That is rather high and may cause side effects for most people.
(Those are: tingling in fingers, vivid dreams, and especially bad nausea and stomach pain. Also higher testosterone and dramatically higher sex drive, though maybe you like that.)
I agree, and I don’t recommend anyone take zinc before getting their zinc levels tested. Or if they know they have genetic issues with zinc and zinc deficiency.
But the side effects from the zinc could be from a deficiency as well.
If you are low in serotonin and dopamine and take zinc, it will increase these, and since you were low for so long, the reaction to higher levels will be more pronounced. The increase in serotonin is usually what causes stomach upset, and diarrhea.
So it’s probably better for people who haven’t taken zinc who are deficient to start slowly.
> For nearly 40 years, neurologist Francisco Lopera at the University of Antioquia in Medellín, Colombia, has been following an extended family whose members develop Alzheimer’s in their forties or earlier. Many of the approximately 6,000 family members carry a genetic variant called the paisa mutation that inevitably leads to early-onset dementia.
Does he, like, tell them? Do they tell people they're dating? It's not clear how this perpetuates.
I remember a podcast where I believe a lady could smell Alzheimers (or possibly Dementia) years before it showed any symptoms. I have no idea how real it is, but the ethical dilemma is similar. She decided never to tell anyone if my memory is correct
Yeah, she could smell Parkinson's. I believe it. Dogs can smell all sorts of things humans cannot, and it is possible that a human mutation could grant her such a gift (or curse).
My wife and I smell different scents with differing sensitivities, so I can believe it. (I still remember the smell of roaches from when I was a young child.)
But then one day, about 10 years into the marriage, when Les was 31, he came home, and strangely, Joy says, he smelled different. "His lovely male musk smell had got this overpowering sort of nasty yeast smell," she says.
Yesterday an article was published showing a strong link with trichloroethylene. Apparently some of Fort Bragg's drinking water was contaminated with it and the incidence of Alzheimer's among soldiers being present there was way high.
People can choose to give a blood sample for the study, but they are not being told if they carry the mutation. I’m unclear if they even tell people they have found through the genealogical tree (that did not provide a blood sample) that they are part of it.
Which drug are you thinking of? Because the recent one that was approved was both highly controversial because the efficacy is extremely questionable[1] and the entire theory of disease is in question as well [2].
Yes, this too. This one though appears to have some side effects of brain swelling as mentioned in the article.
Though the one announced in 2021 made the headlines and appeared to be more of a success than it was. You could say a new drug being approved after 20 years is still a relative success (it does have some statistically significant results which led it to being approved).
If you're referring to the (likely) falsified research of Sylvain Lesné, my understanding is that researchers universally agree that it was not central to the beta-amyloid hypothesis, and therefore didn't change much. The story appears to have been widely mischaracterized in the press, even by Science, who broke the story.
It's good then that we now have another solution to tackle this like mentioned in OP, such as targeting reelin or APOE. And if anti-amyloids, or reducing amyloids are only a part solution. Hopefully, the findings keep continuing to cure Alzheimers.
How far are we from being able to simulate every molecule and folding in our body, tell a neural net what the desire outcome is and have it point out everything that prevents the desired outcome and what to do about it in a way that also doesnt prevent the desired outcome
Here's an interesting paper that looks at blood plasma protein contents and uses bioinformatics processes including learned models to identify plausible biofeedback pathways responsible for protein concentrations deviated from baseline. It's not what you are asking for, but it's the closest thing I've seen to date:
Plasma Proteome of Long-covid Patients Indicates Hypoxia-mediated Vasculo-proliferative Disease With Impact on Brain and Heart Function (Preprint)
> In Fig. 7A, hierarchical clustering heatmaps reflect the levels of neurological markers
across the patient groups (markers have been curated by OLINK). The values of the PEA expression levels were hierarchically clustered based on Pearson correlation algorithms. Markers selected through the
above methodology were investigated for functional annotation using tools from the GSEA platform and MSigDB data positories (Fig. 7B). This latest analysis demonstrated that functional clusters were formed
around leukocyte migration, positive immune signals, glial cell differentiation, neurogenesis and MAPK regulatory modules. Taken together, these pathways predict a possible brain-blood barrier
dysfunctionality grounded on cell proliferation. Graphs in Fig. 7C illustrate the expression levels of individual markers from the functional groups presented in Fig. 7B. One of the highly expressed markers, was the amyloid precursor protein (APP; Supplementary Fig. 10) which is known to be a pathognomonic
marker for both Alzheimer disease and brain inflammation [61–65]. Additional markers for brain
dysfunction include JAM2 (endothelial tight junctions protein), SNAPIN (a mediator of neuronal autophagy-lysosomal function in developing neurons), KCNH2 (potassium channel), S100A14 (involved in cell motility adhesion and growth), KIAA0319 (language impairment biomarker), and IROR1 (a receptor tyrosine kinase like orphan receptor 1, which regulates neurites growth in the central nervous system
having also WNT-signaling pathway functions, and being crucial for the auditive apparatus
maintenance).
“The fact that the man stayed mentally healthy for so long despite the many amyloid plaques in his brain suggests that Alzheimer’s is more complicated”. Given researchers still think is amyloid/tau related but still don’t understand why, you don’t say. Is like saying the universe is more complicated than that
It might be low Reelin that protects them. That is the function of must genetic mutations, to slow down the enzyme. So taking Reelin might make you worse.
RELN-COLBOS is a gain-of-function variant showing stronger ability to activate its canonical protein target Dab1 and reduce human Tau phosphorylation in a knockin mouse. A genetic variant in a case protected from ADAD suggests a role for RELN signaling in resilience to dementia.
These molecular systems are deeply complex and will depend on cascades of interactions. Hang tight. The only generic neuroprotective supplement I can recommend is niacinamide (vitamin B3, non-flushing). See:
(yes, in mice! but now in clinical trials for glaucoma and looking good. And yes, glaucoma is not AD, but many/most forms of neurodegenerations are associated with high mitochondrial stress/dysfunction).
wow, you really like dismissing pretty obvious evidence that zinc plays a role in Alzheimer's.
It is not complex, it is simple. I believe it is a metabolic disease caused by metabolic disease and genetic risk. That will be unique for everyone, but for most people I feel the answer will be poor zinc handling.
And Niacin is all you can come up with? Did you know we make niacin if we have enough B6 and B2?
No, not in any way useful in therapeutics yet. It is a large gene and protein. Delivery to the right cells and neurons in adult humans is well beyond state-of-the-art. But we may be able to mimic its effects with small molecules.
I carry four (as far as I know) rare and low frequency homozygous minor allele SNPs in RELN:
rs39335(G;G)
rs3914132(C;C)
rs7696175(C;C)
rs4298437(T;T)
And guess what? I have Bipolar Disorder Schizoaffective type and my therapists keep telling me I have Aspergers.
This gene seems to bind to zinc, and a deficiency of zinc is also found in Alzheimer's.
https://www.jneurosci.org/content/41/13/3025#:~:text=Inflamm....
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3010690/
https://alzres.biomedcentral.com/articles/10.1186/s13195-021...
Zinc has helped me in many ways.
Since the mutation is a GAIN OF FUNCTION mutation, more zinc means less risk of Alzheimer's.