(LLLT Efficacy) Mobilizing Mitochondria May Be Key to Regenerating Damaged Neurons, Zhou, B et. al.

Professor Dr. Bing Zhou of molecular biology and genetics has released a publication yesterday that excited me as it forms a missing piece of my puzzle concerning the efficacy of LLLT.
http://life.tsinghua.edu.cn/english/faculty/faculty/651.html
https://scholar.google.nl/citations?user=YVvMM_MAAAAJ&hl=en&oi=ao

Mobilizing mitochondria may be key to regenerating damaged neurons:
Pupular science article, http://www.neuroscientistnews.com/r...ndria-may-be-key-regenerating-damaged-neurons
Research paper http://jcb.rupress.org/content/early/2016/06/07/jcb.201605101.abstract

As it is the mitochondria that are at fault in neuronal regeneration after injury, there is now a clear connection between LLLT and the neurons since ATP cycling is the primary effect of LLLT.
Apparently adult neurons do not regenerate because of synthaphilin, now the efficacy debate has moved to whether we can help the mitochondrial ATP production despite of it.

 

yes ATP is one important factor
also here:
http://www.nature.com/articles/srep12029
and more detailed
http://www.sciencedirect.com/science/article/pii/S0014483514000682

 

Well I expected everyone to be just as excited as me, I get the feeling that perhaps that won't even happen after we can regenerate the entire CNS.. Maybe I should have named the thread something else... like biggest breakthrough ever that will impact brain injury to the point it will help MS patients..
I was so excited when I read this with my morning tea that the pointer sisters came on and stayed on for half an hour.

The Pointer Sisters - I'm So Excited

You see ATP is the primary action of LLLT and this paper now clinically proves its mechanism of action quite expertly.

 

I was excited. You were just too far away to hear me. Or maybe The Pointer Sisters drowned me out.

 

I had an eccentric pioneering professor in college who used electrotherapy for all sorts of ingenious, off the beaten track treatments. He is long gone. Sad. I had him back in the 1980s. (NOT the 1890s).

 

Haha, when I showed this paper to someone today he said "well I guess Freud was on to something with his electrotherapy", might be right It's still used for pain and such.

 

@Cityjohn, in your case it was the high dose of MSG that caused the sh*tstorm. Do you think it killed hair cells or damaged the afferent neurons connected to the inner hair cells? Or perhaps it may have disrupted the outer hair cells or their corresponding efferent neurons?

 

@Cityjohn , Can I ask you the best cost effective way to give lllt a shot?

You seem knowledgeable on this and I would love to try to see if it helps me.

Is there a good say to do this? I would go buy a laser, but many of the kits are 2000+$ ;/.

Any ideas on easy way to get a good laser to try this soon?

 

I'm pretty sure it caused an inflammation in my entire brain, my brainstem felt inflamed at one point and I had hypothalamic dysfunction to the point of hypothermia. I think most damage was done to the dorsal cochlear nucleus and the epithelial cells, I'm not leaning too strongly toward IHC or OHC damage. I had tremendous pain in my head and ears so perhaps it damaged most of everything... but the general idea is that since it was systemic most problems would occur in the ears and near the circumventricular organs.

We'll find out soon

Don't buy the laser... it's really expensive for what it does. I'm developing a way this Juli, you can follow my thread, search for DIY LLLT. Please be very careful when trying this on yourself and ask people here, or me, what is safe.

 

I'm still curious on why is this so exciting and how on earth you plan to remove "synthaphilin" (whatever that is) from whatever it is you remove it from, also this is just early research (a hypothesis basically) and the good old fact that it works on mice.
AUT00063 worked great on mice.

 

Oke, so.. you don't extract the synthaphilin, you stimulate the cells to produce ATP despite of it. This researcher just figured out why and how LLLT would work on the nervous system without even being aware of LLLT. For this exact reason university's are creating multidisciplinary studies around the world so that absolutely crucial research gets linked.
Microstructure research in animals is not quite like substance research, nerves are nerves, they all function in the much the same way because there's only one law of nature and we have common ancestry. If you want a quantitative analysis you can see this study: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0046683.
So this is the single most useful piece of research that has ever been published for me personally, and should be for everyone with brain trauma such as tinnitus. He tested his hypothesis in this very paper.

 

"Strikingly, enhancing mitochondrial transport via genetic manipulation facilitates regenerative capacity by replenishing healthy mitochondria in injured axons, thereby rescuing energy deficits."

