Posted 28 March 2017 - 10:16 PM
Posted 28 March 2017 - 10:31 PM
Substantial amount of excitement in the dementosphere about:
http://journals.plos...al.pmed.1002258
Interested in when you will experience dementia?
Posted 15 April 2017 - 03:05 PM
PLoS One. 2017 Apr 14;12(4):e0175369.
Metabolic changes and inflammation in cultured astrocytes from the 5xFAD mouse model of Alzheimer's disease: Alleviation by pantethine.
van Gijsel-Bonnello M1, Baranger K1, Benech P1, Rivera S1, Khrestchatisky M1, de Reggi M1, Gharib B1.
Astrocytes play critical roles in central nervous system homeostasis and support of neuronal function. A better knowledge of their response may both help understand the pathophysiology of Alzheimer's disease (AD) and implement new therapeutic strategies. We used the 5xFAD transgenic mouse model of AD (Tg thereafter) to generate astrocyte cultures and investigate the impact of the genotype on metabolic changes and astrocytes activation. Metabolomic analysis showed that Tg astrocytes exhibited changes in the glycolytic pathway and tricarboxylic acid (TCA) cycle, compared to wild type (WT) cells. Tg astrocytes displayed also a prominent basal inflammatory status, with accentuated reactivity and increased expression of the inflammatory cytokine interleukin-1 beta (IL-1β). Compensatory mechanisms were activated in Tg astrocytes, including: i) the hexose monophosphate shunt with the consequent production of reducing species; ii) the induction of hypoxia inducible factor-1 alpha (HIF-1α), known to protect against amyloid-β (Aβ) toxicity. Such events were associated with the expression by Tg astrocytes of human isoforms of both amyloid precursor protein (APP) and presenilin-1 (PS1). Similar metabolic and inflammatory changes were induced in WT astrocytes by exogenous Aβ peptide. Pantethine, the vitamin B5 precursor, known to be neuroprotective and anti-inflammatory, alleviated the pathological pattern in Tg astrocytes as well as WT astrocytes treated with Aß. In conclusion, our data enlighten the dual pathogenic/protective role of astrocytes in AD pathology and the potential protective role of pantethine.
PMID: 28410378
Posted 21 April 2017 - 03:17 AM
Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia.
In 2013, a UK Medical Research Council team stopped brain cells dying in an animal for the first time, creating headline news around the world.
But the compound used was unsuitable for people, as it caused organ damage.
Now two drugs have been found that should have the same protective effect on the brain and are already safely used in people.
[...]
Prof Mallucci told the BBC News website: "Both were very highly protective and prevented memory deficits, paralysis and dysfunction of brain cells."
The best known drug of the pair is trazodone, which is already taken by patients with depression.
The other, DBM, is being tested in cancer patients.
Posted 21 April 2017 - 07:06 PM
Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia.
In 2013, a UK Medical Research Council team stopped brain cells dying in an animal for the first time, creating headline news around the world.
But the compound used was unsuitable for people, as it caused organ damage.
Now two drugs have been found that should have the same protective effect on the brain and are already safely used in people.
[...]
Prof Mallucci told the BBC News website: "Both were very highly protective and prevented memory deficits, paralysis and dysfunction of brain cells."
The best known drug of the pair is trazodone, which is already taken by patients with depression.
The other, DBM, is being tested in cancer patients.
looks like trazodone is easy to get online and cheap. Assuming you trust the source.
Posted 21 April 2017 - 07:25 PM
Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia.
[source]In 2013, a UK Medical Research Council team stopped brain cells dying in an animal for the first time, creating headline news around the world.
But the compound used was unsuitable for people, as it caused organ damage.
Now two drugs have been found that should have the same protective effect on the brain and are already safely used in people.
[...]
Prof Mallucci told the BBC News website: "Both were very highly protective and prevented memory deficits, paralysis and dysfunction of brain cells."
The best known drug of the pair is trazodone, which is already taken by patients with depression.
The other, DBM, is being tested in cancer patients.
looks like trazodone is easy to get online and cheap. Assuming you trust the source.
Posted 21 April 2017 - 07:40 PM
I dont think he expects it to be a cure. He wants to do clinical trials to see if it slows down the progression in humans. It may be like everything else and only work in the mice and not us big rats. Now, I dont know anything about this guy or is credibility but here is the source article.
https://academic.oup...eIF2-P-mediated
Posted 22 April 2017 - 01:35 AM
I or my rat have no reason to use it so it will go in the deep freeze if I am successful at making it.
I think you will be as the process is pretty much foolproof.
Next, I will look at making other useful phages that might be good for general health. So far all I have seen on the market is the product floraphage but I'm not convinced it's all that beneficial.
In fact I think anyone watching the video you posted and taking head of what the selective elimination of bad bacteria, including senescent cell preservation, can do, is ahead of the game.
This is especially true in the gut with its cell turnover of 5 days = short telomeres.
The systemic effect of reducing NF-kB on telomerase, cell signalling, replacement by stem cells etc, NAD+, SIRT etc upregulation due to CD38 reduction, etc-etc is potentially unparalleled IMHO. (Gut feeling 
)
I for one would gladly visit you and donate bacteria for bacteriophages 'research' specific to the the bacteria I want dead.
