Bhupesh Prusty: "we are on a perfect path for identifying potential transferable factors in ME/CFS blood that can cause mito dysfunction..." GoFundMe
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Treeman
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They found viruses and gave her treatments that cured her. No they didn't specifically say anti viral. I also read an article with the girl, which I can no longer find where she said she took anti virals that cured her. It used to be on the Stanford Medicine ME/CFS Initiative web site.
"Martin Lerner became acquainted with Chronic Fatigue Syndrome in a very direct way: he caught it in 1988 and was disabled by it until 1996. He recovered using valtrex, an antiviral." After that he went back to work and died working at the age of 86 in 2015. I think that’s one example of a cure.
https://www.healthrising.org/chronic-fatigue-syndrome-mecfs-doctor-resource-center/dr-martin-lerner/
If you don't want to believe it please yourself.
gbells
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I disagree. Latent HSV6 and EBV infection is common in the population and they remain in latent states reactivating occasionally. A 2006 study by Chapenco found that ME patients had a higher rate of dual infections vs controls:
These viruses are anti-apoptotic so that means that a virus which normally be limited to one area of the body can now spread to other tissues provided they are primed by the other virus. A large accumulation of virally seeded tissue is a big energy drain and inflammation trigger. However, if there is a high antibody count there shouldn't be detectable viral DNA. I'm not saying that I think antivirals are worth taking but that the viruses are the underlying mechanism for ME.
gbells
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For the RNA virus Covid-19.
andyguitar
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At 3.25 min on the video inflammation is reffered to as the "core" of the illness.
andyguitar
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Lerner took antivirals for years. As his illness could have just got better on it's own during that time his case is not evidence of anything.
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Treeman
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As I said before, If you don't want to believe it please yourself
Treeman
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6 years, so he lived another 19 cured without taking them.
ME/CFS is an illness where there is little evidence of anything if I’m honest, that’s why I’m here. I'm just passing on information that some people diagnosed with ME/CFS who have taken anti virals after finding high viral loads, inform they have recovered and/or being cured. I believe them, I'm accepting people’s accounts, including respected former members of the medical ME/CFS community. As many have said, ME/CFS probably has many route causes, I’m not ruling any of them out in the hope that at least one sufferer (including me) could recover from a specific treatment.
MonkeyMan
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Here's more evidence of the relationship between mitochondrial fragmentation (Prusty) and neuroinflammation (Younger). The same treatment described earlier (P110) is discussed here. I wonder if we patients could get our hands on P110 on an experimental basis? And I wonder if Ron Davis has tested this stuff in his nanoneedle (esp. given that Mochly-Rosen is his colleague at Stanford).
https://med.stanford.edu/news/all-n...ed-in-several-neurodegenerative-diseases.html
Achilles’ heel identified in several neurodegenerative diseases
A Stanford research team has identified an oddball way brain cells spread inflammation in several neurodegenerative diseases — and an approach that could counter them all.
Sep 23 2019
Daria Mochly-Rosen is the senior author of a study that implicates two types of normally protective brain cells called glial cells in tripping off neuronal destruction.
Many neurodegenerative diseases have a common feature that may make them amenable to the same treatment, investigators at the Stanford University School of Medicine have found.
“We’ve identified a potential new way to reduce nerve-cell death in a number of diseases characterized by such losses,” said Daria Mochly-Rosen, PhD, professor of chemical and systems biology at Stanford.
A paper describing the researchers’ findings was published today in Nature Neuroscience. Mochly-Rosen is the senior author. The lead author is postdoctoral scholar Amit Joshi, PhD.
Alzheimer’s disease, Huntington’s disease and amyotrophic lateral sclerosis, or Lou Gehrig’s disease, share a common mode of damaging brain cells, the scientists learned in studying both human cells in culture and mouse models of the diseases. This damage can be blocked by administering a substance that inhibits a critical step in that process.
The new study implicates two types of normally protective brain cells called glial cells in tripping off neuronal destruction: Microglia monitor the brain for potential trouble — say, signs of tissue injury or the presence of invading microbial pathogens — and scavenge debris left behind by dying cells or protein aggregates. Astrocytes, which outnumber the brain’s neurons nearly 5 to 1, release growth factors, provide essential metabolites and determine the number and placement of the connections neurons make with one another.
