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Member
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Join Date: Nov 2006
Posts: 290
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Member
Join Date: Nov 2006
Posts: 290
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Now, let's get serious.
Much of this has already been posted elsewhere, but for this to make sense, all of the significant parts should be together. This will not, however concentrate on the role of the Blood-Brain Barrier nor the role of specific agents of inflammation. It will concentrate, however, on the role of the Vagus Nerve and its function as a conduit for the transfer of such substances from their point of insult to the Substantia Nigra. It will also cite the role of the Vagus nerve in presenting other symptoms that are outside of the symptoms that have come to define Parkinson's disease.
The increasing toxicity of our planet should be a much more pressing subject of our concern than it seems to be. This should be the most important health issue before congress, and it should be placed on the very top of the items being considered for funding. Every day, the mountain of compiled information grows. It grows at an alarming rate. So why hasn't the alarm been sounded more loudly? Epidemiologists are beginning to see more and more evidence that indicates that all life on this planet could soon be in danger of extinction if a new course of action is not set and adhered to. We are talking about the possibility of a major catastrophe in the annals of human history. Obviously, it's not going to conclude tomorrow or the next day, but conclude it will if we don't stop polluting our planet.
http://lansbury.bwh.harvard.edu/pd_reviews_2003.htm
Quote:
Braak, H., U. Rub, et al. (2003). "Idiopathic Parkinson's disease: possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen." J Neural Transm 110(5): 517-36.
The progressive, neurodegenerative process underlying idiopathic Parkinson's disease is associated with the formation of proteinaceous inclusion bodies that involve a few susceptible neuronal types of the human nervous system. In the lower brain stem, the process begins in the dorsal motor nucleus of the vagus nerve and advances from there essentially upwards through susceptible regions of the medulla oblongata, pontine tegmentum, midbrain, and basal forebrain until it reaches the cerebral cortex. With time, multiple components of the autonomic, limbic, and motor systems become severely impaired. All of the vulnerable subcortical grays and cortical areas are closely interconnected. Incidental cases of idiopathic Parkinson's disease may show involvement of both the enteric nervous system and the dorsal motor nucleus of the vagus nerve. This observation, combined with the working hypothesis that the stereotypic topographic expansion pattern of the lesions may resemble that of a falling row of dominos, prompts the question whether the disorder might originate outside of the central nervous system, caused by a yet unidentified pathogen that is capable of passing the mucosal barrier of the gastrointestinal tract and, via postganglionic enteric neurons, entering the central nervous system along unmyelinated praeganglionic fibers generated from the visceromotor projection cells of the vagus nerve. By way of retrograde axonal and transneuronal transport, such a causative pathogen could reach selectively vulnerable subcortical nuclei and, unimpeded, gain access to the cerebral cortex. The here hypothesized mechanism offers one possible explanation for the sequential and apparently uninterrupted manner in which vulnerable brain regions, subcortical grays and cortical areas become involved in idiopathic Parkinson's disease.
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http://psychiatrictimes.com/p0104vagus.html
Quote:
George et al. cited evidence that VNS prompts changes in norepinephrine and serotonin, the neurotransmitters most closely associated with mood regulation, as well as GABA and glutamate. They noted that VNS can activate the locus ceruleus, the main source of central nervous system norepinephrine-containing neuronal cell bodies, and is associated with increased cerebrospinal fluid levels of 5-hydroxyindoleacetic acid, a serotonin metabolite.
The researchers also observed that there has been a historical association of autonomic nervous system dysfunction mediated by the vagus, including heart rate variability, in patients with depression. They speculated, "If depressed patients have abnormalities in brain regions that control the vagus nerve (top-down regulation), then stimulating the vagus nerve might theoretically engage this dysfunctional circuit (a bottom-up approach
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