Waardeloos onderzoek -
[URL="http://www.wetenschap24.nl/nieuws/artik ... rzoek.html"][U]Proeven met muizen[/U][/URL] zeggen vrijwel niets over ontstekingen bij mensen
[QUOTE]Onderzoek naar acute ontstekingsziekten bij muizen leidt vrijwel nooit tot nieuwe medicijnen voor mensen. Nu is duidelijk hoe dat komt: het afweersysteem van de knaagdieren werkt heel anders dan dat van ons. Miljarden onderzoeksgeld zijn de afgelopen decennia dus voor niets uitgegeven.[/QUOTE]
Muismodel
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june
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MarcC
Laten we het positieve ervan inzien: nu duidelijk wordt dat muizen niet geschikt zijn als model voor ontstekingen in mensen, moet er iets anders gebruikt worden. En dan zou het zo maar eens kunnen zijn dat men flink dichterbij de oplossing voor het genezen van MS komt.
Vraag is tuurlijk wat dat andere zou kunnen zijn. Testen op mensen zelf?
groetjes, Marc
Vraag is tuurlijk wat dat andere zou kunnen zijn. Testen op mensen zelf?
groetjes, Marc
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Marsei
Lesions and Relapses--Part One
Lesions and Relapses--Part One
Van Marie op [URL="https://www.facebook.com/notes/ccsvi-in ... 9538792211"][U]FB[/U][/URL]: Lesions and Relapses--Part One
[QUOTE]The bottom line is, that for some years, Ebers and his team of researchers have been saying that lesions and relapses are not appropriate surrrogate markers to predict progression in MS. His comments detailed in the link take a pharma-unfriendly position-- by saying that lesions and relapses should no longer be endpoints in MS research. These comments shockingly resulted in the NMSS removing funding of the Sylvia Lawry center where his research was done.[/QUOTE]
[QUOTE]Suppression of lesions seen on MRI does not correlate with MS progression.
He is not the first person to make this observation. Since the early 2000's, epidemiology has shown that relapses and their accompanying lesions are only weakly associated with eventual disability level. [/QUOTE]
[QUOTE]Other researchers notice this too; in progressive MS lesions are not associated with disability and in relapsing MS there is a only a small association.[/QUOTE]
[QUOTE]All MS drugs were approved based on lesion loads and relapse activity. All of the upcoming new drugs use the same criteria.[/QUOTE]
[QUOTE]But there's another way to evaluate MS-- by looking at population studies. We have areas in the world where MS patients are ALL monitored for many years and information about what happens to them over time is recorded for others to review for research purposes. London, Ontario and Lyon, France are two areas where we have decades of information about people with MS that researchers can mine for data to see what is real about MS outside of our theories and assumptions.
What has emerged from this study of thousands of patient years is something really damning for the lesion focus in MS: Because relapses and their associated lesions do not predict MS disability.[/QUOTE]
[QUOTE]Dr. Ebers did the unthinkable; not only did he observe this disconnect, he also had the chutzpah to take this information a step further and say that patients should not be subjected to clinical trials when the outcome is relapses- because such outcome measures do not predict how well the drug works to decrease the only thing that really matters: how disabled a person will become. He also said that the drug companies use relapses as their primary outcome because they know they can make a drug that will show a positive effect when reducing relapses is the endpoint.
Drugs that showed reduction in relapses and lesion loads have now been around long enough to reveal their long term effectivness, and unfortunately they do NOT reduce accumulated progression after sufficient time is allowed to see if real progression (not relapse related losses) was present[/QUOTE]
[QUOTE]But in spite of this other data MS specialists insist on seeing lesions and relapses as the main problem in MS:
1. They adopted the belief that lesions and lesion activity, even silent activity, is always bad and associated with greater disability in a linear fashion ignoring the other data listed above.
2. They also continue to advance the idea that if we stop lesions/relapses we will stop the disease and MS will be managable. They also notice when relapses/lesions are greatly reduced vs pre-treatment then they point to the MRI as proof they are managing patient's long term outcome.