Neuronal bits and fragments are perceived as foreign and targeted for clearance by microglia. But a vicious cycle of glial-cell activation and inflammation can occur in the absence of neuronal debris.
Mochly-Rosen, the George D. Smith Professor in Translational Medicine, and her colleagues discovered that mitochondria, essential components of cells, were conveying deleterious signals from microglia to astrocytes and from astrocytes to neurons. Mitochondria are tiny power packs: They furnish cells with energy. A typical nerve cell contains thousands of them. Their ability to communicate death signals from one cell to another was unexpected.
Convoluted tubular networks
Viewed close up, mitochondria are convoluted tubular networks that are perpetually being right-sized in a dynamic dance of fusion and fission, performed by opposing assemblies of enzymes. Mitochondria frequently get shuffled around from one part of a cell to another and must shift their shapes accordingly to accommodate their environments: Too much fusion, and they become too tubby to get around or work well. Too much fission, and they break up into dysfunctional fragments.
An enzyme called Drp1 that facilitates mitochondrial fission can be catapulted into hyperactivity by neurotoxic protein aggregates such as those linked to Alzheimer’s, Parkinson’s or Huntington’s diseases or to amyotrophic lateral sclerosis. About seven years ago, Mochly-Rosen’s team designed a tiny protein snippet, or peptide, called P110, that specifically blocks Drp1-induced mitochondrial fission when it’s proceeding at an excessive pace, as happens when a cell is damaged.
The study showed that sustained P110 treatment via a subcutaneous pump over periods of several months lowered the microglial and astrocytic activation and inflammation in the brains of mice.
Then, experimenting with microglia in culture, the researchers introduced toxic proteins that cause different neurodegenerative diseases. Each of these manipulations kicked the microglia into an inflamed state, and they released, into the broth they were bathed in, something that could trip off inflammatory responses in astrocytes. But adding P110 to the microglial culture dishes substantially dialed down this subsequent transfer of microglial inflammation to the astrocytes. Something the microglia had expelled was providing the signal.
Likewise, something in the culture broth in which inflamed astrocytes had been immersed killed neurons. But P110 blunted that destruction, as well. Additional experiments showed that both types of glial cells were expelling damaged mitochondria into the broth.
'Lethal for nearby neurons'
“Most people have thought that mitochondria situated outside of cells must be ghosts of dead or dying cells,” Mochly-Rosen said. “But we found plenty of high-functioning mitochondria in the culture broth, along with damaged ones. And the glial cells releasing them appear very much alive.”
As has been recently reported, even healthy cells routinely release mitochondria into their surrounding environment. This can be beneficial if those mitochondria are healthy, too. However, the mitochondria released by inflamed microglia and astrocytes were more apt to be damaged. When expelled mitochondria are in bad shape, it’s lethal for nearby neurons.
Blocking this mitochondrial fragmentation with P110 in the microglia or in the astrocytes was enough to significantly reduce neuronal death.
How do expelled mitochondria that are damaged produce inflammation and neuronal cell death? “We’re working hard to find that out,” she said.
Joshi and Mochly-Rosen have filed for a patent on P110 and its utility in Huntington’s disease, ALS and other neurodegenerative diseases.
Mochly-Rosen is a member of Stanford Bio-X, the Stanford Cardiovascular Institute, the Stanford Maternal & Child Health Research Institute, the Stanford Cancer Institute and the Wu Tsai Neurosciences Institute at Stanford, a faculty fellow of Stanford ChEM-H, and founder and co-director of SPARK At Stanford and the founder and president of SPARK Global.
Other Stanford co-authors of the study are medical student Paras Minhas; former postdoctoral scholar Shane Liddelow, PhD; Bereketeab Haileselassie, MD, instructor in pediatric clinical care medicine; and Katrin Andreasson, MD, professor of neurology and neurological sciences. Researchers from the Washington University School of Medicine also contributed to the study.
The study is dedicated to the memory of the late Stanford neuroscientist Ben Barres, MD, PhD, who first identified many of the crucial roles of glial cells.
