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==== Triggers and associations ==== | ==== Triggers and associations ==== | ||
- | - Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.(({{pubmed> | + | - Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.(({{pmid> |
BACKGROUND: Multiple sclerosis (MS) incidence is higher among those who live at high latitudes before adulthood. This is usually attributed to lower levels of Vitamin D, caused by lower UV levels. However direct damage of the optic nerve by near-horizon sunshine is a possible alternative explanation. | BACKGROUND: Multiple sclerosis (MS) incidence is higher among those who live at high latitudes before adulthood. This is usually attributed to lower levels of Vitamin D, caused by lower UV levels. However direct damage of the optic nerve by near-horizon sunshine is a possible alternative explanation. | ||
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Multiple sclerosis etiology – an Epstein Barr hypothesis. | Multiple sclerosis etiology – an Epstein Barr hypothesis. | ||
- | (({{pubmed> | + | (({{pmid> |
The pathogenesis of multiple sclerosis: reconsideration of | The pathogenesis of multiple sclerosis: reconsideration of | ||
- | the role of viral agents and defence mechanisms. (({{pubmed> | + | the role of viral agents and defence mechanisms. (({{pmid> |
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Anti-tumor necrosis factor | Anti-tumor necrosis factor | ||
- | treatment restores the gut barrier in Crohn’s disease. | + | treatment restores the gut barrier in Crohn’s disease. |
- | Changes in gastrointestinal permeability in celiac disease. | + | Changes in gastrointestinal permeability in celiac disease. |
Increased intestinal permeability as a cause of fluctuating postprandial | Increased intestinal permeability as a cause of fluctuating postprandial | ||
- | blood glucose levels in Type 1 diabetic patients. | + | blood glucose levels in Type 1 diabetic patients. |
Role of the intestinal tight junction modulator zonulin in the | Role of the intestinal tight junction modulator zonulin in the | ||
- | pathogenesis of type I diabetes in BB diabetic-prone rats. (({{pubmed> | + | pathogenesis of type I diabetes in BB diabetic-prone rats. (({{pmid> |
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- | Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.(({{pubmed> | + | Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.(({{pmid> |
- | Non-MS autoimmune demyelination.(({{pubmed> | + | Non-MS autoimmune demyelination.(({{pmid> |
- | Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. (({{pubmed> | + | Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. (({{pmid> |
- | Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.(({{pubmed> | + | Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.(({{pmid> |
- | Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.(({{pubmed> | + | Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.(({{pmid> |
- | Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease.(({{pubmed> | + | Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease.(({{pmid> |
- | Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid (({{pubmed> | + | Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid (({{pmid> |
- | Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis? | + | Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis? |
- | MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.(({{pubmed> | + | MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.(({{pmid> |
- | Multiple sclerosis: infectious hypothesis. | + | Multiple sclerosis: infectious hypothesis. |
- | Role of viruses in etiology and pathogenesis of multiple sclerosis. | + | Role of viruses in etiology and pathogenesis of multiple sclerosis. |
- | Infection and the etiology and pathogenesis of multiple sclerosis. (({{pubmed> | + | Infection and the etiology and pathogenesis of multiple sclerosis. (({{pmid> |
Part I: the role of infection. | Part I: the role of infection. | ||
- | Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the " | + | Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the " |
- | **Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases.**(({{pubmed> | + | **Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases.**(({{pmid> |
- | **The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment.** | + | **The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment.** |
- | **Epidemiology and etiology of multiple sclerosis.**(({{pubmed> | + | **Epidemiology and etiology of multiple sclerosis.**(({{pmid> |
Detection of EBV-infected B-cells in patients' | Detection of EBV-infected B-cells in patients' | ||
- | (({{pubmed> | + | (({{pmid> |
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This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens. | This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens. | ||
- | (({{pubmed> | + | (({{pmid> |
===== Of further interest ===== | ===== Of further interest ===== | ||
By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments. | By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments. | ||
- | (({{pubmed> | + | (({{pmid> |
- | In a collaborative GWAS involving 9772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the Class I region. Immunologically relevant genes are significantly over-represented amongst those mapping close to the identified loci and particularly implicate T helper cell differentiation in the pathogenesis of multiple sclerosis. | + | In a collaborative GWAS involving 9772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the Class I region. Immunologically relevant genes are significantly over-represented amongst those mapping close to the identified loci and particularly implicate T helper cell differentiation in the pathogenesis of multiple sclerosis. |
- | Antibiotic Use (({{pubmed> | + | Antibiotic Use (({{pmid> |
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- | {{http:// | + | {{https:// |
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- | **Occupational exposure to UV light and mortality from multiple sclerosis**(({{pubmed> | + | **Occupational exposure to UV light and mortality from multiple sclerosis**(({{pmid> |
< | < | ||
- | " | + | " |
Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group). | Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group). | ||
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- | [{{ home: | + | [{{home: |
- | Low prevalence in Russia, although it varies by ethnic region. | + | Low prevalence in Russia, although it varies by ethnic region.}}] **map from msrc.co.uk** |
- | **map from msrc.co.u}}] | + | |
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- | ==== Myelin sheath ==== | + | ===== Myelin sheath |
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- | 2018 This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS (({{pubmed> | + | 2018 This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS (({{pmid> |
2019 [[https:// | 2019 [[https:// | ||
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• Calcium influx from the extracellular space drives axon degeneration | • Calcium influx from the extracellular space drives axon degeneration | ||
• Nanoscale ruptures allow entry of calcium across the axonal plasma membrane | • Nanoscale ruptures allow entry of calcium across the axonal plasma membrane | ||
+ | | ||
===== Member experience ===== | ===== Member experience ===== | ||
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First: Greg Blaney some years ago... | First: Greg Blaney some years ago... | ||
- | [[http:// | + | [[https:// |
Next: Dr Roswitha Goetze-Pelka, | Next: Dr Roswitha Goetze-Pelka, | ||
- | [[http:// | + | [[https:// |
- | Our simplified article in [[http:// | + | Our simplified article in [[https:// |
{{tag> | {{tag> | ||
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+ | < | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
removed FAILED LINK --- //Sallie Q 01.18.2019// | removed FAILED LINK --- //Sallie Q 01.18.2019// | ||
- | {{http:// | + | {{https:// |
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< | < | ||
- | [[http:// | + | [[https:// |
2011. "A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis." | 2011. "A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis." | ||
- | | + | |
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- | May 2005: Interesting new abstract about MS as an infection (({{pubmed> | + | May 2005: Interesting new abstract about MS as an infection (({{pmid> |
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Here is an example of the type of study which had initially side-tracked me into thinking viruses might play a part in MS | Here is an example of the type of study which had initially side-tracked me into thinking viruses might play a part in MS | ||
- | http:// | + | https:// |
But what these scientists are forgetting is that a monkey is not a human. Animal models have failed to predict human autoimmune disease time after time. So, while this study sounds very persuasive, it will fail to be replicated in man. | But what these scientists are forgetting is that a monkey is not a human. Animal models have failed to predict human autoimmune disease time after time. So, while this study sounds very persuasive, it will fail to be replicated in man. | ||
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Here is a paper on cytokine profiles in MS | Here is a paper on cytokine profiles in MS | ||
- | http:// | + | https:// |
They concluded that the Th1 profile is predominant, | They concluded that the Th1 profile is predominant, | ||
- | http:// | + | https:// |
however their raw data seem reliable, and it indicates Th1 is dominant. | however their raw data seem reliable, and it indicates Th1 is dominant. | ||
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Proc Natl Acad Sci U S A. 2010 Apr 6; | Proc Natl Acad Sci U S A. 2010 Apr 6; | ||
- | UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.(({{pubmed> | + | UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.(({{pmid> |
Becklund BR, Severson KS, Vang SV, DeLuca HF. | Becklund BR, Severson KS, Vang SV, DeLuca HF. | ||
Department of Biochemistry, | Department of Biochemistry, | ||
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Abstract | Abstract | ||
Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, | Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, | ||
- | PMID: 20308557 | + | PMID: 20308557 |
</ | </ | ||
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From: Varia | From: Varia | ||
Date: 2010-07-07 15:47:41 | Date: 2010-07-07 15:47:41 | ||
- | Reply: | + | Reply: |
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Phillyguy: Probably explains one of the reasons why the incidence of autoimmune disease is lower in developing countries and infectious disease is higher. | Phillyguy: Probably explains one of the reasons why the incidence of autoimmune disease is lower in developing countries and infectious disease is higher. | ||
- | (({{pubmed> | + | (({{pmid> |
PMID: 21277637 </ | PMID: 21277637 </ | ||
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Abstract | Abstract | ||
It has recently been suggested that, rather than being an autoimmune disease, multiple sclerosis (MS) is an example of a neurocristopathy, | It has recently been suggested that, rather than being an autoimmune disease, multiple sclerosis (MS) is an example of a neurocristopathy, | ||
- | (({{pubmed> | + | (({{pmid> |
PMID: 21547536 [</ | PMID: 21547536 [</ | ||
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In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, | In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, | ||
- | http:// | + | https:// |
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Department of Neuroimmunology, | Department of Neuroimmunology, | ||
Abstract | Abstract | ||
- | Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, | + | Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, |
PMID: 22031325 | PMID: 22031325 | ||
</ | </ | ||
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< | < | ||
- | http:// | + | https:// |
</ | </ | ||
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- | - Review Finds Marijuana May Help MS Patients - http:// | + | - Review Finds Marijuana May Help MS Patients - https:// |
< | < | ||
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- | ===== References ===== | + | ===== References =====</ |