A Post Infectious Illness?
Some time ago we looked at post-infectious illnesses. From Giardia to Epstein-Barr Virus (infectious mononucleosis) to the Ebola virus we found that significant numbers of people who remain sick after an infection have been mostly been left adrift by the medical profession.
Those diseases are bad news but Alzheimer's - striking over five million people in the U.S. - a number that will only grow - is on a different level, altogether. Alzheimer's is a disease that can't be ignored; it's causing too much misery and expense for that. Recent evidence suggests, to most researchers surprise, that it could be another post-infectious illness.
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[/fright]The hypothesis suggests that even a mild infection could result in Alzheimer's. The scenario goes like this: some pathogen (a virus, bacteria or fungi) sneaks into the brain through a leaky blood-brain barrier. The immune cells in the brain surround the pathogen and block it off by building a protein wall build out of amyloid proteins. The pathogen dies and disappears - but the amyloid deposits are left behind in patients who have difficulty removing them.
Robert Moir of Harvard noticed that a similar process occurs in the body; the immune system typically immobilizes invaders by building walls around them and then attacks them. Moir asked why that process might not be happening in the brain as well. Could amyloid, he asked, have beneficial effects?
When Moir injected salmonella into the brains of mice that did not produce amyloid they died while mice able to produce amyloid plaques survived. In fact, the amyloid deposits appeared almost overnight- and at the center of each was a bacterium. That was the game-changer; the amyloid at the heart of Alzheimer’s appears to be the result of an immune reaction to a pathogen.
That's a pretty shocking finding for Alzheimer's researchers. A recent overview of the immune system's role in AD never mentioned pathogens at all.
could redefine how we understand Alzheimer’s disease. More interesting for people with ME/CFS is the fact that the pathogen at the heart of Alzheimer’s is mostly like a herpesvirus (but could also be the bacteria that causes Lyme disease, or candida or spirochetes.)
The Danger of Unaddressed Assumptions
It took a researcher who looked behind the assumption that amyloids were some sort of waste product to get to this point. Unaddressed assumptions, of course, have gotten the medical profession in deep water many times before. Consider the tragic history of radical mastectomies (RM's). From 1895 to the 1970's the gold standard for treatment of breast cancer was the radical mastectomy; a procedure in which the breast, the chest muscles around the breast and sometimes the lymph nodes were removed. Not only was the procedure disfiguring but it could leave a woman in pain for the rest of her life.
[fleft]
[/fleft]The hypothesis behind RM's seemed to make sense. If cancer expanded exponentially from a focal point it made sense to clear out as much tissue as possible. That assumption was false, however. It turns out that cancer does not expand exponentially from a central point. When cancer's become malignant they grow in one place and then spread to different parts of the body. The massive amounts of tissue the surgeons were removing had no effect, whatsoever, in spreading the cancer.
The tragedy was that much pain could have been avoided if the medical profession had been willing to question it’s strongly held beliefs. Questions about the effectiveness of radical mastectomy were raised early by surgeons who had data showing that a less invasive technique was equally as effective. (See the Biography of Cancer").
The surgical communities resistance to employing less invasive techniques, however, meant it took decades to mount a full study. In the end it took just one large, well-designed study to prove that radical mastectomies were unnecessary. Once that happened the practice of treating breast cancer with radical mastectomies essentially disappeared; they are rarely performed anymore.
A Herpesvirus Disease?
Now it may be Alzheimer's turn. The possibility that an infection – a herpes virus infection, no less – triggers Alzheimer’s Disease is actually nothing new.
Two years ago, a clearly frustrated Dr. Ruth Itzhaki of the University of Manchester in the U.K., wrote a review article claiming that there’s a strong likelihood that herpes simplex virus contributes to Alzheimer’s.
Herpes simplex virus type 1 and Alzheimer’s disease: increasing evidence for a major role of the virus. Ruth F. Itzhaki, Frontiers in Aging Neuroscience www.frontiersin.org August 2014 | Volume 6 | Article 202 | 1
She felt that three 10-20 year-old publications had unduly influenced the field. Beliefs had hardened into dogma and once that dogma was set nothing - not even studies to the contrary - could shake it.
Positive studies, and she cites 37 of them, had not, she felt, been given their due. In fact, Itzhaki believes that the link between chronic HSV infection and Alzheimer’s is so strong that she can’t believe that there’s anything controversial about it.