The work was funded by the National Institutes of Health (grants R01HL52141, R01AG058047, R01AG058047 and R35HL135736), a Stanford Discovery Innovation Award, the Paul & Daisy Soros Foundation and the Glenn Foundation.
Stanford’s Department of Chemical and Systems Biology also supported the work.
https://med.stanford.edu/news/all-n...ed-in-several-neurodegenerative-diseases.html
Achilles’ heel identified in several neurodegenerative diseases
A Stanford research team has identified an oddball way brain cells spread inflammation in several neurodegenerative diseases — and an approach that could counter them all.
Sep 23 2019
Daria Mochly-Rosen is the senior author of a study that implicates two types of normally protective brain cells called glial cells in tripping off neuronal destruction.
Many neurodegenerative diseases have a common feature that may make them amenable to the same treatment, investigators at the Stanford University School of Medicine have found.
“We’ve identified a potential new way to reduce nerve-cell death in a number of diseases characterized by such losses,” said Daria Mochly-Rosen, PhD, professor of chemical and systems biology at Stanford.
A paper describing the researchers’ findings was published today in Nature Neuroscience. Mochly-Rosen is the senior author. The lead author is postdoctoral scholar Amit Joshi, PhD.
Alzheimer’s disease, Huntington’s disease and amyotrophic lateral sclerosis, or Lou Gehrig’s disease, share a common mode of damaging brain cells, the scientists learned in studying both human cells in culture and mouse models of the diseases. This damage can be blocked by administering a substance that inhibits a critical step in that process.
The new study implicates two types of normally protective brain cells called glial cells in tripping off neuronal destruction: Microglia monitor the brain for potential trouble — say, signs of tissue injury or the presence of invading microbial pathogens — and scavenge debris left behind by dying cells or protein aggregates. Astrocytes, which outnumber the brain’s neurons nearly 5 to 1, release growth factors, provide essential metabolites and determine the number and placement of the connections neurons make with one another.
Neuronal bits and fragments are perceived as foreign and targeted for clearance by microglia. But a vicious cycle of glial-cell activation and inflammation can occur in the absence of neuronal debris.
Mochly-Rosen, the George D. Smith Professor in Translational Medicine, and her colleagues discovered that mitochondria, essential components of cells, were conveying deleterious signals from microglia to astrocytes and from astrocytes to neurons. Mitochondria are tiny power packs: They furnish cells with energy. A typical nerve cell contains thousands of them. Their ability to communicate death signals from one cell to another was unexpected.
Convoluted tubular networks
Viewed close up, mitochondria are convoluted tubular networks that are perpetually being right-sized in a dynamic dance of fusion and fission, performed by opposing assemblies of enzymes. Mitochondria frequently get shuffled around from one part of a cell to another and must shift their shapes accordingly to accommodate their environments: Too much fusion, and they become too tubby to get around or work well. Too much fission, and they break up into dysfunctional fragments.
An enzyme called Drp1 that facilitates mitochondrial fission can be catapulted into hyperactivity by neurotoxic protein aggregates such as those linked to Alzheimer’s, Parkinson’s or Huntington’s diseases or to amyotrophic lateral sclerosis. About seven years ago, Mochly-Rosen’s team designed a tiny protein snippet, or peptide, called P110, that specifically blocks Drp1-induced mitochondrial fission when it’s proceeding at an excessive pace, as happens when a cell is damaged.
The study showed that sustained P110 treatment via a subcutaneous pump over periods of several months lowered the microglial and astrocytic activation and inflammation in the brains of mice.
Then, experimenting with microglia in culture, the researchers introduced toxic proteins that cause different neurodegenerative diseases. Each of these manipulations kicked the microglia into an inflamed state, and they released, into the broth they were bathed in, something that could trip off inflammatory responses in astrocytes. But adding P110 to the microglial culture dishes substantially dialed down this subsequent transfer of microglial inflammation to the astrocytes. Something the microglia had expelled was providing the signal.
Likewise, something in the culture broth in which inflamed astrocytes had been immersed killed neurons. But P110 blunted that destruction, as well. Additional experiments showed that both types of glial cells were expelling damaged mitochondria into the broth.
