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Alzheimer's protocol — dissolve & detoxify

aβ plaques plaques oleuropein hepps epps taurine tau

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#331 Turnbuckle

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Posted 15 October 2018 - 03:28 PM

J147 inhibits ATP Synthase activity.

 

https://onlinelibrar...1111/acel.12715

 

 

I stand corrected. However, according to that paper, J147 increases Δψ, which will potentially protect defective mitochondria from QC, as the QC process labels mitochondria with low Δψ for destruction. So the end result is the same. 



#332 Empiricus

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Posted 15 October 2018 - 04:58 PM

FWIW, this is what ACTGene HEPPS looks like. I know the quality is not good. I also took a picture with a proper camera, but can't find the USB cord to it. If I find it, or get a new one, I'll upload it if it's still relevant. 

 

Thank you for the photo. The texture looks like mine, clumpy like mine, though yours appears yellow, whereas mine is white.

 

 

I should be more specific about how to taste HEPPS. You need to add a small amount of water and then swish it around to detect the chemical taste, as taste buds are distributed around the tongue in a pattern.

 

This stuff has very little taste. 

 


Edited by Empiricus, 15 October 2018 - 04:59 PM.


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#333 tunt01

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Posted 15 October 2018 - 05:04 PM

 

Thank you for the photo. The texture looks like mine, clumpy like mine, though yours appears yellow, whereas mine is white.

 

 

If this does anything for you, I have some HEPPS.  It's pure white.

 

MALcxBZ.jpg


Edited by tunt01, 15 October 2018 - 09:41 PM.

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#334 Moumou

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Posted 16 October 2018 - 01:55 AM

Are you saying that in AD, all the sensory and motor functions that you listed are the first to show signs of the disease?

 

You will not likely be able to diagnose an AD with the primary "infected" zones I've listed, because many disease share same signs or symptoms. Even more, you won't be able acknowledge the sensory losses, because of habituation. For exemple a loss of smell can grow for decades before you percieve the loss, even if you acknowledged a sensory loss you would need for exemple an old olfactive test to refer and prove it, based on the differential.

 

 

Isn't it things that memory, problem-solving, decision-making, inability to complete tasks which were very easy before that are signs of AD?

 

 

The first zone affected by "AD" is the enthorinal cortex, close to the olfactive tubercule and hippocampus. It is to be the location of convergence between vision, auditory and olfactory signals, all together to build and organize memory.  Second zone affected by "AD" is hippocampus.

 

 


All these apply to me, yet I have no problems with vision, hearing, etc.

 

 

I think it is easier to diagnose early AD with a test of free seric copper and  maybe soon, circulating tau and amyloid beta, than from analysing your sensory losses.

 

o Elevated serum copper and ceruloplasmin levels in Alzheimer’s disease : https://onlinelibrar...1111/appy.12077

 

Or you saying that stresses to these parts of the CNS is what causes memory, thinking and other issuers?

 

 

"AD" is only the terminal phase of a cascade process which emerge principaly from aged, stressed, injuried zones, because Amyloid Beta isn't a bad peptide in itself, AB is usefull in some situations but beyond a threshold it builds an autogenerating loops that secrete the uncontrolled AB plaques of "AD". Some people won't have the disease even with AB and plaques, because they can clear and heal better, then they won't pass the "AD" threshold.

 


If not, then how "cognitive and sensorial understimulation ... and isolation" fit in within this taxonomy?

 

 

Understimulation and isolation are more of a neuroplasticity and maybe a neurogenesis problematic. Someone understimulated and isolated will have a tendency to regress cognitively, brains need various interactions and stimulations to behave well. When I speak of stimulations I obviously exclude violent stimuluses, for exemple someone who listened to soft noises isn't someone submitted to harsh noises (large scale epidemiologic studies found more "AD" people next to noisy locations). Neuroplasticy and neurogenesis only compensate and slow the cognitive loss in the process which leads to neurodegenerations like AD. For exemple transcranial stimulations improve patients condition by improving neuroplastogenesis.