The question is; how to isolate said bad bacteria?
Edited by Logic, 22 April 2017 - 01:52 AM.
Posted 22 April 2017 - 02:03 AM
The professor is nuts. There is no evidence that trazodone prevents or cures neuradegenerative diseases.
Even the paper says the mice are still loaded with prions or misfolded proteins. It's not actually clearing misfolded proteins. Trazodone won't be much more than symptomatic relief or at best be a very downstream intervention.
Posted 22 April 2017 - 03:22 AM
I or my rat have no reason to use it so it will go in the deep freeze if I am successful at making it.
I think you will be as the process is pretty much foolproof.
Next, I will look at making other useful phages that might be good for general health. So far all I have seen on the market is the product floraphage but I'm not convinced it's all that beneficial.
In fact I think anyone watching the video you posted and taking head of what the selective elimination of bad bacteria, including senescent cell preservation, can do, is ahead of the game.
This is especially true in the gut with its cell turnover of 5 days = short telomeres.
The systemic effect of reducing NF-kB on telomerase, cell signalling, replacement by stem cells etc, NAD+, SIRT etc upregulation due to CD38 reduction, etc-etc is potentially unparalleled IMHO. (Gut feeling
I for one would gladly visit you and donate bacteria for bacteriophages 'research' specific to the the bacteria I want dead.
The question is; how to isolate said bad bacteria?
Turns out the price the lab gave me was better than I thought. I only asked for a small amount so thats what he quoted me. Later I found out that I could have the entire batch for that price which is several ml but noone seemed interested so I let it go. If we ever had 10 or so people interested it would actually be affordable and safer.
Posted 23 April 2017 - 02:34 PM
I or my rat have no reason to use it so it will go in the deep freeze if I am successful at making it.
I think you will be as the process is pretty much foolproof.
Next, I will look at making other useful phages that might be good for general health. So far all I have seen on the market is the product floraphage but I'm not convinced it's all that beneficial.
In fact I think anyone watching the video you posted and taking head of what the selective elimination of bad bacteria, including senescent cell preservation, can do, is ahead of the game.
This is especially true in the gut with its cell turnover of 5 days = short telomeres.
The systemic effect of reducing NF-kB on telomerase, cell signalling, replacement by stem cells etc, NAD+, SIRT etc upregulation due to CD38 reduction, etc-etc is potentially unparalleled IMHO. (Gut feeling
I for one would gladly visit you and donate bacteria for bacteriophages 'research' specific to the the bacteria I want dead.
The question is; how to isolate said bad bacteria?
Turns out the price the lab gave me was better than I thought. I only asked for a small amount so thats what he quoted me. Later I found out that I could have the entire batch for that price which is several ml but noone seemed interested so I let it go. If we ever had 10 or so people interested it would actually be affordable and safer.
Do you mean for M13 specifically?
It was you who posted the video on home bacteriophage isolation wasn't it?
I want to kill off many different bacteria!
Posted 25 April 2017 - 11:45 AM
I'd be willing to try it
If you are willing to try, the most likely drug that can prevent and cure Alzheimer's is Niagen. A trial will start soon. My father has improved after 4 months of Niagen.
Are you referring to this study?: https://clinicaltria...how/NCT02942888
May I ask what dosage your father take?
Posted 30 April 2017 - 10:05 PM
These studies are not primarily focused on Alzheimer's. They are on hearing loss and traumatic brain injury, though they talk a little about how it relates to Alzheimer's and dementia. This first one below is from a few days ago, the next one is from 2016, and it references another study from 2013, all by the same authors.
Free Radic Biol Med. 2017 Apr 21. pii: S0891-5849(17)30546-4.
Like CTE, the ongoing neurodegeneration associated with bTBIs has been shown to be a Tau protein-linked disorder, or tauopathy [10, 11]. In uninjured brains, the soluble microtubule-associated protein, Tau, is enriched in neuronal axons where it plays a key role in stimulating microtubule formation, outgrowth, and subsequent maintenance of cytoskeletal stability, thus promoting axonal and dendritic transport [12]. However, Tau is susceptible to stress-induced hyperphosphorylation in response to single or repetitive neurotraumas. Hyperphosphorylated Tau is prone to misfolding and aggregation, leading to destabilization of microtubules and, thus, compromised neuronal viability and function. Moreover, once initiated, stress-induced destabilization of Tau can result in propagative waves of Tau dysfunction, as hyperphosphorylated Tau inclusions have a propensity to recruit and subvert functional Tau proteins in a prion-like manner that can progress in a transcellular fashion [13, 14]. Although the neurofibrillary tangles (NFTs) that result from this pathophysiological process have long been appreciated as a central feature of neuropathies, such as Alzheimer's disease and dementia, it is now recognized that the oligomeric “seeds” of hyperphosphorylated Tau that initiate the formation of NFTs are sufficient for the neuronal cell death and cognitive deficits associated with these disorders [15]. Thus, early intervention strategies aimed at attenuating or eliminating the etiological precursors of NFTs would have significant clinical impact on both the acute and chronic manifestations of bTBI-related cognitive dysfunction.
