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New Theory Links Depression to Chronic Brain Inflammation

Discussion in 'Other Health News and Research' started by guest, Oct 21, 2010.

  1. guest

    guest Guest

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    Science progresses extremely fast the last years.

    http://www.sciencedaily.com/releases/2010/10/101020091857.htm

     
  2. tymewarp#9

    tymewarp#9

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    Thanks for this, Diesel; I'm going to need to mull this over a while! Seems like it might be simple (relatively) to experiment with - tho I don't like popping ibuprofen, acetominophen, etc. Interesting, nonetheless!
     
  3. guest

    guest Guest

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    Yes, I don't like using ibuprofen etc. as well and I wonder if they meant certain anti-inflammatory drugs. Kofi just posted the pubmed abstract to the study above.

     
  4. slayadragon

    slayadragon Senior Member

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    My experience is that depression is the first sign that I get that an inflammatory response (e.g. from a mold or other biotoxin exposure) is occurring.

    If I feel that sensation, and then get away right away, I can keep from getting sick from the exposure.

    Thus, maybe the depression is a warning sign - and thus a good, functional thing.....to help me to stay well.

    Best, Lisa
     
  5. FancyMyBlood

    FancyMyBlood Senior Member

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    Michael Maes (also a ME/CFS researcher) has been saying this for years. He is a strong opponent of Wessely, Reeves and the Dutch psychiatric lobby (as a neuropsychiatrist himself).

    And guess what happened with visionaries like him, they get reviled and ridiculed by the establishment. If only scientist would be more open-minded and would let go the old psychiatric dogmas, we'd be much further in these neurobiological diseases.
     
  6. pictureofhealth

    pictureofhealth XMRV - L'Agent du Jour

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    Inflammation seems to be the culprit in a lot of disease, including heart disease, autoimmune conditions, ME/CFS. But why does one person get one illness, whereas someone else gets an entirely different one? Perhaps inflammation is the key to most chronic illnesses, and the different disease names and symptoms and parts of the body in which they appear are just the 'weak link'.
     
  7. guest

    guest Guest

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    And here we have some more evidence, that inflammation of the brain plays an important role in disease.

    http://www.sciencedaily.com/releases/2010/11/101101151310.htm

    Arthritis Drugs Could Help Prevent Memory Loss After Surgery, Study Suggests
    ScienceDaily (Nov. 1, 2010) — Anti-inflammatory drugs currently used to treat diseases such as rheumatoid arthritis may also help prevent cognitive problems after surgery, according to a new study by researchers at Imperial College London and University of California, San Francisco (UCSF).

    The research also reveals for the first time that a specific inflammatory response in the brain may explain why many patients experience memory loss or other forms of cognitive dysfunction after surgery or critical illness.
    The findings, from research in mouse models, could lead to human clinical trials within a year, the authors say. Their work is published in the journal Proceedings of the National Academy of Sciences.
    For years, anesthesiologists and neurologists have struggled to explain why some patients, especially the elderly, experience confusion, learning disorders and memory loss after surgery -- a condition clinicians call post-operative cognitive decline. While typically short-term, this delirium occurs widely in intensive care units, affecting between 28 and 92 per cent of hospitalized patients, depending on their age, health status and type of surgery. It also has been linked to poorer surgical outcomes, as well as an increased risk of mortality, inability to cope and possible permanent dementia.
    Until now, researchers have not clearly understood what causes the disorder or how to treat it. The new research suggests that it is caused by cell-to-cell signalling molecules called cytokines released by cells of the immune system. There are drugs already in use that target the activity of cytokines so it is possible that these drugs could be effective against cognitive decline.
    The senior author of the study is Mervyn Maze, MB ChB, Professor and Chair of the Department of Anesthesiology and Perioperative Care at UCSF and a Visiting Professor in the Department of Surgery and Cancer at Imperial College London.
    "Antibody therapies already are widely used against cytokines to prevent or treat inflammation, so we know that these are effective in humans," said Professor Maze, who began the research at Imperial before moving to UCSF. "This study suggests that one day we also might be able to use these therapies as a single, pre-surgical dose to prevent cognitive decline in susceptible patients."
    Previous studies have linked post-operative cognitive decline with the rise in blood levels of a cytokine called interleukin-1 beta (IL-1β), which is involved in inflammation. For this study, Maze and his colleagues studied another cytokine called tumour necrosis factor (TNF-α), which is known to regulate the immune system's inflammatory response before interleukin-1 is produced.
    Working with Professor Sir Marc Feldmann -- a pioneer in cytokine research in inflammatory disorders and Head of the Kennedy Institute of Rheumatology at Imperial College London -- the team gave a single dose of anti-TNF antibody to mice before giving them surgery. They found that the treatment decreased blood levels of IL-1β, limited inflammation in the brain and prevented the mice from showing behavioural signs of cognitive decline.
    The research suggests that TNF acts "upstream" of IL-1 and triggers a cascade of immune responses during surgery that provokes the production of IL-1 in the brain, Professor Maze said. That in turn contributes to cognitive decline after surgery or critical illness.
    "This is an important observation, as it demonstrates that cytokines are potential therapeutic targets in a wider range of diseases, not just autoimmune disease and cancer for which they are known targets," Professor Feldmann said. "Moreover, effective therapeutics already are available, with a known safety profile and modest cost if used short term."
    The study was supported by the Westminster Medical School Research Trust, in London, the Mathilda and Terence Kennedy Institute of Rheumatology Trust, and Arthritis Research UK.
    Arthritis Research UK-funded research at its Kennedy Institute of Rheumatology was instrumental in showing the substantial health benefits of anti-TNF therapy in patients with rheumatoid arthritis and has transformed the lives of millions of people worldwide. Medical director of the charity Professor Alan Silman said: "This research shows the potential that these drugs have in other areas of health."
     