'Lethal for nearby neurons'
“Most people have thought that mitochondria situated outside of cells must be ghosts of dead or dying cells,” Mochly-Rosen said. “But we found plenty of high-functioning mitochondria in the culture broth, along with damaged ones. And the glial cells releasing them appear very much alive.”
As has been recently reported, even healthy cells routinely release mitochondria into their surrounding environment. This can be beneficial if those mitochondria are healthy, too. However, the mitochondria released by inflamed microglia and astrocytes were more apt to be damaged. When expelled mitochondria are in bad shape, it’s lethal for nearby neurons.
Blocking this mitochondrial fragmentation with P110 in the microglia or in the astrocytes was enough to significantly reduce neuronal death.
How do expelled mitochondria that are damaged produce inflammation and neuronal cell death? “We’re working hard to find that out,” she said.
Joshi and Mochly-Rosen have filed for a patent on P110 and its utility in Huntington’s disease, ALS and other neurodegenerative diseases.
Mochly-Rosen is a member of Stanford Bio-X, the Stanford Cardiovascular Institute, the Stanford Maternal & Child Health Research Institute, the Stanford Cancer Institute and the Wu Tsai Neurosciences Institute at Stanford, a faculty fellow of Stanford ChEM-H, and founder and co-director of SPARK At Stanford and the founder and president of SPARK Global.
Other Stanford co-authors of the study are medical student Paras Minhas; former postdoctoral scholar Shane Liddelow, PhD; Bereketeab Haileselassie, MD, instructor in pediatric clinical care medicine; and Katrin Andreasson, MD, professor of neurology and neurological sciences. Researchers from the Washington University School of Medicine also contributed to the study.
The study is dedicated to the memory of the late Stanford neuroscientist Ben Barres, MD, PhD, who first identified many of the crucial roles of glial cells.
The work was funded by the National Institutes of Health (grants R01HL52141, R01AG058047, R01AG058047 and R35HL135736), a Stanford Discovery Innovation Award, the Paul & Daisy Soros Foundation and the Glenn Foundation.
Stanford’s Department of Chemical and Systems Biology also supported the work.
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gbells
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Actually according to your theory we just need to create nanobot mitochondria to spit out ATP to replace the missing ones. Of course that wouldn't stop the underlying inflammation.
Here's more evidence of the relationship between mitochondrial fragmentation (Prusty) and neuroinflammation (Younger). The same treatment described earlier (P110) is discussed here. I wonder if we patients could get our hands on P110 on an experimental basis? And I wonder if Ron Davis has tested this stuff in his nanoneedle (esp. given that Mochly-Rosen is his colleague at Stanford).
https://med.stanford.edu/news/all-n...ed-in-several-neurodegenerative-diseases.html
Achilles’ heel identified in several neurodegenerative diseases
A Stanford research team has identified an oddball way brain cells spread inflammation in several neurodegenerative diseases — and an approach that could counter them all.
Sep 23 2019
Daria Mochly-Rosen is the senior author of a study that implicates two types of normally protective brain cells called glial cells in tripping off neuronal destruction.
Many neurodegenerative diseases have a common feature that may make them amenable to the same treatment, investigators at the Stanford University School of Medicine have found.
“We’ve identified a potential new way to reduce nerve-cell death in a number of diseases characterized by such losses,” said Daria Mochly-Rosen, PhD, professor of chemical and systems biology at Stanford.
A paper describing the researchers’ findings was published today in Nature Neuroscience. Mochly-Rosen is the senior author. The lead author is postdoctoral scholar Amit Joshi, PhD.
Alzheimer’s disease, Huntington’s disease and amyotrophic lateral sclerosis, or Lou Gehrig’s disease, share a common mode of damaging brain cells, the scientists learned in studying both human cells in culture and mouse models of the diseases. This damage can be blocked by administering a substance that inhibits a critical step in that process.
The new study implicates two types of normally protective brain cells called glial cells in tripping off neuronal destruction: Microglia monitor the brain for potential trouble — say, signs of tissue injury or the presence of invading microbial pathogens — and scavenge debris left behind by dying cells or protein aggregates. Astrocytes, which outnumber the brain’s neurons nearly 5 to 1, release growth factors, provide essential metabolites and determine the number and placement of the connections neurons make with one another.