3. They encourage interpretation of current drug failure to stop MS as an problem of tweaking; the drug doesn't do enough or the right kind of immune suppression and therefore invisible inflammatory lesions not seen on MRI invisibly drive the disease. They suggest this requires a different drug or stronger drugs even though they will cause immune deficiency diseases (like PML), believing this is justified because relapse and lesion reduction in current therapies "proves" the beliefs and interpretations are absolutely right.
These assumptions drive our current standard MS model and unfortunately we still see studies focused on these same outcome measures. Sadly, patient experience does not jive with this storyline and the result is a patient who realizes his disease is not "managed"-- causing distrust and frustration with the whole medical community. [/QUOTE]
[QUOTE]This frustration extends to disbelief as each successive wave of ever more toxic drugs come out to once again address relapses and lesion loads. Ignored in this scenario are brain atrophy, grey matter degeneration and the issue of supporting regeneration, perhaps with stem cells or dietary factors that may maximize what is still working. On top of the ignored pile is the issue of circulation, which is well documented over many non-CCSVI studies as poor in MS patients and possibly contributing to our degeneration and poor brain-healing ability. [/QUOTE]
Van Marie op [URL="https://www.facebook.com/notes/ccsvi-in ... 9538792211"][U]FB[/U][/URL]: Lesions and Relapses--Part One
[QUOTE]The bottom line is, that for some years, Ebers and his team of researchers have been saying that lesions and relapses are not appropriate surrrogate markers to predict progression in MS. His comments detailed in the link take a pharma-unfriendly position-- by saying that lesions and relapses should no longer be endpoints in MS research. These comments shockingly resulted in the NMSS removing funding of the Sylvia Lawry center where his research was done.[/QUOTE]
[QUOTE]Suppression of lesions seen on MRI does not correlate with MS progression.
He is not the first person to make this observation. Since the early 2000's, epidemiology has shown that relapses and their accompanying lesions are only weakly associated with eventual disability level. [/QUOTE]
[QUOTE]Other researchers notice this too; in progressive MS lesions are not associated with disability and in relapsing MS there is a only a small association.[/QUOTE]
[QUOTE]All MS drugs were approved based on lesion loads and relapse activity. All of the upcoming new drugs use the same criteria.[/QUOTE]
[QUOTE]But there's another way to evaluate MS-- by looking at population studies. We have areas in the world where MS patients are ALL monitored for many years and information about what happens to them over time is recorded for others to review for research purposes. London, Ontario and Lyon, France are two areas where we have decades of information about people with MS that researchers can mine for data to see what is real about MS outside of our theories and assumptions.
What has emerged from this study of thousands of patient years is something really damning for the lesion focus in MS: Because relapses and their associated lesions do not predict MS disability.[/QUOTE]
[QUOTE]Dr. Ebers did the unthinkable; not only did he observe this disconnect, he also had the chutzpah to take this information a step further and say that patients should not be subjected to clinical trials when the outcome is relapses- because such outcome measures do not predict how well the drug works to decrease the only thing that really matters: how disabled a person will become. He also said that the drug companies use relapses as their primary outcome because they know they can make a drug that will show a positive effect when reducing relapses is the endpoint.
Drugs that showed reduction in relapses and lesion loads have now been around long enough to reveal their long term effectivness, and unfortunately they do NOT reduce accumulated progression after sufficient time is allowed to see if real progression (not relapse related losses) was present[/QUOTE]
[QUOTE]But in spite of this other data MS specialists insist on seeing lesions and relapses as the main problem in MS:
1. They adopted the belief that lesions and lesion activity, even silent activity, is always bad and associated with greater disability in a linear fashion ignoring the other data listed above.
2. They also continue to advance the idea that if we stop lesions/relapses we will stop the disease and MS will be managable. They also notice when relapses/lesions are greatly reduced vs pre-treatment then they point to the MRI as proof they are managing patient's long term outcome.
3. They encourage interpretation of current drug failure to stop MS as an problem of tweaking; the drug doesn't do enough or the right kind of immune suppression and therefore invisible inflammatory lesions not seen on MRI invisibly drive the disease. They suggest this requires a different drug or stronger drugs even though they will cause immune deficiency diseases (like PML), believing this is justified because relapse and lesion reduction in current therapies "proves" the beliefs and interpretations are absolutely right.
