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Smith:

Gc-MAF

heeft positief effect op

de groei en stofwisseling

van neuronen

en neuropatische pijn

 

 

 

 


 

 

 

Volgens een studie van Smith stimuleert Gc-MAF niet alleen de werking van macrofagen (klik hier),

maar ook (dosis-afhankelijk) de "levendigheid" en mitochondriale activiteit van neuronen.

 

Volgens de auteurs duiden vormwijzigingen en de toename van cAMP op groei van de zenuwcellen.

 

Ook zou Gc-MAF een positief hebben op de neuropatische pijn bij proefkonijnen (o nee, proefratten),

die tot stand gebracht werd door een glycolyse-remmer, resulterend in "artrose" bij de ratten.

 

Volgens de Vereniging tegen de Kwakzalverij wordt Gc-MAF voorgeschreven door kwakzalvers.

 

 


 

 

 

Effects of GC-macrophage activating factor in human neurons; implications for treatment of chronic fatigue syndrome.

Am J Immunol. 2013; 9 (4): 120-129. doi : 10.3844/ajisp.2013.120.129.

Smith RL, Thyer E, Ward E, Meacci E, Branca JJV, Morucci G, Gulisano M, Ruggiero M, Pacini A, Paternostro F, L Di Cesare Mannelli, Noakes DJ, Pacini S.

 

 

Abstract

 

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

is a debilitating disease of multifactorial aetiology

characterized by immune system dysfunction, widespread inflammation,

multisystemic neuropathology and persistent pain.

 

Given

the central role of the immune system in the pathogenesis of the syndrome,

we studied the effects of a potent modulator of the immune system in in vitro and in vivo models

that could help clarifying its role and indications in ME/CFS treatment.

 

To this end,we studied

the effects of vitamin D-binding protein-derived macrophage activating factor

(also designated as Gc-Macrophage Activating Factor or (GcMAF)))

on human neuronal cells and

on the persistent pain induced by osteoarticular damage in rats.

 

GcMAF at pM concentration increased neuronal cell viability and metabolism

through increased mitochondrial enzyme activity.

 

These effects were accompanied by cAMP formation and by morphological changes

that were representative of neuronal differentiation.

 

We hypothesize that these effects are to be ascribed to

the interconnection between the GcMAF and Vitamin D Receptor (VDR) signalling pathways.

 

The results presented here confirm at the experimental level

the therapeutic effects of GcMAF in ME/CFS and

elucidate the mechanisms of action through which

GcMAF might be responsible for such therapeutic effects.

 

 

 

Received 2013-10-29,

Revised 2013-11-05;

Accepted 2013-11-06

 

 

 

Keywords:

 

Chronic Fatigue Syndrome, Immunotherapy, Vitamin D, Macrophage Activating Factor, GcMAF

 

 

http://thescipub.com/abstract/10.3844/ajisp.2013.120.129

http://thescipub.com/pdf/10.3844/ajisp.2013.120.129