As thiamine facilitates nerve conduction I would like to know if it might help the development of the myeline theath generated by the oligodendrocites.
Hi Hernán, Thiamine (via B1) is for sure a key factor in many body processes, especially in the nervous system. In fact deficiency of vitamin B1 affects mainly the nervous and the cardiovascular systems (in humans). I would not however link directly thiamine to myelin production. Indirectly myelin requires energy and oligodendrocytes needs thiamine to generate energy. Thiamine pyrophosphate is a coenzyme of dehydrogenases relevant for cell energy generation.
Hola Rafael, thanks for your answer, As I am a clinical neurologist dealing mostly with aged patients, I look for some therapeutic agent that could help to reduce the simptomatology related to White matter microcirculatory déficit. Currently I use Pentoxyfiline and I think it would do no harm adding thiamine.
I am very pleased to talk abaut link Thiamina Myelin
Thiamine is important for the brain (see beri beri and neuropathology associated with vitamin deficiency B1) and especially the combination with alcoholism, and in this Gabrielli certainly has more knowledge than me. I believe that neurological damage is especially directed to the myelin that is home to active Krebs cycle, as our paper on Biochimie that I enclose. We state that we are proposing a radical change of paradigm about myelin and you can read all about our papers (I am attaching one). Furthermore thiamine is a cofactor of the very important enzyme Transchetolase of the pentose phosphate shunt that in the brain and in particular in myelin is particularly active. Such a shunt is on membrane and the key enzyme is Hexose Phosphate dehydrogenase (H6PD) that is in the membrane and not in citosol as the classical P Glucose6 P dehydrogenase (G6PD)..
In fact the H6PD deficit is very serious, and it is not that of G6PD. Extraordinary: the H6PD deficit (not the 6PGD) causes severe demyelination also in humans, and H6PD is risk gene associated with multiple sclerosis (see attached paper)! This appearas an important link. Do you agree?
I would like to stay in touch with you. It must convince us that the myelin is not a passive "electrical insulator" (but where is the electricity in neurons?) And instead nourishes the axon which is why that increases the speed of the action potential.
I have seen many innovations in the lab I'd like to discuss with you all. Tomorrow I'm in Zagreb and meet Jan Homolak..
I think that the administration of B1 to people with multiple sclerosis is benefical, but it remains to be seen . Best regards,
As a clinical neurologist I actually deal mostly with aged patients affected with white matter microcirculatory alterations and its relation with cognition and gait and balance alterations. The pathophisiology underlying this condition is chronic hypoperfusion that in turn generates disruption of the blood brain barrier and demyelination. Apart of managing vascular risk factors we have no proven means for dealing with the above-rmentioned pathophysiology, so many years ago, I started using pentoxifyline because of its vasodilator and hemorheologic properties, adding more recently thiamine because my previous good experience in relation with other demyelinating conditions, namely alcoholic peripheral neuropathy, diabetic polineuropayhy, trigeminal neuralgia,etc. Occasionally I add Citicoline because of its properties of promoting rapid repair of injured neuronal membrane by increasing the synthesis of phospholipids.
Obviously my results are purely observational ; I never detected serious side effects and the results are good, especially in what has to do with gait and balance disorders and to less extent with cognitive impairment, probably in this latter case because of the common association with neurodegenerative pathology