Ginseng: a promising neuroprotective strategy in stroke

Is anyone ever going to write up a stroke protocol for this kind of stuff?  My god, neurons are dying by the trillions every day because our stroke medical people will not get off their asses and put this together.  This is not somebody else's problem to solve, it's yours. So buckle down and put some f*cking neuroprotective stroke protocols together.  My ideas here:
these 31 hyperacute possibilities I'm going to insist my doctor give me the first week. 

http://journal.frontiersin.org/article/10.3389/fncel.2014.00457/full? 

Vaibhav Rastogi^1,2, Juan Santiago-Moreno¹ and Sylvain Doré^1,2,3,4*

• ¹Departments of Anesthesiology, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA
• ²Departments of Neurology, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA
• ³Departments of Psychiatry, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA
• ⁴Departments of Neuroscience, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA

Ginseng is one of the most widely used herbal medicines in the world. It has been used in the treatment of various ailments and to boost immunity for centuries; especially in Asian countries. The most common ginseng variant in traditional herbal medicine is ginseng, which is made from the peeled and dried root of Panax Ginseng. Ginseng has been suggested as an effective treatment for a vast array of neurological disorders, including stroke and other acute and chronic neurodegenerative disorders. Ginseng’s neuroprotective effects are focused on the maintenance of homeostasis. This review involves a comprehensive literature search that highlights aspects of ginseng’s putative neuroprotective effectiveness, focusing on stroke. Attenuation of inflammation through inhibition of various proinflammatory mediators, along with suppression of oxidative stress by various mechanisms, including activation of the cytoprotective transcriptional factor Nrf2, which results in decrease in reactive oxygen species, could account for its neuroprotective efficacy. It can also prevent neuronal death as a result of stroke, thus decreasing anatomical and functional stroke damage. Although there are diverse studies that have investigated the mechanisms involved in the efficacy of ginseng in treating disorders, there is still much that needs to be clarified. Both in vitro and in vivo studies including randomized controlled clinical trials are necessary to develop in-depth knowledge of ginseng and its practical applications.

Introduction

Ginseng is a broad term that refers to a group of 11 species of perennial plants belonging to the Panax genus under the family Araliaceae. The commercially available herbal formulations of ginseng are extracted from the root of these plants. It has been used for more than 2000 years mainly in China, Korea and Japan. The most commonly used herbal derivative of ginseng is Korean ginseng which is derived from the peeled, steamed, and dried root of Panax ginseng also commonly known as Korean ginseng. Although there are other variants of ginseng that contain many of the same compounds and medicinal properties, we will mainly focus on Panax ginseng and its constituents. The chemical constituents of ginseng include triterpene saponins, polysaccharides, peptidoglycans, nitrogen-containing compounds, fatty acids, carbohydrates and phenolic compounds (Sticher, 1998). It also contains essential oil-containing polyacetylenes and sesquiterpenes (Sticher, 1998). Ginsenosides are the major active components in ginseng; they are a form of triterpene glycosides (saponins). Of the 150 ginsenosides that have been isolated from ginseng, 40 have been found in Panax ginseng alone (Christensen, 2009). These mainly include Rb1, Rb2, Rc, Rd, Rg1, Rg2, Rh1, and Re (Attele et al., 1999).

The Greek word “panax” means “cure-all” and true to its name, ginseng has proven to have a wide variety of medicinal uses. Ginseng can improve pulmonary lung function in stable chronic obstructive pulmonary disorder patients (An et al., 2011). Korean ginseng has been shown to provide symptomatic relief in the patients with complaints of erectile dysfunction (Hong et al., 2002). A large number of carcinomas, including those associated with smoking, could potentially be prevented by the regular use of ginseng (Yun and Choi, 1995). Ginseng’s efficacy in type-2 diabetics has been illustrated by the fact that the patients had a decrease in the fasting blood glucose, weight loss and HbA1c (glycated hemoglobin) along with improvement in mood and psychophysical performance (Sotaniemi et al., 1995). Ginseng also possesses numerous cardiovascular benefits that are mainly due to its cardioprotective and anti-hypertensive effects; it can also attenuate myocardial hypertrophy and heart failure (Karmazyn et al., 2011).

Ginseng is also known to affect various aspects of neurodevelopmental, neurodegenerative and neuropsychiatric disorders (Kim et al., 2013). Stroke is the 4th leading cause of death in United States with an estimated 1 death every 4 min. Stroke recurs in 1 out of every 4 stroke patients. Approximately 87% of strokes are a result of ischemic insult and 13% are hemorrhagic strokes. Subarachnoid hemorrhage (SAH) accounts for approximately 3% of all strokes, has an incidence rate of 30,000 cases per year (King, 1997) and is mostly seen after brain aneurysm rupture or in traumatic brain injury (TBI) patients. Stroke is also one of the leading causes of long term disability (Go et al., 2013). These are reasons for stroke’s high magnitude of mortality and morbidity. From this information, one can see that present preventive and treatment strategies are not sufficient to curb this health menace. Because of this, there is a need to look for other treatment modalities and ginseng has shown promising evidence in this regard.