Neuronal bits and fragments are perceived as foreign and targeted for clearance by microglia. But a vicious cycle of glial-cell activation and inflammation can occur in the absence of neuronal debris.
Mochly-Rosen, the George D. Smith Professor in Translational Medicine, and her colleagues discovered that mitochondria, essential components of cells, were conveying deleterious signals from microglia to astrocytes and from astrocytes to neurons. Mitochondria are tiny power packs: They furnish cells with energy. A typical nerve cell contains thousands of them. Their ability to communicate death signals from one cell to another was unexpected.
Convoluted tubular networks
Viewed close up, mitochondria are convoluted tubular networks that are perpetually being right-sized in a dynamic dance of fusion and fission, performed by opposing assemblies of enzymes. Mitochondria frequently get shuffled around from one part of a cell to another and must shift their shapes accordingly to accommodate their environments: Too much fusion, and they become too tubby to get around or work well. Too much fission, and they break up into dysfunctional fragments.
An enzyme called Drp1 that facilitates mitochondrial fission can be catapulted into hyperactivity by neurotoxic protein aggregates such as those linked to Alzheimer’s, Parkinson’s or Huntington’s diseases or to amyotrophic lateral sclerosis. About seven years ago, Mochly-Rosen’s team designed a tiny protein snippet, or peptide, called P110, that specifically blocks Drp1-induced mitochondrial fission when it’s proceeding at an excessive pace, as happens when a cell is damaged.
The study showed that sustained P110 treatment via a subcutaneous pump over periods of several months lowered the microglial and astrocytic activation and inflammation in the brains of mice.
Then, experimenting with microglia in culture, the researchers introduced toxic proteins that cause different neurodegenerative diseases. Each of these manipulations kicked the microglia into an inflamed state, and they released, into the broth they were bathed in, something that could trip off inflammatory responses in astrocytes. But adding P110 to the microglial culture dishes substantially dialed down this subsequent transfer of microglial inflammation to the astrocytes. Something the microglia had expelled was providing the signal.
Likewise, something in the culture broth in which inflamed astrocytes had been immersed killed neurons. But P110 blunted that destruction, as well. Additional experiments showed that both types of glial cells were expelling damaged mitochondria into the broth.
'Lethal for nearby neurons'
“Most people have thought that mitochondria situated outside of cells must be ghosts of dead or dying cells,” Mochly-Rosen said. “But we found plenty of high-functioning mitochondria in the culture broth, along with damaged ones. And the glial cells releasing them appear very much alive.”
As has been recently reported, even healthy cells routinely release mitochondria into their surrounding environment. This can be beneficial if those mitochondria are healthy, too. However, the mitochondria released by inflamed microglia and astrocytes were more apt to be damaged. When expelled mitochondria are in bad shape, it’s lethal for nearby neurons.
Blocking this mitochondrial fragmentation with P110 in the microglia or in the astrocytes was enough to significantly reduce neuronal death.
How do expelled mitochondria that are damaged produce inflammation and neuronal cell death? “We’re working hard to find that out,” she said.
Joshi and Mochly-Rosen have filed for a patent on P110 and its utility in Huntington’s disease, ALS and other neurodegenerative diseases.
Mochly-Rosen is a member of Stanford Bio-X, the Stanford Cardiovascular Institute, the Stanford Maternal & Child Health Research Institute, the Stanford Cancer Institute and the Wu Tsai Neurosciences Institute at Stanford, a faculty fellow of Stanford ChEM-H, and founder and co-director of SPARK At Stanford and the founder and president of SPARK Global.
Other Stanford co-authors of the study are medical student Paras Minhas; former postdoctoral scholar Shane Liddelow, PhD; Bereketeab Haileselassie, MD, instructor in pediatric clinical care medicine; and Katrin Andreasson, MD, professor of neurology and neurological sciences. Researchers from the Washington University School of Medicine also contributed to the study.
The study is dedicated to the memory of the late Stanford neuroscientist Ben Barres, MD, PhD, who first identified many of the crucial roles of glial cells.
The work was funded by the National Institutes of Health (grants R01HL52141, R01AG058047, R01AG058047 and R35HL135736), a Stanford Discovery Innovation Award, the Paul & Daisy Soros Foundation and the Glenn Foundation.
