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.

Friday, April 14, 2023

A mild dose of aspirin promotes hippocampal neurogenesis and working memory in experimental ageing mice

Ask your doctor is this is enough to have this intervention immediately post stroke or do you need to wait for human testing which will occur in 50 years?

 A mild dose of aspirin promotes hippocampal neurogenesis and working memory in experimental ageing mice

emi Feiona Vergil Andrews1

Divya Bharathi Selvaraj1

Akshay Kumar1

Syed Aasish Roshan1

Muthuswamy Anusuyadevi1

Mahesh Kandasamy1

Email

Bharathidasan University

https://doi.org/10.21203/rs.3.rs-2789201/v1

This work is licensed under a CC BY 4.0 License

Aspirin treatment is the most widely used preventive measure against cardiovascular diseases. Aspirin is also expected to provide beneficial effects on the brain. However, the association between aspirin treatment and neurocognitive functions is a subject of debate. Ample reports strongly advocate that a mild dose of aspirin positively modulates hippocampal plasticity responsible for memory. Aspirin is a selective cyclooxygenase (COX)-2 inhibitor but the underlying mechanism through which aspirin modulates neuroplasticity remains unclear. Adult neurogenesis in the hippocampus has been established as an underlying basis of learning and memory. Therefore, aspirin treatment might be linked to the regulation of hippocampal neurogenesis. Thus, this study revisited the effect of low-dose aspirin on learning and memory in correlation with the regulation of hippocampal neurogenesis in the brains of ageing experimental mice. Results from the novel object recognition (NOR) test, Morris water maze (MWM), and cued radial arm maze (cued RAM) revealed that aspirin treatment enhances working memory in experimental ageing mice. Further, the co-immunohistochemical assessments on the brain sections indicated an increased number of doublecortin (DCX) positive immature neurons and bromodeoxyuridine (BrdU)/neuronal nuclei (NeuN) double-positive newly generated neurons in the hippocampi of mice in aspirin-treated group compared to the control group. Recently, enhanced activity of acetylcholinesterase (AChE) in circulation has been identified as an indicative biomarker of dementia. The biochemical assessment in the blood of aspirin-treated mice showed decreased activity of AChE than that of the control group. This study supports the procognitive effects of aspirin which can be translated to treat dementia.

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