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While this paper primarily relates to the influence of the immune system in major depressive disorder it also proposes the more general need to distinguish between 'neuroinflammation' associated with diseases such as Alzheimers' and Parkinsons where there is progressive and irreversible damage to the CNS and lower level immune activation which may be transitory and reversible.
They suggest that making this distinction should avoid confusion as to what exactly 'neuroinflammation' means.
Hopefully if central immune activation plays a role in ME/CFS it's the latter type :
Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder
http://journal.frontiersin.org/article/10.3389/fnins.2014.00309/full
They suggest that making this distinction should avoid confusion as to what exactly 'neuroinflammation' means.
Hopefully if central immune activation plays a role in ME/CFS it's the latter type :
Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder
Classically, inflammation involves swelling, heat, and pain, coupled with a coordinated infiltration of various immune cells into the affected area. In many neurological conditions, this large-scale damage is not seen unless in terminal stages, or in cases of major BBB compromise. Thus, the use of “neuroinflammation” to refer to central immune activity can become confusing, and a clear distinction between high magnitude and submaximal immune states is required.
We thus propose the use of the terms “increased neurokine signaling” or “increased central immune signaling” to apply to these sub-inflammatory states, and only when there is large-scale damage as a result of immune cell derived neurotoxicity and inflammation should the term “neuroinflammation” be applied in order to reduce confusion within the literature.
http://journal.frontiersin.org/article/10.3389/fnins.2014.00309/full