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.

Monday, March 25, 2024

New Data Support Viagra for Alzheimer’s Prevention

 

But is it the drug or the amount of sex they are having? An easy piece of research to accomplish; WHOM will do that? What about for women?

Sex linked to better brain power in older age

 My doctor said it wasn't proven enough to do this.

But this for the negative view: Does Viagra really help prevent Alzheimer’s? Not so fast

The latest here:

New Data Support Viagra for Alzheimer’s Prevention

A new study provides more evidence that sildenafil (Viagra) which is used to treat erectile dysfunction (ED) may help protect against Alzheimer's disease (AD).

The large real-world analysis of patient data from two databases showed a 30%-54% reduced prevalence in AD among patients who took sildenafil (Viagra) than those who did not, after adjusting for potential confounding factors.

This observation was further supported by mechanistic studies showing decreased neurotoxic protein levels in brain cells exposed to the phosphodiesterase type 5 inhibitor (PDE5i).

"Our findings provide further weight to repurposing this existing FDA-approved drug as a novel treatment for Alzheimer's, which is in great need of new therapies," Feixiong Cheng, PhD, director of the Cleveland Clinic Genome Center, who led the research, said in a news release. 

"We used artificial intelligence to integrate data across multiple domains which all indicated sildenafil's potential against this devastating neurological disease," Cheng noted. 

The study was published online on March 1, 2024, in the Journal of Alzheimer's Disease

Neuroprotective?

Using real-world patient data from the MarketScan Medicare Supplemental database (2012-2017) and the Clinformatics database (2007-2020), the researchers conducted propensity score-stratified analyses after adjusting for gender, age, race, and comorbidities. 

They searched for all individuals with pharmacy claims for sildenafil or four comparator drugs — bumetanide, furosemide, spironolactone, and nifedipine. Results showed that sildenafil use was associated with reduced likelihood of AD relative to the control drugs. 

For example, sildenafil use was associated with a 54% reduced incidence of AD in MarketScan (hazard ratio [HR], 0.46; 95% CI, 0.32-0.66) and a 30% reduced prevalence of AD in Clinformatics (HR, 0.70; 95% CI, 0.49-1.00) compared with spironolactone.

The findings support a study published earlier this year that found a potential protective effect of PDE5i treatment on AD risk, as previously reported by Medscape Medical News.

However, this research and the current study are contradicted by another paper published in Brain Communications in late 2022 which showed no such link between ED meds and reduced AD risk.

The investigators also found that sildenafil reduces tau hyperphosphorylation (pTau181 and pTau205) in a dose-dependent manner in both familial and sporadic AD patient induced pluripotent stem cell (iPSC)-derived neurons. 

They further demonstrated through RNA-sequencing data analysis that sildenafil specifically targets AD related genes and pathobiological pathways, mechanistically supporting the beneficial effect of sildenafil in AD.

"We believe our findings provide the evidence needed for clinical trials to further examine the potential effectiveness of sildenafil in patients with Alzheimer's disease," Cheng said. 

The study was primarily supported by the National Institute on Aging (NIA) and the National Institute of Neurological Disorders and Stroke (NINDS). Cheng had no relevant disclosures.

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