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, October 30, 2014

May BDNF be Implicated in the Exercise-Mediated Regulation of Inflammation? Critical Review and Synthesis of Evidence

You'll have to ask your doctor about the benefits of exercising and producing BDNF. Some articles to bring to their attention.

Gradually Increased Training Intensity Benefits Rehabilitation Outcome after Stroke by BDNF Upregulation and Stress Suppression

Serum Brain-Derived Neurotrophic Factor and the Risk for Dementia

Promoting neuroplasticity for motor rehabilitation after stroke: considering the effects of aerobic exercise and genetic variation on brain-derived neurotrophic factor

Microglia Promote Learning-Dependent Synapse Formation through Brain-Derived Neurotrophic Factor

Newly identified protein helps explain how exercise boosts brain health 

Brain Derived Neurotrophic Factor Key Element in Recovery from Stroke

Individual Differences in Novelty Seeking Predict Subsequent Vulnerability to Social Defeat through a Differential Epigenetic Regulation of Brain-Derived Neurotrophic Factor Expression 



The latest here:
May BDNF be Implicated in the Exercise-Mediated Regulation of Inflammation? Critical Review and Synthesis of Evidence555411.abstract?
  1. Elizabeth D. E. Papathanassoglou, PhD, MSc, RN1
  2. Panagiota Miltiadous, PhD1
  3. Maria N. Karanikola, PhD, MSc, RN1
  1. 1Department of Nursing, Cyprus University of Technology, Limassol, Cyprus
  1. Elizabeth D. E. Papathanassoglou, PhD, MSc, RN, Department of Nursing, Cyprus University of Technology, 15 Vragadinou str., 3041 Limassol, Cyprus. Email: e.papathanassoglou@cut.ac.cy

Abstract

Introduction: Exercise attenuates inflammation and enhances levels of brain-derived neurotrophic factor (BDNF). Exercise also enhances parasympathetic tone, although its role in activating the cholinergic anti-inflammatory pathway is unclear. The physiological pathways of exercise’s effect on inflammation are obscure.
Aims: To critically review the evidence on the role of BDNF in the anti-inflammatory effects of exercise and its potential involvement in the cholinergic anti-inflammatory pathway.
Methods: Critical literature review of studies published in MEDLINE, PubMed, CINAHL, Embase, and Cochrane databases.
Results: BDNF is critically involved in the bidirectional signaling between immune and neurosensory cells and in the regulation of parasympathetic system responses. BDNF is also intricately involved in the inflammatory response: inflammation induces BDNF production, and, in turn, BDNF exerts pro- and/or anti-inflammatory effects. Although exercise modulates BDNF and its receptors in lymphocytes, data on BDNF’s immunoregulatory/anti-inflammatory effects in relation to exercise are scarce. Moreover, BDNF increases cholinergic activity and is modulated by parasympathetic system activation. However, its involvement in the cholinergic anti-inflammatory pathway has not been investigated.
Conclusion: Converging lines of evidence implicate BDNF in exercise-mediated regulation of inflammation; however, data are insufficient to draw concrete conclusions. We suggest that there is a need to investigate BDNF as a potential modulator/mediator of the anti-inflammatory effects of exercise and of the cholinergic anti-inflammatory pathway during exercise. Such research would have implications for a wide range of inflammatory diseases and for planning targeted exercise protocols

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