This is caused by consuming insect larvae that contain a cooking-resistant thiaminase which causes a functional thiamine deficiency. Seasonal ataxia mainly affects women. I consider this to be a paradox within a paradox. Is it possible seasonal consumption of thiaminase somehow upregulates a pathway that is protective against thiamine deficiency or increases efficiency of thiamine utilization (a kind of hormesis)? I don't know if there is a connection to CXCR3, but I am looking into the literature. I found article suggesting that due to the metabolic demands of infection, thiamine can be depleted, and that IV thiamine benefitted hospitalized people with infection-related encephalopathy. Certain types of infections can increase risk of AD. That's all I have for now.
* epidemiologists adjust for age, so lower life expectancy in Nigeria isn't responsible for the lower AD rates in comparison to other countries
oh - and just to be clear, females have 2 X chromosomes and thus 2 copies of CXCR3, whereas males only have 1. Higher copy number can increase gene expression. Usually one X chromosome is inactivated, but sometimes genes escape the inactivation process, leading to higher expression levels.
@@rhyothemisprinceps1617 Sorry but it is not clear.
@@MrSupremeYann sorry, that was the 2nd part of a longer comment that got deleted. I will try again, but YT may delete this comment.
1st - It is good to be curious😺 Low B1 status is associated with Alzheimer (AD), women are at higher risk for AD, and women are more affected by B1 deficiency. APOE4 increases AD risk, but Nigeria has low AD rates (at least among those who have a traditional diet), despite high prevalence of APOE4 - this is known as the Nigerian Paradox. Interestingly, in Nigeria they also have something called seasonal ataxia, which is caused by eating insect larvae containing thiaminases, resulting in functional thiamine deficiency which somewhat resembles Wernicke's Encephalopathy. Women are more affected by seasonal ataxia. Sort of a paradox within a paradox. I've wondered if there is something about occasional thiaminase consumption that increases functional thiamine level or increases efficiency of thiamine utilization - a kind of hormetic effect. I'm looking at the literature to see if there is a connection between CXCR3 and thiamine - nothing really obvious so far. However, I found a paper suggesting that the metabolic demands of infection can cause thiamine deficiency and IV thiamine ameliorated infection-related encephalopathy. So there might be some link between infection, metabolism, thiamine, and CXCR3 expression. That's the best I can do in YT comments.
2:40 the James Webb Telescope would like to send a copyright notice to your house and know your location.