Neuroimmunity by Michal Schwartz

Author:Michal Schwartz
Language: eng
Format: epub
Publisher: Yale University Press
Published: 2015-10-24T16:00:00+00:00

Over the past two decades, neurodegenerative diseases have often been linked to chronic inflammatory processes within the brain or the spinal cord tissue. Again, as we have seen in this book, it was commonly believed that in the diseased central nervous system, overactivated immune cells could create a vicious self-perpetuating cycle resulting in a prolonged, unregulated inflammation that drives the chronic progression of such diseases.15

Based on this assumption, many clinicians treated Alzheimer’s, ALS, and other neurodegenerative diseases with anti-inflammatory drugs and steroids, yielding conflicting results. The immunosuppressant Minocycline showed promising results in mice with ALS but showed no benefit in human patients, and in some cases even exacerbated the disease. A similar hope that anti-inflammatory drugs might prevent the onset of Alzheimer’s didn’t pan out; the drugs failed to help patients.16

According to my theory, at the root of this approach lies a misconception about the nature of inflammation. As we have emphasized, every condition associated with inflammation in the central nervous system has traditionally been linked to autoimmune inflammatory pathologies, as in multiple sclerosis, in which the circulating immune system attacks the brain.

Now we know that inflammation within the brain starts out as a good thing: It is the body’s physiological response, a way of using the immune system against risk factors within the brain that may cause chronic neurodegenerative conditions. When this immune response isn’t switched off on time, it becomes an unresolved process that can contribute to disease progression. With more and more pro-inflammatory effector immune cells engaged in a desperate and unsuccessful attempt to contain the disease, it seems like a vicious cycle that further exacerbates the disease. While it begins as a defense process, physiological inflammation can soon become pathological inflammation. The belief of clinical researchers that we can break such a vicious cycle by suppressing the immune system outside the brain has turned out to be an illusion. As we understand from our studies, suppressing the immune system outside the brain to shut off chronic inflammation within brain tissue can be counterproductive, as it denies the diseased brain the immune assistance it needs from the blood. This assistance includes that provided by blood-borne immune cells, recruited to the damaged site, which eventually help extinguish the vicious cycle of inflammation within the brain. Thus general immune suppression might dampen the response of such immune cells that serve as “cease-firing,” immune-resolving cells. As an alternative to the ineffective general immune suppression, we suggest augmenting recruitment of the appropriate immune assistance from the blood to the brain.17

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