Agreed on all your points, bigger and better trials for early prevention need to be conducted.
I’d guess that this info will be used to fine tune other GLP1 type peptides for a more focused therapy, if the mechanistic data holds up for that expenditure.
In the meantime, my weekly shot will continue 
Looking at AD brains on autopsy, I am pessimistic about “reversal” of AD, unless it’s very early stage. The late AD brain is hollowed out by the disease, there’s massive loss of tissue and I don’t understand how you’re supposed to get it all back. You could reach for an analogy, like losing a limb - you can arrest early gangrene and save the leg, but once the leg has been removed any talk of “reversal” is pointless. Only it’s worse than that with AD. There is a future possibility of regrowing limbs salamander-like if we can crack the code, but the brain is not like a limb, it’s the repository of your identity, your memories and life experience - after a massive loss of tissue, all that is gone… even if you could reintroduce brain tissue, it’s no longer you, it’s a clean slate, tabula rasa. Early, limited damage that still has most brain tissue preserved at least has the potential of migration of function to any prospective new (or current) tissue. But once the massive AD damage has been done, the horse is out of the barn.
Bottom line, I think it’s a distraction to focus on AD reversal (unless very early MCI), prevention and amelioration is where it’s at. Although quite frankly I find it depressing that we seem to have so little in the way of pharma interventions after so much research effort over the decades. Still, no choice but to keep grinding forward.
Hope this goes mainstream ASAP, would be good to know before it’s too late.
IMO: Doesn’t really matter until someone actually produces a cure. The Alzheimer’s and dementia drugs that are now on the market only provide minor relief.
This falls into the category of testing that I never use because knowing the results of the test wouldn’t change what I am already doing.
Knowing years before it became apparent, would be beneficial for those at risk. Agreed there is no cure but it can be slowed with lifestyle changes and some other drugs are showing promise in slowing it down. Plus there is some planning required to address the final stages. Something I’d like to participate in before it’s decided for me.
Just because dementias have no cure does not mean it’s useless to detect it as early as possible for some people. I’m one of those even though I don’t have the bad genes and it’s not in our family history, every familial generation has it’s weaknesses and strengths the previous generation didn’t have.
It’s not like prostate testing where it’s now becoming the standard to not do testing. AZ will put you in a care home for 10 to 15 years before it kills you. The cost of that is astronomical and can easily wipe out a lifetime of savings that could be better used by the living.
My solution is already in place, the MAID program will be used if/when appropriate.
I think this study is demonstrating changes in individuals who already have significant disease.
I think the use of p-Tau 217 / Beta Amyloid 42:40 ratio yields much more as a earlier warning (or if normal reassurance!) in regards to disease, probably 5-10 years or early before MCI occurs. I think that is a valuable piece of data that can be tracked yearly, and will have some individual really pursue everything known to delay disease progression.
Once you have significant disease, which was my take on this EEG study … we don’t have much in the way of action points or levers to pull. I think we do, at the point where a Beta Amyloid 42:40 is abnl, but the p-Tau 217 is still normal … or even if the p-Tau 217 is a little abnormal - this is likely early disease if no MCI … that is a valuable tool letting individuals know they must get very serious about everything.
See:
On semaglutide here’s another comment:
Here’s the video, worth watching (and short):
Very interesting. The issue is duration and intensity of therapy to show a result. A positive result should not be improvement, but should be slowing in the expected rate of decline.
I suspect that just like statins for CAD, it may take many years of therapy to show results.
However, my major interest is in prevention - I personally don’t manage any individuals who already have a diagnosis of AD, but do take care of individuals who have PD, but without advanced disease.
Anyone can recommend a brand of Lithium Orotate that does not smell stale? I bought KAL Lithium Orotate 5mg, it smells terrible. Thanks
I asked my PCP for a script of methylphenidate (Ritalin) for my husband. He has MCI and had been experiencing extreme lethargy. The methylphenidate does seem to be helping.
I use Nutricost Lithium Orotate 5 mg from Amazon. It is in capsule form with no taste and no smell, as far as I can perceive.
@Jonas,
I just went and smelled my bottle and I don’t detect anything, so I wonder if you might have a bad bottle?
Perhaps contact the company and perhaps they’ll send you one?
FWIW, I too went ahead and smelled my KAL 5mg Lithium Orotate bottle, and detected no particular odor. I’ve been using it steadily for months - my wife 5mg daily, I 5mg twice weekly and 5 times weekly 1mg the Life Extension Lithium Orotate. No issues that I can tell. Perhaps you have a defective bottle?
My 5mg KAL Lithium Orotate was manufactured 03/25 and expires 08/28 according to the dates on the bottom of the bottle. There’s also the LOT# listed on the bottom, you may want to contact KAL and give them the lot number with your complaint and see if they take some kind of action.
Thanks will do!
How about Nicotine as it’s great for Parkinson’s and Alzheimer’s? Also it doesn’t appear to be particularly addictive in isolation. Nicotine lozenges is probably the safest way to consume but I think even vapes aren’t that harmful and would probably net benefit humanity if we were all on them.
lol at vaping. you’re joking right?
I won’t put in the 15 pages of discussion Vera Health.ai gave on this query with Nicotine … but here is the summary. I think this is why nicotine is not presently on my list. It does a great job of dopamine release, but doesn’t seem to modify progression or symptoms sadly.
Exactly. Nicotine doesn’t help in PD at all. Smoking does but it’s probably hypoxia and/or carbon monoxide. There are ongoing RCTs to test those hypotheses. Answer soon.
The accelerated aging in Naked Mole Rats should inform people studying PD. I linked to it on another topic on this site.
Seems like people with both APOE3 and 4 need to be more focused on this topic:
Researchers based at University College London claim that the ε3 and ε4 variants of the APOE gene are responsible for most cases of Alzheimer’s disease.
As reported in npj Dementia, an analysis using individuals with two copies of the protective ε2 variant as a comparator, 71–93% of Alzheimer’s and cerebral amyloidosis was attributable to ε3 and ε4 and around 44% of dementia.
“When we consider the contributions of ε3 and ε4, we can see that APOE potentially has a role in almost all Alzheimer’s disease. Consequently, if we knew how to reduce the risk that the ε3 and ε4 variants confer to people, we may be able prevent most disease from occurring,” said lead researcher Dylan Williams from the UCL Division of Psychiatry and Unit for Lifelong Health and Ageing at UCL.
The APOE ε4 variant, carried by around 25% of Americans, is a known risk factor for Alzheimer’s disease. Only around 2.3% of people in the U.S. carry two copies of ε4 but 22-23% of the population carry one copy. Those homozygous for ε4 can have as much as a 15% increase in risk for Alzheimer’s compared to the general population risk.
The APOE ε2 variant is rare and protective. Estimates suggest up to 13% of people carry one copy of the allele, with only around one percent of people carrying two, but the large majority of the population (up to 65%) have two copies of the ε3 gene.
In the past, most studies have used ε3/ε3 to denote standard risk, but in this study the authors chose to use ε2/ε2 as a control.
Open Access Paper:
The proportion of Alzheimer’s disease attributable to apolipoprotein E