 

I think Turnbucle Mito and C60 protocols could help you for your depression as they improve neuroplastogenesis.

 

o Protecting Mitochondrial Health: A Unifying Mechanism in Adult Neurogenesis:  https://www.ncbi.nlm...les/PMC5508253/

 

o Social isolation is associated with reduced neurogenesis, impaired spatial working memory performance, and altered anxiety levels in male rats:
https://www.dovepres...xt-article-OAAP

o Social Isolation Stress Induces Anxious-Depressive-Like Behavior and Alterations of Neuroplasticity-Related Genes in Adult Male Mice:
https://www.hindawi....p/2016/6212983/

 

o The Role of Neural Plasticity in Depression:

 

"Overall, neural plasticity is a vital feature of the brain in response to intrinsic and extrinsic stimuli, including stress and depression. Mounting clinical and basic research studies have illuminated the correlations between neural plasticity and depression. As the summaries in Tables 1 and 2, the effects of depression on neural plasticity are complex pathophysiological processes, involving multiple encephalic regions, such as the hippocampus, prefrontal cortex, and amygdala as well as complicated interactions of many signal pathways, such as NMDA, glutamate, and glucocorticoid. On the other hand, the changes in neural plasticity induced by stress and other negative stimuli can contribute to the onset and development of depression. The majority of antidepressant treatments, including psychotherapies, physiotherapies, and medications, exert antidepressant effects associated with neural plasticity. Unfortunately, to date, no ideal and completely effective treatment has been found for depressed patients."

 

 

o Transcranial magnetic stimulation of the precuneus enhances memory and neural activity in prodromal Alzheimer's disease : https://www.scienced...053811917310728

 

 

In the case of Alzheimer, I believe like Turnbuckle ; that it is better to prevent than heal it. Plaques builds from soluble AB accumlation. When putted together they are structured like biofilms and are then more difficult to dissolve and clear. On the long run, too much soluble AB will trigger the emergent phenomenon AB plaques.

 

But...

"Another important consideration in targeting these devastating diseases is when in the amyloid aggregation cascade or disease process to intervene. This consideration is exacerbated by the dynamic nature of the precursors of amyloid formation that are unfolded, non-native or partially folded, precluding structure-based drug design.  Decreasing  the  concentration  of  monomer would reduce the total amount of protein available to form amyloid, but such strategies could be deleterious if the monomer has a vital functional role. Interestingly, however,  the  function  of  several  amyloid  proteins remains unresolved. Perturbing oligomer formation may offer a route to treatment, but the dynamic nature of these species makes them difficult to target, and no high-resolution amyloid oligomer structures are currently available to guide such efforts. Decreasing the population of any one oligomer may drive the equilibrium towards a more toxic assembly. Small molecules could be sought to prevent oligomer formation or, conversely, to promote fibrillation, which, in turn, would decrease the lifetime and hence toxic potential of the oligomeric species. Designing interventions that promote the assembly of less toxic fibril polymorphs might also reduce disease severity."

 

A new era for understanding amyloid structures and disease: https://www.nature.c...1580-018-0060-8

 

 


Edited by Moumou, 16 October 2018 - 02:03 AM.

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#335 tolerant

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Posted 18 October 2018 - 12:05 AM

I am experiencing difficulty splitting posts into individual quotes for some unknown reason, so I'll respond without quoting.

 

Thank you tunt01 and Turnbuckle for your response on J147. After what you've said I know I won't be getting it. 

 

Thank you Momou for your detailed response. With regards to testing, we've got the following tests here:

 

Caeruloplasmin

Copper - 24hr urine 
Copper - random urine 
Copper - red cell Copper 
Copper - serum/plasma
Copper - tissue Copper
Copper oxidase

 

Caeruloplasmin and copper - serum/plasma speak for themselves, but is there anything on that list which is free copper?

 

I have ordered all of the ingredients for Turnbuckle's mito QC and stem cell protocols, however I've experienced an unpleasant reaction of C60, so I will be addressing imminently how I proceed with that.

