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, July 7, 2014

A 'switch' in Alzheimer's and stroke patient brains that prevents the generation and survival of neurons

This is a fascinating conundrum since nitric oxide has many health benefits. You'll have to have your doctor sort out all the claims and provide you with the way to go. Don't  let your doctor dismiss your questions without providing a clear answer to all the linked research.

You do expect your doctor to actually know something about your stroke recovery? Don't you?

We are really f*cking screwed if we can't use exercise to create neurogenesis because the same process that creates new neurons also creates NO that prevents neurogenesis?
Damnable Catch-22.

What is your doctors solution? 

Vigorous treadmill exercise improves reactivity of cerebral arterioles and reduces brain injury following transient focal ischemia - In rats

Exercise creates NO.

Enhanced endothelial nitric oxide production impairs cerebrovascular tone after brain trauma

How Mouthwash Can Affect Stroke Risk

Chlorhexidine kills nitrite production in your body, which prevents blood vessels from dilating.

Research Focuses on Beet Juice After Stroke

Creation of nitric oxide via Breath of Fire

 

The role of nitric oxide in pre-synaptic plasticity and homeostasis

 

  Physical activity improves long-term stroke outcome via endothelial nitric oxide synthase-dependent augmentation of neovascularization and cerebral blood flow.

 

  Sun's blood pressure benefits 'may outdo cancer risks'

 

 Nasal NO is known to be increased 15-to20 fold by humming compared with quiet exhalation.

  The role of nitric oxide in pre-synaptic plasticity and homeostasis

  Benefits of Nose Breathing & Nitric Oxide

Tea, flavonoids, and cardiovascular health: endothelial protection

A comparative study of NONOate based NO donors: Spermine NONOate is the best suited NO donor for angiogenesis

Atherosclerosis: Evolving Vascular Biology and Clinical Implications

Pleiotropic effects of statins include improvement of endothelial dysfunction, increased nitric oxide bioavailability, antioxidant properties, inhibition of inflammatory responses, and stabilization of atherosclerotic plaques.  

Intranasal pyrrolidine dithiocarbamate decreases brain inflammatory mediators and provides neuroprotection after brain hypoxia–ischemia in neonatal rats

Inhibition of inducible nitric oxide synthase after brain HI reduced brain tissue loss.

Effect of a single intrastriatal rotenone injection on oxidative stress and neurodegeneration in the rat brain

I'm not sure I'd want a pesticide injected into my brain even if nitric oxide and CoQ10 increased.

Modulation of Adult Neurogenesis by the Nitric Oxide System

Efficacy of Nitric Oxide in Stroke' (ENOS) study 

Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury 

 

  Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury

 

  Regulation of Injury-Induced Neurogenesis by Nitric Oxide

 

 Nitric Oxide and the Biological Cascades Underlying Increased Neurogenesis, Enhanced Learning Ability, and Academic Ability as an Effect of Increased Bouts of Physical Activity

  Inhalation of nitric oxide could help improve blood flow to ischemic brain

  Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

 

  Cerebrovascular protection by various nitric oxide donors in rats after experimental stroke

 

Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

Don't do your own research on this, your doctor needs to take the lead. This is all provided to you so you can ask your doctor leading questions. 

The new research here:

http://medicalxpress.com/news/2014-07-alzheimer-patient-brains-survival-neurons.html
A new study by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) has identified a chemical "switch" that controls both the generation of new neurons from neural stem cells and the survival of existing nerve cells in the brain. The switch that shuts off the signals that promote neuron production and survival is in abundance in the brains of Alzheimer's patients and stroke victims. The study, published July 3 in Cell Reports, suggests that chemical switch, MEF2, may be a potential therapeutic target to protect against neuronal loss in a variety of neurodegenerative diseases, such as Alzheimer's, Parkinson's and autism.

"We have shown that when nitric oxide (NO)—a highly reactive free radical—reacts with MEF2, MEF2 can no longer bind to and activate the genes that drive neurogenesis and neuronal survival," said Stuart Lipton, M.D., Ph.D., director and professor in the Neuroscience and Aging Research Center at Sanford-Burnham, and a practicing clinical neurologist. "What's unique here is that a single alteration to MEF2 controls two distinct events—the generation of new neurons and the survival of existing neurons," added Lipton, who is senior author of the study.
In the brain, transcription factors are critical for linking external stimuli to protein production, enabling neurons to adapt to changing environments. Members of the MEF2 family of have been shown to play an important role in neurogenesis and neuronal survival, as well as in the processes of learning and memory. And, mutations of the MEF2 gene have been associated with a range of neurodegenerative disorders, including Alzheimer's and autism.
The process of NO-protein modifications—known as S-nitrosylation—was first described by Lipton and collaborators some 20 years ago. S-nitrosylation has important regulatory functions under normal physiological conditions throughout the body. However, with aging, environmental toxins, or stress-related injuries, abnormal S-nitrosylation reactions can occur, contributing to disease pathogenesis.
"Our laboratory had previously shown that S-nitrosylation of MEF2 controlled neuronal survival in Parkinson's disease," said Lipton. "Now we have shown that this same reaction is more ubiquitous, occurring in other neurological conditions such as stroke and Alzheimer's disease. While the major gene targets of MEF2 may be different in various diseases and brain areas, the remarkable new finding here is that we may be able to treat each of these neurological disorders by preventing a common S-nitrosylation modification to MEF2.
"The findings suggest that the development of a small therapeutic molecule—one that can cross the blood-brain barrier and block S-nitrosylation of MEF2 or in some other way increase MEF2 transcriptional activity—could promote new brain cell growth and protect existing cells in several neurodegenerative disorders," added Lipton.
"We have already found several such molecules in our high-throughput screening and drug discovery efforts, so the potential for developing new drugs to attack this pathway is very exciting," said Lipton.

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