These assumptions drive our current standard MS model and unfortunately we still see studies focused on these same outcome measures. Sadly, patient experience does not jive with this storyline and the result is a patient who realizes his disease is not "managed"-- causing distrust and frustration with the whole medical community. [/QUOTE]
[QUOTE]This frustration extends to disbelief as each successive wave of ever more toxic drugs come out to once again address relapses and lesion loads. Ignored in this scenario are brain atrophy, grey matter degeneration and the issue of supporting regeneration, perhaps with stem cells or dietary factors that may maximize what is still working. On top of the ignored pile is the issue of circulation, which is well documented over many non-CCSVI studies as poor in MS patients and possibly contributing to our degeneration and poor brain-healing ability. [/QUOTE]
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joge
Tja, probeer dat neurologenparadigma maar eens te veranderen... Dat kost een paar generaties neuro's vrees ik. Artsen en farmaceuten houden elkaar in een soort houdgreep. Loslaten is gezichtsverlies?
Ondertussen staat de patiënt aan de zijlijn vergeefs te wachten op een concept dat echt werkt. Jammer.
Ondertussen staat de patiënt aan de zijlijn vergeefs te wachten op een concept dat echt werkt. Jammer.
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Marsei
Lesions and Relapses- Part Two
Lesions and Relapses- Part Two
[URL="https://www.facebook.com/notes/ccsvi-in ... 9646747211"][U]Deel 2[/U][/URL]: Lesions and Relapses
[URL="https://www.facebook.com/notes/ccsvi-in ... 9646747211"][U]Deel 2[/U][/URL]: Lesions and Relapses
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Marsei
MS muis model is niet hetzelfde als MS bij mensen
MS muis model is niet hetzelfde als MS bij mensen
X-Ray Phase Contrast Tomography Reveals [URL="https://www.ncbi.nlm.nih.gov/pubmed/28724999"][U]Early Vascular Alterations and Neuronal Loss in a Multiple Sclerosis Model[/U][/URL]
[QUOTE][B]Abstract[/B]
The degenerative effects of multiple sclerosis at the level of the vascular and neuronal networks in the central nervous system are currently the object of intensive investigation. Preclinical studies have demonstrated the efficacy of mesenchymal stem cell (MSC) therapy in experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis, but the neuropathology of specific lesions in EAE and the effects of MSC treatment are under debate.
Because conventional imaging techniques entail protocols that alter the tissues, limiting the reliability of the results, we have used non-invasive X-ray phase-contrast tomography to obtain an unprecedented direct 3D characterization of EAE lesions at micro-to-nano scales, with simultaneous imaging of the vascular and neuronal networks.
We reveal EAE-mediated alterations down to the capillary network. Our findings shed light on how the disease and MSC treatment affect the tissues, and promote X-ray phase-contrast tomography as a powerful tool for studying neurovascular diseases and monitoring advanced therapies.[/QUOTE]
X-Ray Phase Contrast Tomography Reveals [URL="https://www.ncbi.nlm.nih.gov/pubmed/28724999"][U]Early Vascular Alterations and Neuronal Loss in a Multiple Sclerosis Model[/U][/URL]
[QUOTE][B]Abstract[/B]
The degenerative effects of multiple sclerosis at the level of the vascular and neuronal networks in the central nervous system are currently the object of intensive investigation. Preclinical studies have demonstrated the efficacy of mesenchymal stem cell (MSC) therapy in experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis, but the neuropathology of specific lesions in EAE and the effects of MSC treatment are under debate.
Because conventional imaging techniques entail protocols that alter the tissues, limiting the reliability of the results, we have used non-invasive X-ray phase-contrast tomography to obtain an unprecedented direct 3D characterization of EAE lesions at micro-to-nano scales, with simultaneous imaging of the vascular and neuronal networks.
We reveal EAE-mediated alterations down to the capillary network. Our findings shed light on how the disease and MSC treatment affect the tissues, and promote X-ray phase-contrast tomography as a powerful tool for studying neurovascular diseases and monitoring advanced therapies.[/QUOTE]
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zeiler
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Moderator