• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Mitochondrial length plays role in Dementia and Alzheimers

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Hi August59, I read an article on this recently, not the one you posted but I don't recall where it was, and its very interesting. Mitochondria have to move in nerves. Nerves are long and narrow. Effectively they become blocked and cannot move if they are too large, which might mean that while part of the nerve has enough energy, the other part is deficient. The nerve then dies. Bye, Alex
 

jeffrez

Senior Member
Messages
1,112
Location
NY
That's interesting, I wonder if mitochondrial length is an issue in ME/CFS mitochondrial dysfunction, and whether the drugs they're developing for these "mitochondrial dynamics" issues would have applicability in ME/CFS?
 

August59

Daughters High School Graduation
Messages
1,617
Location
Upstate SC, USA
Hi August59, I read an article on this recently, not the one you posted but I don't recall where it was, and its very interesting. Mitochondria have to move in nerves. Nerves are long and narrow. Effectively they become blocked and cannot move if they are too large, which might mean that while part of the nerve has enough energy, the other part is deficient. The nerve then dies. Bye, Alex

That is what I saw on TV last night about them moving along the nerves and if they were to long they would move way to slow.

It would be very interesting to see if a person with ME/CFS has abnormal shape to the mitochondria. I pretty sure that most of us have mitochondrial dysfunction to some degree, but I would have never thought about just the fact that they were a little bit elongated could possibly be the reason behind Alzheimers. All they had to do was get the mitochondrial back to normal shape and they not only moved along the nerves at the speed that they needed to, but it also helped the mitochondrial remove all or the excessive "tau" from the mitochondrial.

I can't help but think that there is at least some possibilty that this may at least shed some light on the understanding of what may be going on with people with ME/CFS.

Is there anyone that is doing a study on mitochondria for people with ME/CFS right now?
 

August59

Daughters High School Graduation
Messages
1,617
Location
Upstate SC, USA
That's interesting, I wonder if mitochondrial length is an issue in ME/CFS mitochondrial dysfunction, and whether the drugs they're developing for these "mitochondrial dynamics" issues would have applicability in ME/CFS?

I don't know jeffrez, but I would surely like someone to take a look at it. I would think the possibilty of this being an issue to at least minor extent would be pretty high.

I know Dr. Bariniuk first spinal fluid study found some abnormal misfolded amyloid in the mitochondria i believe.

I'm going try and find that more in depth write up about this that alex was referring to and I'll add it to the first post. If someone is doing a study on mitochondria of people with ME/CFS, I would like to find a way for someone here on the forum to get this information just in case.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Its been a very long term finding (from 1988 I think) that some with CFS have mitochondria that look like "ragged red fibers". This is a classic sign of mitochondrial damage.

I am not sure that most of us have the same kind of damage as found in Alzheirmers'. I think the evidence is that most of the damage is to do with mitochondrial membrane transport (Myhill's research). It would be good to see more research on this though.

Bye, Alex
 

lansbergen

Senior Member
Messages
2,512
I am not sure that most of us have the same kind of damage as found in Alzheirmers'. I think the evidence is that most of the damage is to do with mitochondrial membrane transport (Myhill's research). It would be good to see more research on this though.Bye, Alex

Anyone ever checked the intregity of the nicotine receptors?

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031361

Galyna Gergalova1, Olena Lykhmus1, Olena Kalashnyk1, Lyudmyla Koval1, Volodymyr Chernyshov1, Elena Kryukova2, Victor Tsetlin2, Sergiy Komisarenko1, Maryna Skok1*
1 Department of Molecular Immunology, Palladin Institute of Biochemistry, Kyiv, Ukraine, 2 Department of Molecular Bases of Neurosignaling, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia

Abstract

Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that mediate synaptic transmission in the muscle and autonomic ganglia and regulate transmitter release in the brain. The nAChRs composed of α7 subunits are also expressed in non-excitable cells to regulate cell survival and proliferation. Up to now, functional α7 nAChRs were found exclusively on the cell plasma membrane. Here we show that they are expressed in mitochondria and regulate early pro-apoptotic events like cytochrome c release. The binding of α7-specific antibody with mouse liver mitochondria was revealed by electron microscopy. Outer membranes of mitochondria from the wild-type and β2−/− but not α7−/− mice bound α7 nAChR-specific antibody and toxins: FITC-labeled α-cobratoxin or Alexa 555-labeled α-bungarotoxin. α7 nAChR agonists (1 µM acetylcholine, 10 µM choline or 30 nM PNU-282987) impaired intramitochondrial Ca2+ accumulation and significantly decreased cytochrome c release stimulated with either 90 µM CaCl2 or 0.5 mM H2O2. α7-specific antagonist methyllicaconitine (50 nM) did not affect Ca2+ accumulation in mitochondria but attenuated the effects of agonists on cytochrome c release. Inhibitor of voltage-dependent anion channel (VDAC) 4,4′-diisothio-cyano-2,2′-stilbene disulfonic acid (0.5 µM) decreased cytochrome c release stimulated with apoptogens similarly to α7 nAChR agonists, and VDAC was co-captured with the α7 nAChR from mitochondria outer membrane preparation in both direct and reverse sandwich ELISA. It is concluded that α7 nAChRs are expressed in mitochondria outer membrane to regulate the VDAC-mediated Ca2+ transport and mitochondrial permeability transition.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Hi Lansbergen, I have known since 2000 that vascular acetylcholine muscarinic receptors might have issues. I am not sure about mitochondrial nicotinic receptors. I do not recall that anything has been investigated. Bye, Alex