Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Tuesday, April 11, 2017

Molecular Mechanisms of Brain-Derived Neurotrophic Factor in Neuro- protection: Recent Developments

BDNF is good for our recovery. What the hell is your doctors' protocol to ensure your levels are good and you are getting enough?


http://www.sciencedirect.com/science/article/pii/S0006899317301440

Highlights

Neuronal cell injury is the primary pathological mechanism responsible for most types of brain injury.
Brain-derived neurotrophic factor (BDNF) may facilitate protective and regenerative effects following injury.
BDNF is involved in several pathological conditions, including hypoxic brain injury, stroke, Alzheimer’s disease and Parkinson’s disease.
Targeting BDNF can be applied in clinical settings and can serve as a new therapeutic strategy against neuronal injury.

Abstract

Neuronal cell injury, as a consequence of acute or chronic neurological trauma, is a significant cause of mortality around the world. On a molecular level, the condition is characterized by widespread cell death and poor regeneration, which can result in severe morbidity in survivors. Potential therapeutics are of major interest, with a promising candidate being brain-derived neurotrophic factor (BDNF), a ubiquitous agent in the brain which has been associated with neural development and may facilitate protective and regenerative effects following injury. This review summarizes the available information on the potential benefits of BDNF and the molecular mechanisms involved in several pathological conditions, including hypoxic brain injury, stroke, Alzheimer’s disease and Parkinson’s disease. It further explores the methods in which BDNF can be applied in clinical and therapeutic settings, and the potential challenges to overcome.

Abbreviations

  • PKA, protein kinase A;
  • cAMP, cyclic AMP;
  • CREB, cAMP response element binding;
  • AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor;
  • NMDA, N-methyl-D-aspartate receptor;
  • CAMK, Ca2+-calmodulin-dependent protein kinase;
  • BDNF, brain derived neurotrophic factor. MAPK, mitogen-activated protein kinase;
  • MEK, MAPK/ERK kinase;
  • ERK, extracellular signal-regulated kinase;
  • GAB1, GRB-associated binder 1;
  • Ins(1,4,5)P3, inositol-1,4,5-trisphosphate;
  • DAG, diacylglycerol;
  • PKC, protein kinase C;
  • Ca2+/CaM, Ca2+/calmodulin;
  • CaMK, Ca2+/calmodulin-dependent protein kinases

Keywords

  • Brain-derived neurotrophic factor;
  • Neuroprotection;
  • Brain injury
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Corresponding author. Address: Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, London, UK (Daqing Ma). Department of Anesthesiology, Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China, (Qingquan Lian)

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