  8. glenp

    glenp "and this too shall pass"

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    Very interesting, thank you for posting. I have had some improvement in cognition - I am more able to add numbers and dont make as many mistakes paying my bills, after taking minocyclin which is also supposed to help many sufferers of rheumatoid arthritis and HIV I wonder what drugs would help more?

    glen
     
  9. guest

    guest Guest

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    GABA is one of the most important neurotransmitters we have. Problems with GABA always seem to result in neuropsychiatric disorders like autism and schizophrenia.

    http://www.sciencedaily.com/releases/2010/11/101110131155.htm

    Inhibitory Neurons Key to Understanding Neuropsychiatric Disorders
    ScienceDaily (Nov. 10, 2010) — The brain works because 100 billion of its special nerve cells called neurons regulate trillions of connections that carry and process information. The behavior of each neuron is precisely determined by the proper function of many genes.

    In 1999, Baylor College of Medicine researcher Dr. Huda Zoghbi and her colleagues identified mutations in one of these genes called MECP2 as the culprit in a devastating neurological disorder called Rett syndrome . In new research in mice published in the current issue of the journal Nature, Zoghbi and her colleagues demonstrate that the loss of the protein MeCP2 in a special group of inhibitory nerve cells in the brain reproduces nearly all Rett syndrome features.
    Children, mostly girls, born with Rett syndrome, appear normal at first, but stop or slow intellectual and motor development between three months and three years of age, losing speech, developing learning and gait problems. Some of their symptoms resemble those of autism.
    These inhibitory (gamma-amino-butyric-acid [GABA]-ergic) neurons make up only 15 to 20 percent of the total number of neurons in the brain. Loss of MeCP2 causes a 30 to 40 percent reduction in the amount of GABA, the specific signaling chemical made by these neurons. This loss impairs how these neurons communicate with other neurons in the brain. These inhibitory neurons keep the brakes on the communication system, enabling proper transfer of information.
    "In effect, the lack of MeCP2 impairs the GABAergic neurons that are key regulators governing the transfer of information in the brain," said Dr. Hsiao-Tuan Chao, an M.D./Ph.D student in Zoghbi's laboratory and first author of the report.
    Chao made the discovery by developing a powerful new tool or mouse model that allowed researchers to remove MeCP2 from only the GABAergic neurons.
    "We did this study thinking that perhaps all we would see was a few symptoms of Rett syndrome," said Chao. "Strikingly, we saw that removing MeCP2 solely from GABAergic neurons reproduced almost all the features of Rett syndrome, including cognitive deficits, breathing difficulties, compulsive behavior, and repetitive stereotyped movements. The study tells us that MeCP2 is a key protein for the function of these neurons."
    Once the authors determined that the key problem rested with the GABAergic neurons, they sought to find out how the lack of MeCP2 disturbed the function of these neurons. Chao discovered that losing MeCP2 caused the GABAergic neurons to release less of the neurotransmitter, GABA. This occurs because losing MeCP2 reduces the amount of the enzymes required for the production of GABA.
    Intriguingly, prior studies showed that expression of these enzymes is also reduced in some patients with autism, schizophrenia and bipolar disorder, said Chao.
    "This tells us a lot about what is going on in the brains of people with Rett syndrome, autism or even schizophrenia," said Chao. "A child is born healthy. She starts to grow and then begins to lose developmental milestones. Communication between neurons is impaired, in part due to reduced signals from GABAergic neurons."
    "This study taught us that an alteration in the signal from GABAergic neurons is sufficient to produce features of autism and other neuropsychiatric disorders," said Zoghbi
    , a Howard Hughes Medical Institute investigator and director of the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital.
    Others who took part in this work include Hongmei Chen, Rodney C. Samaco, Mingshan Xue, Maria Chahrour, Jong Yoo, Jeffrey L. Neul, Hui-Chen Lu, Jeffrey L. Noebels and Christian Rosenmund, all of BCM, John L.R. Rubenstein of University of Calfornia in San Francisco, Marc Ekker of University of Ottawa in Ontario, and Shiaoching Gong and Nathaniel Heintz of The Rockefeller University in New York.
    Funding for this work came from the Howard Hughes Medical Institute, the National Institute of Neurological Disorders and Stroke, the Simons Foundation, the Rett Syndrome Research Trust, the Intellectual and Developmental Disability Research Centers, the International Rett Syndrome Foundation, Autism Speaks, the National Institute of Mental Health, Baylor Research Advocates for Student Scientists and McNair Fellowships.
    Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.
     