See, @Cityjohn , there are those who celebrate with you, just a few miles and countries away.

 

@Cityjohn Hope I'm not coming off as rude or anything, but hasn't LLLT already been tested for tinnitus and the results marginal at best? Could this be one of those things that works great in scientific theory but doesn't translate to significant results in reality? I'm open to the idea, just trying to understand it more. Thanks.

 

Not at all, well, some of the research done on LT it is so badly designed that I had cracked jokes about it for days. When researchers say that you should never consider one work on its own, what they mean is, there's some serious crap out there and you need to be trained to distinguish between the good and the bad.
As far as I can tell the theory is sound and the practice is often too lacking to provide clear insight. That's exactly why I'll be doing my own study. There is nothing in the theory that would suggest tinnitus can be helped much with an ear laser for example.

To be clear, at this moment I hypothesize, based on sound theory and experiments, that using light on nervous system tissues can be restorative given that there is still tissue i.e the glia have not removed the synapses. This patching up could be enough to completely treat tinnitus. Because all we need to do is provide the body with the ability to restore the filtering threshold by spreading the signal.
The problems are getting enough of the right light inside your brain without burning your head, the possibity that the neurons are damaged beyond repair or have been removed by the glia, and then any unforseen complications.

This research paper has solved the problem I had previously, which was with proof that ATP metabolism would principally work to directly restore CNS functioning at all. It provides me and I hope everyone interested in neurology with crucial evidence. I personally believe, and this may sound cheeky, that nobody has done LT right yet when it comes to tinnitus because it's really hard and they either lack will or imagination.

 

Hey @Cityjohn , absolutely thrilled to see the research and thought you are putting into LLLT. I hope this question isn't out of place, I've just seen different answers to this question on TinnitusTalk and I'm curious what your take on it is....

How long is the "window of opportunity" for treating T with LLLT in your opinion? I've seen some people on here claim there is no real timeline, while others say that after a week there is no point. What is your opinion?

I apologize if this question has already been answered or if it's out of place. Appreciate any input!

-Steve

 

Aaah, that is a really good question Perfectly in place too.

So, I've thought about this a bit, especially since I'm doing my therapy a whopping 5 months after getting tinnitus... To keep it short, I'm unsure and can't hazard an educated guess. If the neurons have not been removed by the body, we should be able to kickstart them back to life. But all the research I could find that touches on this subject is not thorough enough to distinguish between removal and degeneration or contradicts other research... However this piece might interest you a great deal. http://www.jneurosci.org/content/29/45/14077.long

Quote:
Although the loss of peripheral terminals of the cochlear neurons was rapid, the death of the cell and the disappearance of the somata were extremely slow. To evaluate this delayed neural degeneration, we counted SGCs in tissue sections (Supplemental Fig. 1, available at www.jneurosci.org as supplemental material) from separate groups of noise-exposed animals. As quantified in Figure 8 d, ganglion cell numbers in the 32 kHz region were close to normal at 2 weeks postexposure. However, by ∼1 year, dramatic loss was seen throughout the basal turn in every ear (Figs. 4 d, 8 d), and by 2 years, cell counts near the 32 kHz region had decreased by ∼50% (Fig. 8 d), comparable to ribbon losses seen in the first 24 h after exposure (Figs. 7, 8 c). Hair cell populations remained intact in corresponding regions. Ganglion cell loss was modest (<10%) in unexposed, aging animals (Fig. 8 d, triangles), mirrored by similarly modest age-related decreases in both IHC ribbon counts (Fig. 8 c, triangles) and suprathreshold neural responses (data not shown).

(Soma is the core of a neuron)

Even if so, it remains unclear whether we can restore the nerves even after they have been removed completely. Or if not, perhaps the remaining neurons can sprout more heads, in which case the tinnitus would also reduce considerably. When the neurons are dead and gone the area is restructured by gliosis (glial scars), I don't understand see why these glia, or astrocytes, could not be stimulated to become fully functioning neurons.

So it's a tough question and I'm afraid I can't answer yet.

 

No it didn't work. Results were misinterpreted partly because of flawed model. Trials with mice was doubted before the human clinical trials. The test model with mice was flawed and now we know it especially well.

 

I wasn't aware of that. I thought that the human trial started because of an overwhelmingly successful mice trial.