New intel re Lithium Orotate

Posted by pb50 @pb50, Dec 31, 2025

I have discussed previously that I have mild cognitive dysfunction and after two rounds of neuropsych testing over two years and Lab & imaging testing confirming my clinical profile, I am taking Lithium Orotate as a nutritional supplement. But I consume professional intel on studies religiously. Like this one.
https://www.psychiatrictimes.com/view/lecanemab-or-lithium-compare-benefits-risks-and-dose
The key question that stood out to me which the physician author (Dr Phelps) asks in his review of studies is below. I highly emcourage reading this. You have to follow some links and jump back and forth a bit but make the effort. For those of you fond of calculating elemental lithium there is a section on calculating equivalent dosing to the mice study.

“Brain lithium prevents amyloid plaque formation and phosphorylation of tau proteins. In the process of AD dementia, lithium is sequestered in plaques, creating a positive feedback loop: more plaque, less lithium, leading to more plaque, and so on. Giving lithium orotate to young adult mice almost completely prevented plaque formation and tau phosphorylation. Starting lithium orotate after plaques and phosphorylated tau have already formed almost completely reversed the expected cognitive impairment. Lithium carbonate is far less effective. If all this were true in humans, lithium orotate would be an obvious treatment both to prevent AD dementia and to treat it once detected.

Of course, skeptics’ first response has been “these are mouse data.” Aron et al point out that lithium levels in human and mouse brains are comparable, supporting the relevance of mouse models for studying the biological effects of lithium. Skeptics, including a prominent neurologist following a national presentation on AD treatment, have said that we should wait for a randomized trial of lithium orotate in humans (personal communication, August 2025). But the recent lithium carbonate randomized trial took 8 years to mount and complete. What shall we suggest to patients and families for the next 8 years?

A healthy lifestyle—including a Mediterranean-like diet, regular physical activity, and avoidance of smoking, excessive alcohol, social isolation, sleep disorders, and hearing loss—is an important means of preserving cognitive function in people at risk of developing dementia.

The subsequent article will compare lecanemab and lithium’s benefits, risks, and costs. With ApoE genotyping and the new pTau/amyloid blood test, patients and families need help now deciding between treatment alternatives.”

Interested in more discussions like this? Go to the Aging Well Support Group.

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@ralpha4 totally separate out of john Hopkins by Christopher Morrow - a geriatric psychiatrist. So his lens is probably Bipolar dosing
The 9 week window is more typical for acute treatment window for psychiatric drug trials
We can still get valuable learnings if it does clear and move amyloid to csf - and it is a fast study

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@pb50
Will they release any outcome data before the end of the trial which I think is in 2029 is a key question?
Also, will they capture any markers that relate to AD, such as tau 217/181, amyloid PET scans , cognitive testing,
I think that using LP’s/CSF testing will discourage participation and enrollment.

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I agree - i just translate a CSF result in my mind to an updated 42-40 ratio since the only time anyone will access csf in me is if it is coming out of my nostrils or I am on the Pathologist’s table 🙂 So for that reason i would not enroll.

I wonder about pet scans too.

But I welcome their results!!!!

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