Posted 09 May 2017 - 11:50 AM
An Australian biotech company is launching a novel attack on Alzheimer's disease. Rather than following the traditional treatment paths, it is taking a new route.
This month the first of 174 patients on an international trial will begin taking a drug to lessen the level of the stress hormone, cortisol, in the brain.
There is evidence to suggest this hormone has role in Alzheimer's. It is not promoted as the sole cause of the disease but rather as a contributing factor.
Current wisdom holds that it is likely that a few factors combine to bring about Alzheimer's. Some think cortisol may be one of them....
The trial aims to use Xanamem, to lower cortisol in the brains of people with early mild Alzheimer's and assess whether this can delay further deterioration.
Read more: http://www.afr.com/l...20170506-gvzk57
Posted 09 May 2017 - 03:08 PM
Good find Rwac. I am only half surprised, it is not the first time cortisol is involved in brain disease, e.g. epilepsy: "...The unbalancing in morning cortisol and DHEAS levels was emphasized by increased C/Dr. Similar changes are present in aging and characterize other neurologic conditions (i.e., primary depression and dementia) (27–30)..."
Galimberti CA, Magri F, Copello F, et al. Seizure frequency and cortisol and dehydroepiandrosterone sulfate (DHEAS) levels in women with epilepsy receiving antiepileptic drug treatment. Epilepsia. 2005;46(4):517-23. If the ratio cortisol/dhea-s turns to be also a possible drug target, it can also be lowered by natural supplementation with DHEA.
Posted 23 May 2017 - 11:35 PM
Bad news for Lithium. I don't think this has been posted yet. It's from a few months ago.
J Clin Psychiatry. 2017 Feb;78(2):e139-e145.
Posted 25 May 2017 - 06:12 AM
Hi mag1, good point. Here's 2c from someone who has tried every neurologically oriented diet in the book, more or less. Some of this is a repeat, but I think it bears repeating...
If only it were the Warburg effect. Cancer cells become cancerous in part because they learn to obtain energy from the glycolytic pathway. This process makes them overly reliant on glucose metabolism. But in the AD brain, this pathway is insufficiently activated to compensate for impaired glucose metabolism and sensitivity. (This would seem to involve damage to PDH, for one thing.) As a result, some neurons die due to poor maintenance and impaired waste efflux, while others enter a senescent state.
A ketogenic diet can often relieve this condition via the provision of acetoacetate and/or beta hydroxybutyrate, which bypass PDH to provide energy. From what I've seen of Dale Breden's work, for example, I must say I'm impressed with the approach.
Personally, as someone with probably impaired zinc transport, it just doesn't work. The reason is that protein intake on this diet is necessarily quite a bit higher, and richer in glutamic acid, than would be the case on a low-calorie but sugar-rich vegan diet. As a result, glutamate runs amok in the brain, resulting in excitotoxicity. Zinc gluconate can ameliorate this condition, but not to a sufficient extent, at least in my rather mild case. Cat's claw works better, but it crushes dopamine levels required for mathematical thinking and visualization, so in my own line of work it's not a longterm solution.
We can sort of choose between the aforementioned 2 diets. In one case, a high-ish protein intake probably results in elevated IGF1 over time. In the other, IGF1 is low (ideally, very low) but fasting glucose may eventually reach diabetic levels. From a cancer standpoint, if Laron syndrome is any clue, this is actually just fine because we need both elevated blood glucose and normal or higher IGF1 to create malignant tumors. (I actually just had an IGF1 test to see how well my protein restriction is going. We'll see.)
In all this, we have to remember that the most successful AD prevention methodology of all time was apparently drinking a few juices per week, if the Kame study is to be believed. Personally, I've taken to buying the more expensive, lower-sugar "greens" powders (not from China), so I can get the benefits of obscure fruits, veggies, and berries, but without the sugar or the hassle of juicing tons of fibrous material. (Beet powder is particularly helpful, I notice.)
The only other thing I have to add in this vein is that I've noticed that hydrogen water seems to help me sleep. It could be coincidence, so I plan to retest this soon. That matters because, in theory, it could potentially prevent the aforementioned excitotoxicity, thereby allowing zinc-impaired people like me to switch to and remain on a ketogenic diet. We'll see.
Posted 25 May 2017 - 11:43 PM
res, I have been very interested in PMID: 25579853 of late.
Bring glucose levels way way down.
This would be such a great test of the entire metabolic approach to cancer.
Seems like a really good to try out, though in most extreme implementation
would need to be done in an ICU; probably best not to be that extreme and
just bring down glucose somewhat more moderately.
Edited by mag1, 25 May 2017 - 11:45 PM.
Posted 26 May 2017 - 08:42 AM
Posted 05 June 2017 - 11:50 PM
PQQ, Blueberry, Green Tea, Carnosine, and Vitamin D:
Heliyon. 2017 Apr 4;3(4):e00279. doi: 10.1016/j.heliyon.2017.e00279. eCollection 2017 Apr.
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