[fright]
[/fright]The problem Itzahki believes is that the medical field in general resists the idea that infections play any role in chronic diseases. Itzahki believes several misconception about pathogens have contributed to the misunderstanding.
Plus the dogma in the medical world is that the microglia and the innate immune response in the brain are part of a disease's progression - not the cause of the disease itself. It's believed that T and B-cells that gain entry to the central nervous system actually initiate the disease process. But there's no evidence that T and B-cells play a strong role in Alzheimer's; instead the innate immune system and the microglia - the two sentinels on watch for pathogens in the brain - are going gang-busters.
Years before the Harvard researchers showed that viruses cause the immune system to produce amyloid depositions in the brain, Itzaki and others showed that HSV causes amyloid products to appear. They also showed that anti-herpesvirus drugs such as valacyclovir reduced the accumulation of amyloid deposits in cell cultures.
Funding for antiviral trials in humans, however, has been denied both at the federal level and by drug companies. This is despite the fact no drugs effectively target disease progression in AD; it remains an essentially untreatable disease.
If the amyloid-infection connection wins out, though, antivirals and antibiotics could be become first-line treatments. Doctors would either find ways to remove the amyloid deposits or prevent them from being posited in the first place.
First, though, researchers have to examine be brains of Alzheimer's patients more closely to identify the pathogens they would want to target. In that they're lucky - they have lots of brain tissue to study.
There's little evidence to suggest that amyloid deposits play a role in ME/CFS or fibromyalgia. (Evidence of amyloid deposits was found Dr. Baraniuk's proteome study but that finding has not been validated.)
The role herpesviruses play in ME/CFS or FM is not clear either but the potential is there. Dr. Pridgen has found herpes simplex viruses in the gut tissues of fibromyalgia patients. A cadaver study found herpes simplex infections in the nerves of about a third of the cadavers studied. We know that HSV reactivation causes canker sores in the mouth and genital herpes and ocular herpes. In the brain it can produce encephalitis. If Itzaki is right it may even be triggering Alzheimer's.
We don’t know that herpesviruses are causing ME/CFS or FM, but if they or another pathogen end up triggering AD the impact on ME/CFS or fibromyalgia could be large.
Given AD's prevalence and cost to society efforts would surely be made to develop more effective herpesvirus drugs. It's possible that better diagnostic tests for herpesviruses could be developed as well. The role that the immune response plays in chronic illness would be highlighted as well, and post-infectious illnesses might finally start to get their due in the medical community.
The evidence presented here for the presence of HSV1 in the elderly human brain, for its reactivation there, its interference with cellular processes and its harmful effects on cognition,is very strong. Itzhaki
Some time ago we looked at post-infectious illnesses. From Giardia to Epstein-Barr Virus (infectious mononucleosis) to the Ebola virus we found that significant numbers of people who remain sick after an infection have been mostly been left adrift by the medical profession.
Those diseases are bad news but Alzheimer's - striking over five million people in the U.S. - a number that will only grow - is on a different level, altogether. Alzheimer's is a disease that can't be ignored; it's causing too much misery and expense for that. Recent evidence suggests, to most researchers surprise, that it could be another post-infectious illness.
[fright]
Robert Moir of Harvard noticed that a similar process occurs in the body; the immune system typically immobilizes invaders by building walls around them and then attacks them. Moir asked why that process might not be happening in the brain as well. Could amyloid, he asked, have beneficial effects?
When Moir injected salmonella into the brains of mice that did not produce amyloid they died while mice able to produce amyloid plaques survived. In fact, the amyloid deposits appeared almost overnight- and at the center of each was a bacterium. That was the game-changer; the amyloid at the heart of Alzheimer’s appears to be the result of an immune reaction to a pathogen.
That's a pretty shocking finding for Alzheimer's researchers. A recent overview of the immune system's role in AD never mentioned pathogens at all.
could redefine how we understand Alzheimer’s disease. More interesting for people with ME/CFS is the fact that the pathogen at the heart of Alzheimer’s is mostly like a herpesvirus (but could also be the bacteria that causes Lyme disease, or candida or spirochetes.)
The Danger of Unaddressed Assumptions
It took a researcher who looked behind the assumption that amyloids were some sort of waste product to get to this point. Unaddressed assumptions, of course, have gotten the medical profession in deep water many times before. Consider the tragic history of radical mastectomies (RM's). From 1895 to the 1970's the gold standard for treatment of breast cancer was the radical mastectomy; a procedure in which the breast, the chest muscles around the breast and sometimes the lymph nodes were removed. Not only was the procedure disfiguring but it could leave a woman in pain for the rest of her life.
