I started to wonder why lab mice with rotenone induced parkinson's benefit, in studies, from all sorts of supplements. Humans are not usually as lucky beyond the beauty of the placebo effect.
The thing I want to know about rotenone mice is, does it cause genetic parkinson's with misfolded alpha synuclean proteins that clog up the works and choke dopaminergic neurons, or, does it directly kill the neurons in an amount limited by the exposure to the chemical, thereby leaving the brain of the mice to allow itself to heal in ways that genetically malfunctioning humans cannot? This is my theory as to why things work in mice and not people.
The Autophagy process is severely diminished in the genetically malfunctioning human brain cells, leading to a cascade of problems including weakened mitochondrial systems, premature dopaminergic cell death and pruning of the interneuronal connections accross the various areas of the brain. All of these neuro-supplements would most likely help the mice speed their recovery, (and is this recovery temporary or permanent upon discontinuation of the supplements?) and I suspect it would be similar for a human that got parkinson's from toxin exposure, trauma, nutritional deficiency or some other cause of non genetic origin.
Does anyone know the answer to this? Am I on the right track?
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Another aspect of this issue that is crucial is whether the proposed treatment is applied before, during, or after the toxic insult. From your reference:
"reducing oxidative damage with antioxidants ... blocked cell death"
If the candidate treatment is an antioxidant and is applied before or during the toxic insult, this will mitigate the damage. However once the damage is done, as in the case of actual Parkinson's, a mere antioxidant is not likely to have much effect on the resulting clumps of alpha-synuclein. So if the treatment is applied before or during the toxic insult, any reported benefit is likely to be illusory.
Oftentimes the timing of the application of a candidate treatment is not disclosed in the abstract of a study and requires a careful reading of the materials and methods section of the fulltext. Even then, in some cases this crucial information is not stated clearly.
You present a very important distinction. My theory is that antioxidants can help reduce further damage and rescue suffering cells. But I believe will do nothing for clearing out alpha synuclein or actual repair. This is why I take Ambroxol in hopes it removes some of the AS but also use various antioxidants in hopes of reducing future damage.
No RX required. It’s being trialed in the UK for PD and in Canada for ALZ Trehalose is similar to mannitol and reduces protein clumping. Might be of interest
Part of what helps the small animals is their metabolic health and fast healing rate, I believe. I've rescued two chickens from hawk attacks on two occasions and despite looking to be fatal wounds and in shock, they literally recover in days as if nothing happened after I sewed them up and hydrated them. They heal INCREDIBLY fast. On the note, I spotted a shocking what looked to be a large dark bug flopping about on my floor just the other night but quickly realized that it was one of my precious beautiful Galaxy Koi Betta who managed to jump out of his aquarium between a small 1/2" gap on the lid. In human terms, it jumped off at least 50 stories and should've been dead, but after I placed him back in the aquarium, he was completely fine after being sedentary for a few hours. Just unbelievable.
I like this correlation you present because it leads me to hypothesize that that supplements and lifestyle interventions can take longer than we have typically presumed.
Yes, generally for you to shift/correct deficiencies homeostatically, it can take months if not years. You should assume that your metabolic health is already compromised to arrive at a diseased state, including poor/inefficient nrf2 as you get older or metabolic blockage due to toxins or deficiencies.
I need to re-research, re-inform myself with the NRF2 process. I need repetition to retain much of this. If you have recommendations on where it is put in to laymen terms, that would be great! Learning about the basics of epigenetics gave me hope. This hope has spurred me on in my quest to heal. Striving to heal instead of “fight off” disease has been a pivotal shift for me. I have you to thank for introducing epigenetics and methylation. ❤️
That article I posted the other day is a decent start as it contains all relevant nrf2 references for you to then further deduce from. It's a rabbit hole for sure, but I have faith you'll get the hang of it. Only YOU are responsible for making the difference and deserve all the kudos for taking actions to get better, including exercise that you absolutely abhorred to start! Kudos to you C!
