MegansMom wrote:These veins are made of mesenchymal tissue, mesenchymal tissue responds to hormones, especially female hormones, the tissue is much more " stretchy" during pregnancy/ lactation. This may explain why there are less MS events during these times
2. Sheer stress and hypoxia both make the endothelium produce "endothelin 1" this "endothelin1" can cause fibrosis ( stiffness) and hypertrophy (thickening) of vessels (arteries and veins) especially valves. So from birth this may cause the veins/ valves to get worse CCSVI over time.
3. Endothelin1 is found in much higher levels in people with MS. It would be interesting to see if they could test if the level goes down after CCSVI angioplasty and normal cerebral venous outflow?
4.could a high level of Endothelin1 influence restenosis/ resumption of reflux after angioplasty?
Over 50% of multiple sclerosis (MS) patients experience cognitive deficits, and hippocampal-dependent memory impairment has been reported in >30% of these patients. While postmortem pathology studies and in vivo magnetic resonance imaging demonstrate that the hippocampus is targeted in MS, the neuropathology underlying hippocampal dysfunction remains unknown. Furthermore, there are no treatments available to date to effectively prevent neurodegeneration and associated cognitive dysfunction in MS. We have recently demonstrated that the hippocampus is also targeted in experimental autoimmune encephalomyelitis (EAE), the most widely used animal model of MS. The objective of this study was to assess whether a candidate treatment (testosterone) could prevent hippocampal synaptic dysfunction and underlying pathology when administered in either a preventative or a therapeutic (postdisease induction) manner. Electrophysiological studies revealed impairments in basal excitatory synaptic transmission that involved both AMPA receptor-mediated changes in synaptic currents, and faster decay rates of NMDA receptor-mediated currents in mice with EAE. Neuropathology revealed atrophy of the pyramidal and dendritic layers of hippocampal CA1, decreased presynaptic (Synapsin-1) and postsynaptic (postsynaptic density 95; PSD-95) staining, diffuse demyelination, and microglial activation. Testosterone treatment administered either before or after disease induction restores excitatory synaptic transmission as well as presynaptic and postsynaptic protein levels within the hippocampus. Furthermore, cross-modality correlations demonstrate that fluctuations in EPSPs are significantly correlated to changes in postsynaptic protein levels and suggest that PSD-95 is a neuropathological substrate to impaired synaptic transmission in the hippocampus during EAE. This is the first report demonstrating that testosterone is a viable therapeutic treatment option that can restore both hippocampal function and disease-associated pathology that occur during autoimmune disease.
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