nAChR, agrin, rapsyn and ME

Nicotinic acatylcholine receptors (nAChRs) are suspected to be involved in the ME pathomechanism (1).

ME patients have dysregulated lipid metabolism (2). This could have an impact on lipid rafts?

Lipid rafts serve as signaling platforms for nAChRs clustering. The clustering is induced by the heparan sulphate proteoglyan, agrin. The nAChRs are anchored into the lipid rafts by rapsyn (3).

A proteomic study on cerebrospinal fluid from ME patients has shown an upregulation of the arin precursor and of the heparan sulfate proteoglyan core protein precursor (4).

The gene RAPSN (protein: rapsyn) has been found epigenetic changed (hypermethylated) in ME (5).

References:

1. Griffith University. https://www.griffith.edu.au/health/national-centre-neuroimmunology-emerging-diseases
2. Naviaux et al: Metabolic features of CFS. www.pnas.org/cgi/doi/10.1073/pnas.1607571113
3. Allen et al: Lipid raft microdomains and neurotransmitter signalling. Nature Reviews, feb 2007, vol 8.
4. Schutzer et al: Distinct Cerebrospinal Fluid Proteomes Differentiate Post- Treatment Lyme Disease from Chronic Fatigue Syndrome. PLOS One February 2011, volume 6, Issue 
5. Vega et al. DNA methylation Modifications associated with CFS. Plos One, aug 2014, vol 9, Issue 8, e104757