Alcohol inhibits Na+ K+ pumps in the cerebellum and this is likely involved in corruption of cerebellar computation and body co-ordination (Ref 2).
ME patients have problems with fine movement and do not tolerate alcohol. Is the cerebellum involved?
ME is suspected to be an autoimmune disease. ME can develop after Epstein-Barr Virus (EBV) infection (mononucleosis) or after Varicella infection (chicken pox).
Antineuronal antibodies are found in acute cerebellar ataxia following EBV infection. Ataxia is a defect defined as incoordination due to errors in the rate, range force and direction of movement.
Centrosome autoantibodies are found in childhood varicella and post-varicella acute cerebellar ataxia. The proteins that react with autoantibodies include pericentrin, ninein, enolase, PCM1 and Mob1. These proteins participate in the function of the microtubule organizing center (MTOC).
Purkinje cells in the cerebellum contain numerous particles of pericentrin and more than one centrosome. That raises the question that purkinje cells are vulnerable to autoimmune attack (Ref 3).
ME is not acute cerebellar ataxia, but is something else going on in the cerebellum?
Marshall Gradisnik et al have found SMPs in TRMP3 in ME patients and refers to a study that shows activation of TRPM3 potentiates glutamergic transmission at cerebellar Purkinje neurons from developing rats. (Ref 4)
Is something wrong with transmission at Purkinje neurons in ME patients?
- Wikipedia: Cerebellum
- Wikipedia: Purkinje Cell
- Fritzler et al. Spectrum of centrosome autoantibodies in childhood varicella and post-varicella acute cerebellar ataxia. BML Pediatrics 2003, 3:11 http://www.biomedcentral.com/1471-2431/3/11
- Examination of Single Nucleotide Polymorphisms (SNPs) in Transient Receptor Potential (TRP); ion Channel in Chronic Fatigue Syndrome Marshall-Gradisnik et al doi: 10.4137/III525247.
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