Stanford’s Department of Chemical and Systems Biology also supported the work.
@Janet Dafoe
@gbells I used the wrong termination there. I didn’t mean none, like none at all, more like not active. The infection rate of all herpes viruses is at near 100% for 18y olds.
As long as we don’t know the real cause of Cfs we should at least try to treat the things we know are wrong right now. The latest lead is mitochondrial fission fusion is disturbed to a point where it could be a big deal. Maybe a year from now this all sounds stupid again if you read it then. But for now it’s worth trying to treat it and see what happens. At least better than taking antivirals for years as a placebo.
As long as we don’t know the real cause of Cfs we should at least try to treat the things we know are wrong right now. The latest lead is mitochondrial fission fusion is disturbed to a point where it could be a big deal. Maybe a year from now this all sounds stupid again if you read it then. But for now it’s worth trying to treat it and see what happens. At least better than taking antivirals for years as a placebo.
gbells
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Sure, have at it.
ljimbo423
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This is a study done by Jose Montoya. Who is a big advocate of viral reactivations being behind ME/CFS.
Note that he uses elevated IgG antibody titers against HHV-6 and EBV as criteria for the study and treatment. However, in the next to the last paragraph, he says
"Viral IgG antibody titers did not differ between arms" after treatment.
To me this says the valganciclovir did not treat the viruses/high antibody titers. So it must have worked in some other way. It doesn't make sense to me that he would use high antibody titers for establishing the cause of these patients ME/CFS and criteria for treatment.
Treat them, note that there was improvement, then say the improvement might be caused by an "antiviral effect", when there was no change in the antibody titer levels. If the antivirals were treating actual HHV-6 or EBV reactivations, it seems to me the high IGG antibody levels would drop but they didn't.
He does say that immunomodulation could be the cause for improvement in the patients and I think he's right about that.
Note that he uses elevated IgG antibody titers against HHV-6 and EBV as criteria for the study and treatment. However, in the next to the last paragraph, he says
"Viral IgG antibody titers did not differ between arms" after treatment.
To me this says the valganciclovir did not treat the viruses/high antibody titers. So it must have worked in some other way. It doesn't make sense to me that he would use high antibody titers for establishing the cause of these patients ME/CFS and criteria for treatment.
Treat them, note that there was improvement, then say the improvement might be caused by an "antiviral effect", when there was no change in the antibody titer levels. If the antivirals were treating actual HHV-6 or EBV reactivations, it seems to me the high IGG antibody levels would drop but they didn't.
He does say that immunomodulation could be the cause for improvement in the patients and I think he's right about that.
Source
@MonkeyMan
p110 wasn't tested in any human yet. So it would be a long long way as a treatment. But could be of interesting for Ron or Prusty to test in the lab.
p110 wasn't tested in any human yet. So it would be a long long way as a treatment. But could be of interesting for Ron or Prusty to test in the lab.
andyguitar
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Yes I expect it's immunomodulation that is providing the benefit. But exactly what is happening is a tough nut to crack. If anyone can come up with something that has the same (as yet unknown) effect then this puzzle might be solved. At least for some. The closest I got was Interleukin 10 levels being raised by some antivirals. IL 10 has been found to be low in me/cfs. But it's also been found to be high!! Which is it?
ljimbo423
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Very true!
This might be the biggest stumbling block in ME/CFS research. Consistent findings in multiple studies is very hard to find. Often, as you point out, they are contradictory.
gbells
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Bingo. It's just an expensive anti-inflammatory drug.
Ding, Zhaoqing; Mathur, Vidhu; Ho, Peggy P.; James, Michelle L.; Lucin, Kurt M.; Hoehne, Aileen; Alabsi, Haitham; Gambhir, Sanjiv S.; Steinman, Lawrence (Feb 10, 2014). "Antiviral drug ganciclovir is a potent inhibitor of microglial proliferation and neuroinflammation". The Journal of Experimental Medicine. 211 (2): 189–198. doi:10.1084/jem.20120696. ISSN 1540-9538. PMC 3920559
gbells
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Honestly, I think some of us are already going this using time released curcumin which surpresses inflammation and a low inflammation diet. It helps lower inflammatory pain but is no ME wondercure.