 

What do you think is the best way to tweak Turnbuckle's Azheimer's protocol to "force" a diagnosis? I've tried taking 2 g HEPPS without any detoxifying agents and got no response. Maybe now I should try 4 g HEPPS on its own? And as far as tau is concerned, I don't know what substance, if any, dissolves tau without clearing it in Turnbuckle's latest protocol. So maybe I should be getting methylene blue and trying increasing doses without niacinamide?

 

I might get a glucose metabolism PET scan and a volumetric MRI in the next few months.


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#336 Empiricus

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Posted 22 October 2018 - 07:51 PM

Having taken a break from the protocol, still experiencing the aforementioned side-effects of the so-called HEPPS from China, yesterday I doubled my intake of taurine which I took throughout the day with oleuropein. 

 

Today I received the first of several orders I placed for HEPPS from various suppliers.  The order I received today is also from China, but another company.  And this HEPPS seems different from the previous.  Very different. 

 

New shipment vs (previous shipment):

- Bright white-yellow (dull transparent white)

- Granular powder (hard crystals)

- Dissolves instantly in water (took a while to dissolve)

- Forms white gobs when dropped into MCT oil (turned into transparent liquified bubbles)

- Mild chemical taste (essentially tasteless)

- has a smell (odorless)

 

Turnbuckle? 


Edited by Empiricus, 22 October 2018 - 08:22 PM.


#337 Empiricus

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Posted 24 October 2018 - 03:04 AM

Didn't some Europeans do a group buy of HEPPS from China? It could be useful to compare notes, as I believe I used the same suppler as the proposed group buy, and have doubts about the product.  The two Chinese products seem too different for them both to be genuine.  I question whether either are genuine. I have long since stopped consuming any from the first supplier, and am not touching the second.  I'm sticking with taurine while I wait for a shipment to arrive from the US.  


Edited by Empiricus, 24 October 2018 - 03:37 AM.


#338 Turnbuckle

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Posted 24 October 2018 - 09:30 AM

Your new new stuff sounds more like HEPPS. I've bought it from 2 US Amazon suppliers and both worked for this protocol. Both were white though one had a slight sienna tinge to it. Real HEPPS is necessary, and small changes to the chemistry can reverse the effect. I tried HEPES early on before I'd seen the research, and I can attest that it makes symptoms worse, not better. Taurine by itself is not going to do the job.


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#339 DeltaWave

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Posted 27 October 2018 - 07:59 AM

Have you tried fluvoxamine (the strongest sigma1 agonist on the market)?

 

https://www.ncbi.nlm...pubmed/29614681

 

 

 

Alzheimer's disease is characterized by abnormal amyloid-β (Aβ) peptide accumulation beginning decades before symptom onset. An effective prophylactic treatment aimed at arresting the amyloidogenic pathway would therefore need to be initiated prior to the occurrence of Aβ pathology. The SIGMAR1 gene encodes a molecular chaperone that modulates processing of the amyloid-β protein precursor (AβPP). Fluvoxamine is a selective serotonin reuptake inhibitor and a potent SIGMAR1 agonist. We therefore hypothesized that fluvoxamine treatment would reduce Aβ production and improve cognition. We firstly investigated the impact of SIGMAR1 on AβPP processing, and found that overexpression and knockdown of SIGMAR1 significantly affected γ-secretase activity in SK-N-MC neuronal cells. We then tested the impact of fluvoxamine on Aβ production in an amyloidogenic cell model, and found that fluvoxamine significantly reduced Aβ production by inhibiting γ-secretase activity. Finally, we assessed the efficacy of long-term treatment (i.e., ∼8 months) of 10 mg/kg/day fluvoxamine in the J20 amyloidogenic mouse model; the treatment was initiated prior to the occurrence of predicted Aβ pathology. Physical examination of the animals revealed no overt pathology or change in weight. We conducted a series of behavioral tests to assess learning and memory, and found that the fluvoxamine treatment significantly improved memory function as measured by novel object recognition task. Two other tests revealed no significant change in memory function. In conclusion, fluvoxamine has a clear impact on γ-secretase activity and AβPP processing to generate Aβ, and may have a protective effect on cognition in the J20 mice.

