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.

Thursday, September 25, 2025

Selenium and brain aging: A comprehensive review with a focus on hippocampal neurogenesis

 

Do you really think your competent? doctor will instruct the dietician to create diet protocols on this in the hospital and for home use? I really doubt you have a functioning stroke doctor as proven by doing nothing with this! I'm doing supplements, don't know if food intake is better and how to get it. I don't have time to wait for that research which will never occur.

Here is how long your doctor has been incompetent! Call the president and ask for competent stroke medical 'professionals' to be hired.  You really should expect your 'professionals' to know more that stroke-addled me!

  • selenium (15 posts to May 2015)

    • Selenium and brain aging: A comprehensive review with a focus on hippocampal neurogenesis


    https://doi.org/10.1016/j.arr.2025.102898Get rights and content

    Highlights

    • •
      Selenium regulates oxidative stress, neuroinflammation, and synaptic plasticity to modulate brain aging via selenoproteins.
    • •
      Selenium influences key molecular pathways (PI3K/Akt/Wnt and BDNF/TrkB) to enhance neural progenitor cell proliferation.
    • •
      The SEPP1-LRP8 axis delivers selenium to the hippocampus, and exercise enhances this system to promote neurogenesis.
    • •
      Selenium prevents ferroptosis and reduces microglial activation, promoting a healthy neurogenic environment.
    • •
      Large clinical trials and longitudinal multi-omics research are needed to confirm selenium’s role in healthy brain aging.

    Abstract

    Brain aging is accompanied by progressive cognitive decline and increased risk of neurodegenerative diseases, with adult hippocampal neurogenesis (AHN) playing a pivotal role in maintaining cognitive resilience. Selenium, an essential trace element, exerts significant neuroprotective and neurogenic effects predominantly through its incorporation into selenoproteins, which regulate oxidative stress, neuroinflammation, and synaptic plasticity. This review synthesizes recent advances delineating selenium’s metabolism, bioavailability, and its multifaceted roles in brain development, function, and aging, emphasizing mechanisms underpinning hippocampal neurogenesis. Key molecular pathways influenced by selenium include phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/Wingless/Integrated (Wnt) and brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) signaling pathways that promote neural progenitor cell proliferation and differentiation. Selenium transport via selenoprotein P and its receptor low-density lipoprotein receptor-related protein 8 (LRP8) is critical for adequate selenium delivery to the hippocampus to support neurogenesis, with exercise demonstrated to potentiate this axis. Selenium also mitigates ferroptosis, preserves mitochondrial integrity, and modulates neuroimmune interactions by attenuating microglial activation and inflammasome signaling, fostering a neurogenic environment. Emerging evidence highlights selenium’s regulatory effects on RNA expression, including microRNAs modifications, further influencing neuronal health. Despite promising preclinical and observational data, clinical translation remains limited by heterogeneous and short-term studies. Future research priorities include multi-omics investigations, longitudinal cohorts, and addressing global selenium intake disparities through policy initiatives and precision nutrition. By consolidating mechanistic insights with clinical perspectives, this review underscores selenium’s potential as a modifiable factor to enhance AHN and cognitive health, advocating for integrated translational strategies to combat brain aging and neurodegeneration.
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