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James Moss May 12, 2013 at 3:46 pm

My wife (also a librarian) is finishing your book.

The review, (and a flurry of other papers) suggest tourette syndrome may have an autoimmune or inflamatory component (may be the whole thing).

The tetracyclines, and minocycline in particular, have been used to erduce the symptoms

(not cure) of autoimmune illnesses including the classic, rheumatoid arthritis.

A number of “spych” conditions are moving under the umbrella of autoimmunity, along with conditions such as COPD, atherosclerosis and more.

This is real.

Jim Moss
Gainesville
Florida

Mov Disord. 2009 Jul 15;24(9):1267-79. doi: 10.1002/mds.22504.

Immunopathogenic mechanisms in tourette syndrome: A critical review.

Martino D, Dale RC, Gilbert DL, Giovannoni G, Leckman JF.

Department of Neurological and Psychiatric Sciences, University of Bari, Italy.
davidemartino@virgilio.it

Tourette syndrome (TS) has a multifactorial etiology, in which genetic,
environmental, immunological and hormonal factors interact to establish
vulnerability. This review: (i) summarizes research exploring the exposure of TS
patients to immune-activating environmental factors, and (ii) focuses on recent
findings supporting a role of the innate and adaptive immune systems in the
pathogenesis of TS and related disorders. A higher exposure prior to disease
onset to group A beta-haemolytic streptococcal (GABHS) infections in children
with tics and obsessive-compulsive (OC) symptoms has been documented, although
their influence upon the course of disease remains uncertain. Increased
activation of immune responses in TS is suggested by changes in gene expression
profiles of peripheral immune cells, relative frequency of lymphocyte
subpopulations, and synthesis of immune effector molecules. Increased activity of
cell-mediated mechanisms is suggested by the increased expression of genes
controlling natural killer and cytotoxic T cells, increased plasma levels of some
pro-inflammatory cytokines which correlate with disease severity, and increased
synthesis of antineuronal antibodies. Important methodological differences might
account for some inconsistency among results of studies addressing autoantibodies
in TS. Finally, a general predisposition to autoimmune responses in TS patients
is indicated by the reduced frequency of regulatory T cells, which induce
tolerance towards self-antigens. Although the pathogenic role of immune
activation in TS has not been definitively proven, a pathophysiological model is
proposed to explain the possible effect of immunity upon dopamine transmission
regulation and the generation of tics.

2009 Movement Disorder Society.

PMID: 19353683 [PubMed – indexed for MEDLINE]

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