[fleft]
The tragedy was that much pain could have been avoided if the medical profession had been willing to question it’s strongly held beliefs. Questions about the effectiveness of radical mastectomy were raised early by surgeons who had data showing that a less invasive technique was equally as effective. (See the Biography of Cancer").
The surgical communities resistance to employing less invasive techniques, however, meant it took decades to mount a full study. In the end it took just one large, well-designed study to prove that radical mastectomies were unnecessary. Once that happened the practice of treating breast cancer with radical mastectomies essentially disappeared; they are rarely performed anymore.
A Herpesvirus Disease?
Now it may be Alzheimer's turn. The possibility that an infection – a herpes virus infection, no less – triggers Alzheimer’s Disease is actually nothing new.
Two years ago, a clearly frustrated Dr. Ruth Itzhaki of the University of Manchester in the U.K., wrote a review article claiming that there’s a strong likelihood that herpes simplex virus contributes to Alzheimer’s.
Herpes simplex virus type 1 and Alzheimer’s disease: increasing evidence for a major role of the virus. Ruth F. Itzhaki, Frontiers in Aging Neuroscience www.frontiersin.org August 2014 | Volume 6 | Article 202 | 1
She felt that three 10-20 year-old publications had unduly influenced the field. Beliefs had hardened into dogma and once that dogma was set nothing - not even studies to the contrary - could shake it.
Positive studies, and she cites 37 of them, had not, she felt, been given their due. In fact, Itzhaki believes that the link between chronic HSV infection and Alzheimer’s is so strong that she can’t believe that there’s anything controversial about it.
[fright]
- The first is the dogma that pathogens only cause temporary problems.
- The second is the idea that the immune system reacts in a consistent way to pathogens. Itzaki asserts that the response to pathogens is very variable in the population; some people beat a particular pathogen off with no trouble while others can get very sick and others have middle of the road responses.
Plus the dogma in the medical world is that the microglia and the innate immune response in the brain are part of a disease's progression - not the cause of the disease itself. It's believed that T and B-cells that gain entry to the central nervous system actually initiate the disease process. But there's no evidence that T and B-cells play a strong role in Alzheimer's; instead the innate immune system and the microglia - the two sentinels on watch for pathogens in the brain - are going gang-busters.
Years before the Harvard researchers showed that viruses cause the immune system to produce amyloid depositions in the brain, Itzaki and others showed that HSV causes amyloid products to appear. They also showed that anti-herpesvirus drugs such as valacyclovir reduced the accumulation of amyloid deposits in cell cultures.
Funding for antiviral trials in humans, however, has been denied both at the federal level and by drug companies. This is despite the fact no drugs effectively target disease progression in AD; it remains an essentially untreatable disease.
If the amyloid-infection connection wins out, though, antivirals and antibiotics could be become first-line treatments. Doctors would either find ways to remove the amyloid deposits or prevent them from being posited in the first place.
First, though, researchers have to examine be brains of Alzheimer's patients more closely to identify the pathogens they would want to target. In that they're lucky - they have lots of brain tissue to study.
There's little evidence to suggest that amyloid deposits play a role in ME/CFS or fibromyalgia. (Evidence of amyloid deposits was found Dr. Baraniuk's proteome study but that finding has not been validated.)
The role herpesviruses play in ME/CFS or FM is not clear either but the potential is there. Dr. Pridgen has found herpes simplex viruses in the gut tissues of fibromyalgia patients. A cadaver study found herpes simplex infections in the nerves of about a third of the cadavers studied. We know that HSV reactivation causes canker sores in the mouth and genital herpes and ocular herpes. In the brain it can produce encephalitis. If Itzaki is right it may even be triggering Alzheimer's.
We don’t know that herpesviruses are causing ME/CFS or FM, but if they or another pathogen end up triggering AD the impact on ME/CFS or fibromyalgia could be large.
Given AD's prevalence and cost to society efforts would surely be made to develop more effective herpesvirus drugs. It's possible that better diagnostic tests for herpesviruses could be developed as well. The role that the immune response plays in chronic illness would be highlighted as well, and post-infectious illnesses might finally start to get their due in the medical community.
