Wednesday, May 26th, 2010 This excellent
review published recently in the journal
Molecular Neurodegeneration elucidates the epidemiologic, pharmacologic and genetic evidence that explains why
inflammation in the brain and the rest of the central nervous system is a key factor in neurodegenerative diseases such as
Alzheimer’s disease,
Parkinson’s disease,
Huntington’s disease and
Amyotrophic Lateral Sclerosis.
“While peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults.”
Inflammatory stimuli include allergens (gluten, etc.), infections, trauma, neurogenic activation of the inflammatory response, and others. Microglia (the immune cells in the brain) are activated and release inflammatory mediators,
the cytokines and chemokines that we measure with lab tests.
“…chronic neuroinflammation is a long-standing and often self-perpetuating neuroinflammatory response that persists long after an initial injury or insult.”
Once chronic neuroinflammation has been established, these inflammatory mediators perpetuate a cascading inflammatory cycle.
Neuroinflammation, neuronal dysfunction and degeneration
“Neurodegenerative CNS disorders, including multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), tauopathies, and age-related macular degeneration (ARMD), are associated with chronic neuroinflammation and elevated levels of several cytokines.”
In other words, microglial activation and the chronic inflammation it perpetuates is the
convergence point for all the kinds of stimuli associated with these neurodegenerative disorders as well as many other conditions affected by compromised brain function.
This is partly why it is of such great practical importance to profile immune dysregulation in the central nervous system with the appropriate lab tests as a basis for rational therapy.
No comments:
Post a Comment