Autoimmunity against a glycolytic enzyme as a possible cause for persistent symptoms in Lyme disease

i am not sure if anyone reading this realizes , if confirmed on large scale study, how important this finding is. In the past, they knew autoimmunity is an issue but nobody managed to detect the autoantigen so far. It is the only one known implicated in chronic borrelia. anti gamma-enolase.

For astroman and the rest that are interested:

enolase is a glycolytic enzyme. It means it's a working part of the process that converts glucose into energy inside the cells (ATP). So this is an essential building block. This is a very complicated process in 10 steps, and enolase is used in the 9th one.

in the brain this enzyme has a special form called gamma-enolase, and it is specific to neurons , it produces energy for neuronal tissue.

The darn borrelia bacteria has something on its surface that looks like gamma-enolase (molecular mimicry). When the bacteria is eaten by white cells it is analyzed and pieces of it are used by the immune system to build detectors (antibodies) to find other borrelia and "tag" them. One of the piece is this borrelia piece that looks like gamma-enolase. The immune system creates an antibody for it and then it sends it throught the body. The antibody attacks the real gamma enolase in the brain and disturbs the energy generation of the neurons, which leads to neuronal death either by it being attacked by the immune cells or directly because the ATP production of energy is disturbed.

It is quite possible this process will continue AFTER the borrelia is completely gone from the body, for a while, but it is not clear how many years. More probable a very small number of borrelia bacteria survive, and they keep the immune system busy producing anti gamma-enolase.

Another option is no borrelia survives but the immune system remains erected for many years, it produces antibodies , cells are killed, and it enters a cycle in which it eats its own neurons...

I will read carefully the entire paper again, and report back.

in the light of these findings, we need to increase the oxygenation/energy production of neural tissue. Things that should be very important to take or to do:
- CoQ10 (probably we need much more than 100mg/day)
- Ginko biloba
- Hawthorn
- Moderate physical activity
- if u afford it, HBOT
- Purchasing/renting an oxygen concentrator and using it throughout the day (im not joking)
- Acetyl-L-Carnitine

the idea is to get as much oxygen to the neural tissue and/or improve the production of ATP. The process is clearly disrupted and this is one of the main problems in PTLDS/chronic neuro lyme.

mpost said...
in the light of these findings, we need to increase the oxygenation/energy production of neural tissue. Things that should be very important to take or to do:
- CoQ10 (probably we need much more than 100mg/day)
- Ginko biloba
- Hawthorn
- Moderate physical activity
- if u afford it, HBOT
- Purchasing/renting an oxygen concentrator and using it throughout the day (im not joking)
- Acetyl-L-Carnitine

the idea is to get as much oxygen to the neural tissue and/or improve the production of ATP. The process is clearly disrupted and this is one of the main problems in PTLDS/chronic neuro lyme.

Strength training again does seem to help my whole body and mind (oxygenate), not to be confused with cardio (which can lower immune strength).

So back to what I was saying about enolase not being the first or only autoantigen implicated in Lyme disease, here are a few things I found this morning that seemed interesting. Still can't find that darned OspA/ganglioside paper. I'm sure it's on my old computer somewhere. Anyways the important thing to remember here is that molecular mimicry is a very very VERY common event. However, not all molecular mimicry = lymphocyte activation. And not all Lymphocyte activation = autoimmune disease. Particularly when extrapolating from in vitro assays to actual disease processes. So we still don't know which autoantigens are responsible for disease symptoms. However, I think the potential here is really cool. Just to know how highly evolved this stupid little thing is to sneak around your body like that pretending to be a piece of you in every possible way that it can come up with. Blows my mind. I also think it helps us to remember that autoimmunity and infection are not separate processes. This is just HOW microorganisms cause illness. It's just a mechanism of injury. It's not a separate disease.

autoantibodies to cardiolipin and ganglioside in neuroborreliosis http://www.jns-journal.com/article/0022-510X(93)90175-X/pdf

This one doesn't talk about OspA specifically, but immunization of whole cell borrelia inducing anti-gangliosides, a common cause of peripheral nerve disorders like CIDP/GBS https://www.ncbi.nlm.nih.gov/pubmed/7558329

Here's an interesting one. 856 peptides cross reactive to Borrelia OspA. Of those, 28 induced an inflammatory response. That doesn't mean they all play a role in disease, but it shows the potential here. "Our data together with other available evidence suggest that cross-reactivity leading to T cell activation is a very frequent event." And this was only in a limited selection of T-cells, and not including B-cells. And only to OspA at that! http://sci-hub.cc/10.1002/1521-4141(200002)30:2%3C448::AID-IMMU448%3E3.0.CO;2-9

This one, though small scale, is provocative in regards to causation. 6 patients develop CIDP and cognitive impairment after vaccination with OspA https://www.ncbi.nlm.nih.gov/pubmed/15363064

And on the topic of vaccines, OspA exacerbates arthritis in live infection (just because I know someone is going to freak out at the implications that a vaccine injury might undermine chronic Lyme. This model suggests live infection may still be necessary.) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC97189/

Post Edited (Psilociraptor) : 11/9/2017 6:30:47 AM (GMT-7)

mpost said...
in the light of these findings, we need to increase the oxygenation/energy production of neural tissue. Things that should be very important to take or to do:
- CoQ10 (probably we need much more than 100mg/day)
- Ginko biloba
- Hawthorn
- Moderate physical activity
- if u afford it, HBOT
- Purchasing/renting an oxygen concentrator and using it throughout the day (im not joking)
- Acetyl-L-Carnitine

the idea is to get as much oxygen to the neural tissue and/or improve the production of ATP. The process is clearly disrupted and this is one of the main problems in PTLDS/chronic neuro lyme.

Very interesting. Agree that we may need more CoQ10. For mitochondrial disease, 5-15 mg of CoQ10 per kg of body weight is often recommended. That would be 340-1,000 mg for a 150 pound person. Taking a water and fat-soluble form can improve absorption, which means we may not need to take as much.

Excited to look more into the other findings.

CoQ 10 isn't supposed to be taken when on Atovaquone.

Astro - I remember about the certain form of CoQ10 but not everyone agrees with that - I can't remember the details either.
My LLND said to take the 'regular' one.