Because mice have the ability to be affected by another mouse's pain or suffering. LYNN NEARY, host: A new study shows that a mouse can sense another mouse's pain. Mice are very social with other mice. Domestic mice are very friendly toward humans and can make good pets for older
They are not mean like us humans, they arenot bullying 86 year-old man, they do not call COVID , a …. Virus.Grown up mice don’t act like a baby mouse. If mice had a forum like HU they would use it in a constructive way not by adding pain and suffering to their kind who were looking for to find a solution for their pain. Yes dear Bass this is why mice are luckier than us humans.
among other things, it is absurd how to understand man scientists observe mice mah! It may seem strange but I have always thought that to understand something you have to observe that thing, not another different one and say that it looks like it. Guys we're not in good hands. Let me tell you.
Rodents do not have dopaminergic neurons with neuromelanin. Our brains are quite different. Yes, I strongly believe that treatments need to be tested in humans over longer time periods. But PD has been "cured" dozens of times in toxin-induced rodent PD models. Repeatedly, when those promising treatments are tested in humans with PD in clinical trials, they fail. Our brain is too different from the rodent brain. Even with advanced aging, they don't get naturally-occurring PD. Although there are "phenocopies" of PD in the animal kingdom, look only to humans to find naturally occurring PD.
I repeat: other animals can have "Parkinsonism" with a parkinsonian phenotype. Whether this corresponds to loss of dopaminergic neurons in the substantia nigra has not been established. Think of all the folks with tremors who don't have PD. CT scan or MRI cannot establish PD. Only autopsy (or, on theory, DatScan), And, yes, I know what the Chinese study claims. Take a look at this, though:
One caveat: A SINGLE cynomolgus monkey was identified by that Chinese lab after screening 1500 such monkeys. It appears to meet most of the hallmarks of PD. including response to levodopa and apomorphine. Due to the monkey's sudden death, they weren't able to collect fresh tissue samples. So, whether the monkey had Lewy body deposits (containing alpha synuclein aggregates) characteristic of human PD is unknown. Other conditions, including dopamine-responsive dystonia, respond to meds used to treat symptoms of PD, so the medication response is not definitive proof of human-equivalent PD.
For those who want to go beyond the press release, here's an article about the finding from a peer reviewed journal: ncbi.nlm.nih.gov/pmc/articl...
Thus, I am willing to acknowledge that a PD-like disorder MAY VERY RARELY occur in a close primate relative of humans. I am on the lookout for more reports like this. Humans have neuromelanin in their dopaminergic neurons. Only very closely related primates have similar (but less) neuromelanin. This makes me think that neuromelanin is a key component in PD pathogenesis.
It's probably best to note that this is a limited population study. Nothing is written in stone, to our best knowledge.
"Thus, the probability of discovering a 10-year-old PD case in our population is about 20 times lower than 0.61. Therefore, we were fortunate to find one PD case in our monkey colony. This rough estimation demonstrates that naturally occurring PD is likely a rare event in monkey colonies within an animal center, and estimation may be biased because of potential inbreeding within the colony. Thus, assessments based on our monkey colony may not accurately reflect the incidence rate of PD in a realistic breeding scenario across wild monkey populations. Moreover, due to greater survival challenges and the fact that PD is a motor deficit disease, we speculate that inflicted animals in the wild may not reach an adequate age to display PD phenotypes. Nonetheless, the occurrence of this disease suggests the possibility that PD-like behaviors may appear in natural wild populations and should be monitored during field observations."
It's interesting, nevertheless, that a case of PD has never been reported in a bonobo or a chimp, our closest primate relatives . They live up to 40 years in captivity. In contrast, Alzheimer's disease with characteristic tau pathology has been found in a number of aging nonhuman primates, including rhesus monkeys, marmosets and chimps.
Yes sure, but not having been officially documented does not equate to non-existence with such rare population incidence, as most can't survive with the motor deficit in the wild. They're also not as readily exposed to toxins, pesticides, pharmaceuticals, empty calories, etc., as humans are.
Agreed. But it is fascinating to me that Alzheimer's and Parkinson's, two conditions for which AGE is undoubtedly the largest risk factor, differ in their identified prevalence among captive primate human relatives.
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