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How We Remove Dead Neurons

Hopeful2021

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Wow .... this is extremely interesting. I'm sending to some friends. Thanks for posting and sharing it.

just did a 60 min Hyperbariac Oxygen session. Feeling good about apoptosis.
 

Wishful

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I'm just guessing that no one has looked into whether neuron removal and replacement is different for ME. We don't know what causes mental lethargy, and this seems like at least a possibility. Think of rush hour traffic with some dead vehicles in the way.

Another possibility is that our neurons are triggering death too easily, and even if they are being replaced, it might take time for the new ones to take over all the tasks of the old one, leading to sluggish brain function.

Hmmm, I forgot to apply my "Does this fit in with temporary remission of ME?" test. We can switch from the ME state to full remission over a period of minutes, so slow-acting mechanisms don't fit that. I'm not sure how fast neuron removal and replacement is.
 

Hopeful2021

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My 14 months of a specific kind of neuroplasticity training gives me the impression that the neurons have been turned off.

connective tissue has "muscle memory too" and like in Alzheimer's patients who their neurologist team would definitely say and have scans to prove two large areas of neurons are "dead" .... however in the presence of ketone type pet scan but not with glucose pet scan ... voila .... those same dead areas are suddenly firing again.

indeed there's lots of new patterns that can be layed down... but as I do my training.... the muscle memory/fascia memory comes back as do those specific movement patterns again. It's remarkable. Blows my mind every time. It is also hard to emotionally process bc then I'm reminded of how much was taken from me. It also doesn't reliably stay. Can fade out and disappear again.

it can also be neither or any of these hypotheses too. So intriguing and complex.
There's still lots even in muscle physiology that's being worked out....so it's a long road for the brain.
 

PatJ

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Another possibility is that our neurons are triggering death too easily, and even if they are being replaced, it might take time for the new ones to take over all the tasks of the old one, leading to sluggish brain function.
Do you remember this thread Wishful? Microglia Induced Cognitive Changes Article - It discusses some of the cognitive changes that can be caused overactive microglia.

And this article looks at Dr. Cheney's information about excitatory neurotoxicity (when the seizure threshold is lowered and excess sensory input can cause neuron death).

This article on Health Rising discusses Glutamate; kindling; and excitotoxicity.
 

Wishful

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Overactive microglia is one thing that I hope researchers think about for ME. The rate of neuron death and the speed (and thoroughness?) of removal and replacement is different. If ME affects glial cells, then it might be affecting how they do their work.

I imagine some researcher reading an idea such as this and thinking "Hey, that would show up on those scans we did several months ago. I'll call up those files and check." Some patterns in data will only be noticed if the person has the right perspective, and asks the right questions.
 

raghav

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Is there any new therapy for removing dead cells due to hippocampal sclerosis ? I have left hippocampal sclerosis with scar tissue namely dense mossy fibers. These trigger seizures and the brain is not able to clear up this mess. We can grow hippocampal volume by cognitive exercises but the scar tissue stays there for life.
 

PatJ

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hippocampal sclerosis
Serrapeptase reduces scar tissue but I don't know if it crosses the blood-brain barrier.

Lithium orotate is useful for hippocampal neuron regeneration:
From: https://nootropicsexpert.com/lithium-orotate/
* [Growth Factors.] Lithium upregulates brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT3) and their receptors. And lithium stimulates the proliferation of stem cells in the brain. All boosting neurogenesis and assisting in repair from all types of brain injury.[iv]
* [Neuroprotection.] Lithium increases brain gray matter, increases DNA replication for neurogenesis, prevents apoptosis, increases N-acetyl-aspartate (NAA), inhibits beta-amyloid secretion and protects against damage once it’s formed, chelates aluminum, and protects against glutamate toxicity.

From http://jeffreydachmd.com/2015/12/lithium-orotate
[Hippocampus regeneration]
Research over the last decade has revealed that lithium’s effects as _mood stabilization and regeneration of new brain cells_ (neurogenesis), are mainly due to the inhibition of a key enzyme called GSK-3β, glycogen synthase kinase-3β. (1) This GSK-3B, in turn, upregulates insulin-like growth factor-I (IGF-I), and brain-derived neurotrophic factor (BDNF) which _stimulates neural stem cells to give rise to new hippocampal neurons throughout adulthood._ Thus, the molecular pathways of how lithium increases new brains cells has been worked out by basic science.
...

Lithium prevents and reverses the loss of brain cells in Bipolar Disorder humans as demonstrated by MRI brain imaging studies. Brain volume increases after lithium treatment.(5-6)(9-10) Similar increases in brain volume have been seen with SSRi antidepressant drugs, suggesting a common mode of action with Lithium. This has launched the “neurotrophic theory of depression”.(21-23) This idea is new and may replace the older theory of neurotransmitter imbalances as a cause of depression. The Neurotrophic theory says that clinical depression is caused by reduced or absent brain neurogenesis, rather than chemical imbalances in the brain. The brain cannot make new cells. Lithium and SSRI antidepressants (24) increase these neurotrophic factors (by inhibiting GSK-3B) thus up-regulating neurogenesis in the hippocampus.