Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, January 31, 2026

Is Lithium Orotate the Key to Preventing Alzheimer’s Disease?

 Dies your doctor even know of your risk of dementia post-stroke? And has EXACT PREVENTION PROTOCOLS? NO? So, you DON'T have a functioning stroke doctor, do you?

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

You need this prevention!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018  

The latest here:

Is Lithium Orotate the Key to Preventing Alzheimer’s Disease?

This transcript has been edited for clarity. 

Hello. I’m Dr JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent exciting and potentially breakthrough study, published in Nature, that suggests a novel approach to preventing Alzheimer’s disease. 

The research was led by Dr Bruce Yankner and colleagues at Harvard Medical School. They conducted a series of studies that pointed to a promising role of lithium orotate in reducing Alzheimer’s risk. I’ll briefly summarize the lines of evidence but want to emphasize that these findings need to be confirmed by a rigorous randomized trial before lithium orotate should be considered ready for primetime. Our research group, in collaboration with Dr Yankner, will soon be launching such a large-scale human trial and appreciate the philanthropic support that has made this possible. 

The lines of evidence supporting a role of lithium orotate in dementia prevention include the following, as reported in the Nature article. The researchers were able to do this research because they had access to post-mortem brain tissue across several groups: people with no cognitive impairment, mild cognitive impairment, and Alzheimer’s disease. They evaluated 27 different metals, and lithium was the only metal that showed significantly lower levels in the postmortem brains of people with cognitive impairment, and especially those with Alzheimer’s disease, compared with cognitively healthy individuals. They also found that the amyloid beta plaques bind and trap lithium, which further reduces lithium availability in the brain and also suggests that lithium loss may be an early and specific biochemical change in the brains of people with Alzheimer’s disease. 

The researchers also conducted studies in mice to assess causation. They fed mice a lithium-restricted diet and found that they developed accelerated amyloid beta and tau pathology, neuroinflammation-reduced myelin, synapse loss, and memory and cognitive deficits. The changes were similar to the hallmark features of human Alzheimer’s disease. They then tested 16 different lithium salts and identified lithium orotate as having several unique and promising features, including low binding to amyloid beta (avoiding the trap that limited other lithium salts), the ability to restore lithium availability in the brain, and cognitive and pathological improvement in the mouse brain. 

In both Alzheimer’s disease mouse models and aging wild-type mice, lithium orotate prevented and reversed amyloid plaque and tau accumulation, other pathological brain changes, and cognitive decline and memory loss.

Prior to this research, only limited data were available on this topic. There were some epidemiologic observational studies, such as a few linking higher lithium levels in drinking water with lower dementia incidence, but prior research on lithium use and dementia risk has been inconclusive. Additionally, high doses of traditional lithium salts, such as lithium carbonate used for bipolar disorder, can be toxic and poorly tolerated, especially in older adults, so we still need confirmatory randomized trials of lithium orotate and dementia prevention in humans. 

The formulation appears to matter. Lithium orotate is an amyloid-evading salt, and it has not been tested in well-controlled human trials. Its safety, efficacy, and long-term tolerability remain unknown. Routine clinical use of lithium orotate isn’t yet ready for prime time until such trials are completed, but these are exciting findings that may hold the key to a novel approach to preventing Alzheimer’s disease.

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