  10. guest

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    And another study to support the headline. Blocking Interleukin 6 can help with depression.

    http://www.sciencedaily.com/releases/2010/11/101116101836.htm

     
  11. guest

    guest Guest

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    Inflammation seems to be key for so many diseases.

    Link Between Depression and Inflammatory Response Found in Mice: New Treatments for Mood Disorders?

    http://www.sciencedaily.com/releases/2010/12/101220150946.htm

     
  12. Angela Kennedy

    Angela Kennedy *****

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    Ok. This is a grand theory. BUT - lots of potential problems. 'Stress' cannot be successfully delineated between psychosocial/physical, or from each other as psychosocial events. These authors are still claiming psychogenic stresses are causing somatic illness. They may also be utilising a 'black box' theory to explain this - so people should not be seeing this as plausible yet - and it may never be so.

    How are they even defining 'depression'?
     
  13. Angela Kennedy

    Angela Kennedy *****

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    From the report you've quoted (your post #1)

    "According to the new theory, severe stress and adverse life events, such as losing a job or family member, prompt neurobiological processes that physically alter the brain."

    This is then used to promote a theory of 'inflammation' CAUSED by 'stress and adverse events'. Direction of causation is a bit ambiguous in this piece, and this is a common phenomenon, but, sooner or later psychogenic explanations tend to be revealed, as here, for example, and in the 'childhood trauma causing neurological and immune dysfunction causing CFS' promoted by Heim et al and utilising Freudian notions as well. : (

    It might look like a grand theory - but it's the links in the chain of reasoning that matter.
     
  14. Tia

    Tia Senior Member

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    They're doing a study about that here where they put the worst depressed patients on though antiinflammatory tablets and see if they see a difference.
    The study starts after they get it aprooved byt the healthpanel here, in the beginning of 2011.
     
  15. D Bergy

    D Bergy

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    I found out by accident, that my own thirty years worth of on again off again depression was caused by low grade chronic inflammation.

    When I was diagnosed with Crohn's Disease, I started to quell the intestinal inflammation with anti-inflammatory supplements, such as Krill Oil, Turmeric, Ginger and others.

    While this was not 100% effective in controlling the Crohn's, it did resolve my depression problem 100%.

    It is easy enough to test out, and with little to no risk.

    Dan
     
  16. Cort

    Cort Phoenix Rising Founder

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    Yes, Maes just put out a paper on that. I've been trying to get an interview with him...He has been like a lone wolf for years....I'm sure he's just loving this!

    I think its important stuff because of the increased incidence of depression/anxiety in CFS. For myself I would not meet the criteria for an anxiety disorder but something is definitely there. I wonder if the pathways for creating fatigue in the brain are close to those that create depression or for that matter, pain.....

    Love to see them open up biological underpinnings of depression.

    Neuroglial dysfunction may also be causing the pain in fibromyalgia...Thanks for posting this.
     
  17. Cort

    Cort Phoenix Rising Founder

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    That's great to hear - was it a combination of all of them?
     
  18. Cort

    Cort Phoenix Rising Founder

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    After I read John Falk's book I realized that some people become depressed without any psychological antecedents. The fact that cytokine production in people who come down with CFS after an infectious appears to be much HIGHER than those that don't makes me wonder if some sort of cytokine cascade get started in the brain?

    I've always thought this was a great explanation for CFS since 'sickness 'behavior'' (ie flu-like symptoms) is definitely triggered by infections and infections seem to trigger many peoples cases of CFS....that's always seemed to fit and actually its a theory that the CDC, believe it or not, is very interested in.
     
  19. Cort

    Cort Phoenix Rising Founder

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    The other thing is that they are just looking at depression! Why stop there with brain inflammation?....that's just the first stop, hopefully,for these researchers.

    I think you should write an article on this Diesel :)
     
  20. Angela Kennedy

    Angela Kennedy *****

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    But again, what do they mean by 'depression'? This is a very important problem. AND, they cannot yet (and may never be able to) substantiate the claim that psychological events will lead to 'inflammation' of the brain, OR that 'inflammation' of the brain leads to 'depression' per se, especially because the definition of 'depression', like many mental health labels, is unstable and confused.

    As for ME/CFS, the claims people have higher levels of 'depression' or 'anxiety' are themselves unsafe, and even where feelings that get labelled as 'depression' (or 'anxiety') do happen, can happen for other reasons such as the terrible situation people are in.

    'Depression' claims in mental health neurology are as unsafe as those around ME/CFS.
     

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