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

If NO is that important why hasn't a therapy protocol been written up for it? There are thousands of neurologists that have known about this for years and every single one has failed in that task.
http://www.frontiersin.org/Journal/10.3389/fncel.2013.00190/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w46-2013
Neil Hardingham^‡, James Dachtler^†‡ and Kevin Fox^*

• School of Biosciences, Cardiff University, Cardiff, UK

Since the observation that nitric oxide (NO) can act as an intercellular messenger in the brain, the past 25 years have witnessed the steady accumulation of evidence that it acts pre-synaptically at both glutamatergic and GABAergic synapses to alter release-probability in synaptic plasticity. NO does so by acting on the synaptic machinery involved in transmitter release and, in a coordinated fashion, on vesicular recycling mechanisms. In this review, we examine the body of evidence for NO acting as a retrograde factor at synapses, and the evidence from in vivo and in vitro studies that specifically establish NOS1 (neuronal nitric oxide synthase) as the important isoform of NO synthase in this process. The NOS1 isoform is found at two very different locations and at two different spatial scales both in the cortex and hippocampus. On the one hand it is located diffusely in the cytoplasm of a small population of GABAergic neurons and on the other hand the alpha isoform is located discretely at the post-synaptic density (PSD) in spines of pyramidal cells. The present evidence is that the number of NOS1 molecules that exist at the PSD are so low that a spine can only give rise to modest concentrations of NO and therefore only exert a very local action. The NO receptor guanylate cyclase is located both pre- and post-synaptically and this suggests a role for NO in the coordination of local pre- and post-synaptic function during plasticity at individual synapses. Recent evidence shows that NOS1 is also located post-synaptic to GABAergic synapses and plays a pre-synaptic role in GABAergic plasticity as well as glutamatergic plasticity. Studies on the function of NO in plasticity at the cellular level are corroborated by evidence that NO is also involved in experience-dependent plasticity in the cerebral cortex.

A Simple Rule for Dendritic Spine and Axonal Bouton Formation Can Account for Cortical Reorganization after Focal Retinal Lesions

Based on this what does your doctor recommend to make sure neuroplasticity is working toward your 100% recovery?
http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1003259

Abstract

Lasting alterations in sensory input trigger massive structural and functional adaptations in cortical networks. The principles governing these experience-dependent changes are, however, poorly understood. Here, we examine whether a simple rule based on the neurons' need for homeostasis in electrical activity may serve as driving force for cortical reorganization. According to this rule, a neuron creates new spines and boutons when its level of electrical activity is below a homeostatic set-point and decreases the number of spines and boutons when its activity exceeds this set-point. In addition, neurons need a minimum level of activity to form spines and boutons. Spine and bouton formation depends solely on the neuron's own activity level, and synapses are formed by merging spines and boutons independently of activity. Using a novel computational model, we show that this simple growth rule produces neuron and network changes as observed in the visual cortex after focal retinal lesions. In the model, as in the cortex, the turnover of dendritic spines was increased strongest in the center of the lesion projection zone, while axonal boutons displayed a marked overshoot followed by pruning. Moreover, the decrease in external input was compensated for by the formation of new horizontal connections, which caused a retinotopic remapping. Homeostatic regulation may provide a unifying framework for understanding cortical reorganization, including network repair in degenerative diseases or following focal stroke.

Author Summary

The adult brain is less hard-wired than traditionally thought. About ten percent of synapses in the mature visual cortex is continually replaced by new ones (structural plasticity). This percentage greatly increases after lasting changes in visual input. Due to the topographically organized nerve connections from the retina in the eye to the primary visual cortex in the brain, a small circumscribed lesion in the retina leads to a defined area in the cortex that is deprived of input. Recent experimental studies have revealed that axonal sprouting and dendritic spine turnover are massively increased in and around the cortical area that is deprived of input. However, the driving forces for this structural plasticity remain unclear. Using a novel computational model, we examine whether the need for activity homeostasis of individual neurons may drive cortical reorganization after lasting changes in input activity. We show that homeostatic growth rules indeed give rise to structural and functional reorganization of neuronal networks similar to the cortical reorganization observed experimentally. Understanding the principles of structural plasticity may eventually lead to novel treatment strategies for stimulating functional reorganization after brain damage and neurodegeneration.