Brainteaser wrote:Recently I was talking to a friend in the US who also has used it but decided to stop as he has learned it adversely affects remyelination. I've looked around the web but can't see anything to support such concerns.
Please if you can.
Voltage-gated potassium channels in multiple sclerosis: Overview and new implications for treatment of central nervous system inflammation and degeneration, pg. 111
In multiple sclerosis (MS), various immune cells are mistakenly triggered to orchestrate an attack against the myelin wrapping on nerve fibers, which leads to impaired nerve function. This review discusses how drugs that block proteins known as potassium channels in the outer membranes of T cells, macrophages, microglia, and dendritic cells may help regulate the detrimental inflammatory immune response underlying MS. Two potassium channels are primary potential therapeutic targets: the Kv1.3 potassium channel that is expressed in each of the fully activated immune cells and the Kv1.5 channel that appears only in activated microglia and dendritic cells. Research in this field focuses on the role of immune cell potassium channels in inflammation and on better drugs for blocking these channels, which will lead to new or improved clinical treatments for MS patients
Conduction studies indicate that neither 4-aminopyridine (4-AP) nor tetraethylammonium alters normal nerve conduction. However, during remyelination, 4-AP profoundly increased both compound action potential amplitude and duration. The level of this effect matched closely the nodal presence of these voltage-dependent K+ channels. Our results suggest that K+ channels may have a significant effect on conduction during remyelination and that Schwann cells are important in K+ channel redistribution and clustering.
Pharmacologic blockade of these potassium channels can increase the safety factor for conduction in demyelinated axons. Restoration of conduction in demyelinated axons, so that action potentials can traverse the zone without myelin, appears to underly clinical remissions in patients with multiple sclerosis and may occur in some patients with spinal cord injury.
In contrast to the demyelinated plaques, all remyelinated lesions are characterized by the detection of aggregates of Nav channels, paranodin/Caspr, Kv channels and Caspr2. Our data suggest that these aggregates precede remyelination, and that Nav channel aggregation is the initial event, followed by aggregation of paranodal and then juxtaparanodal axonal proteins.
Does the following one have a sentence that ends a little too quickly.
and this one is pretty clear...
The adult CNS has the capacity to remyelinate following metabolic, toxic and autoimmune demyelinating insults. In cuprizone-induced demyelination, spontaneous remyelination occurs after the cessation of cuprizone diet. We used the cuprizone model to investigate the role of glial K+ channels in oligodendroglial (OLG) regeneration and remyelination in vivo. We found that treatment with 4-aminopyridine (4-AP), a broad-spectrum K+ channel antagonist, results in: (1) decreased number of oligodendroglial progenitors (OP) and OLGs; (2) diminished astrogliosis; and (3) decreased remyelination in the corpus callosum based on the immunoreactivity to myelin basic protein (MBP), Rip monoclonal antibody, and by electron microscopy. Our findings support the concept that glial K+ channels play an important role during OLG regeneration and remyelination, a crucial factor to be considered during the development of therapeutic strategies to facilitate recovery in demyelinating diseases and spinal cord injury. © 2004 Wiley-Liss, Inc.
No smoking guns here (unless your on a copper diet), i think? I found these by using "potassium channels Multiple sclerosis remyelination" in google. there were more.
The way I look at it was that I would see how I go. I thought it could go one of two ways.
1. The leaking Potasium channels are what trigger remylination, and hence 4-AP would hinder remylination
2. The leaking Potassium channels mean that an electrical charge didnt make it down the full length of the nerve fibre, and hence the end of the axon slowly died.
I felt better about believing option 2.
I found it hard not to go without it when I strarted, and I am pretty certain that I have improved since being on it (while off it ... if you know what I mean...)
So for now, its a win win for me, and I will continue till I recover more, or more is known.