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, February 9, 2026

Aerobic and resistance training similarly enhance hippocampal BDNF expression in aged rats: implications for exercise induced neuroplasticity

Does your competent? doctor have the correct BDNF levels for stroke recovery? Oh, your doctor doesn't even know of the need? Let's see how long your doctor has been incompetent, well over a decade, WOW! And your doctor has no intention of ever becoming competent in stroke rehab?

  • BDNF (195 posts to April 2011)
  •  Aerobic and resistance training similarly enhance hippocampal BDNF expression in aged rats:implications for exercise induced neuroplasticity



    Ricardo Corrêa Cunha1

    Fabiano Salgueirosa1

    Julio Cesar Bassan2

    Marco André Cardoso3

    Rossana Baggio Simeoni4

    Luiz Cesar Guarita - Souza4

    Julio Cesar Francisco5

    Email

    Universidade Positivo,

    Postgraduate Program in Physical Education, Universidade Tecnológica Federal do Paraná,

    Federal University of Technology – Paraná,

    Pontifícia Universidade Católica do Paraná,

    PostGraduate Program in Biomedical Engineering, Universidade Tecnológica Federal do Paraná

    https://doi.org/10.21203/rs.3.rs-8752665/v1

    This work is licensed under a CC BY 4.0 License

    The molecular mechanisms underlying exercise-induced neuroplasticity remain incompletely understood, particularly regarding comparative effects of aerobic versus resistance training on hippocampal neurotrophic signaling in aging. Here we investigated the impact of these two exercise modalities on serum and hippocampal brain-derived neurotrophic factor (BDNF) expression in aged rats. Thirty male Wistar rats (23 months old) were randomly assigned to sedentary (SED), aerobic exercise (AEG), or resistance exercise (REG) groups (n = 10 each). AEG performed progressive treadmill running while REG completed weighted swimming (50–70% body weight), 5 days/week for 8 weeks. Both training protocols significantly reduced serum lactate and increased BDNF concentrations in serum and hippocampus relative to SED (p < 0.05), with no differences between AEG and REG. Densitometric analysis confirmed ~ 35–40% greater BDNF immunoreactivity in the dentate gyrus and CA1-CA3 regions of trained animals (p < 0.01). These findings demonstrate equivalent hippocampal neurotrophic adaptations to aerobic and resistance training in the aged brain, suggesting convergent activation of BDNF-mediated plasticity pathways regardless of exercise modality. Our results support the hypothesis that peripheral metabolic signals (e.g., lactate) and myokines converge on hippocampal BDNF/TrkB signaling during aging-targeted exercise interventions.

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