 

 

Or hesperidine?

 

https://www.ncbi.nlm...pubmed/27068363

 

 

 

Alzheimer's disease (AD) is the most frequent form of neurodegenerative disorder in elderly people. Involvement of several pathogenic events and their interconnections make this disease a complex disorder. Therefore, designing compounds that can inhibit multiple toxic pathways is the most attractive therapeutic strategy in complex disorders like AD. Here, we have designed a multi-tier screening protocol combining ensemble docking to mine BACE1 inhibitor, as well as 2-D QSAR models for anti-amyloidogenic and antioxidant activities. An in house developed phytochemical library of 200 phytochemicals has been screened through this multi-target procedure which mine hesperidin, a flavanone glycoside commonly found in citrus food items, as a multi-potent phytochemical in AD therapeutics. Steady-state and time-resolved fluorescence spectroscopy reveal that binding of hesperidin to the active site of BACE1 induces a conformational transition of the protein from open to closed form. Hesperidin docks close to the catalytic aspartate residues and orients itself in a way that blocks the cavity opening thereby precluding substrate binding. Hesperidin is a high affinity BACE1 inhibitor and only 500 nM of the compound shows complete inhibition of the enzyme activity. Furthermore, ANS and Thioflavin-T binding assay show that hesperidin completely inhibits the amyloid fibril formation which is further supported by atomic force microscopy. Hesperidin exhibits moderate ABTS(+) radical scavenging assay but strong hydroxyl radical scavenging ability, as evident from DNA nicking assay. Present study demonstrates the applicability of a novel multi-target screening procedure to mine multi-potent agents from natural origin for AD therapeutics.

 

 

 


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#340 Turnbuckle

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Posted 27 October 2018 - 09:17 AM

Have you tried fluvoxamine (the strongest sigma1 agonist on the market)?

https://www.ncbi.nlm...pubmed/29614681

 

 

Or hesperidine?

https://www.ncbi.nlm...pubmed/27068363

 

 

Good suggestions,DeltaWave . However, the protocol is about treating the root cause of AD and eliminating it, not in treating symptoms. So I'd say no to fluvoxamine, while flavonoids are a better match. An overview paper--

 

This systematic review suggests that the flavonoids reported have a potential for the treatment of neurodegenerative diseases such as PD and AD and are considered drug candidates in the future clinical research. The studies listed in this review revealed that the main targets of action for Alzheimer's disease therapy were reduction of reactive oxygen species and amyloid beta-protein production. In Parkinson's disease, reduction of the cellular oxidative potential and mechanisms of neuronal death are often involved in the neuroprotective potential of flavonoids.

https://www.ncbi.nlm...les/PMC5971291/

 

 

Some flavonoids are valuable as senolytics (and I am using them for that purpose). For AD, naringenin, rutin, and hesperidin look promising. All are widely available and very cheap.

 

 

 

 

 

 

Edited by Turnbuckle, 27 October 2018 - 09:35 AM.

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#341 tolerant

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Posted 02 November 2018 - 08:39 AM

I think it is easier to diagnose early AD with a test of free seric copper and  maybe soon, circulating tau and amyloid beta, than from analysing your sensory losses.

 

o Elevated serum copper and ceruloplasmin levels in Alzheimer’s disease : https://onlinelibrar...1111/appy.12077

 

The doctor said that these tests will only help in the diagnosis of Wilson's Disease, not AD (even though I included a link to the study in my email to him), so if I want them, I will have to fund them. What do you think?



#342 Turnbuckle

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Posted 02 November 2018 - 01:30 PM

The doctor said that these tests will only help in the diagnosis of Wilson's Disease, not AD (even though I included a link to the study in my email to him), so if I want them, I will have to fund them. What do you think?

 

Once again, get your genetics checked. If you have AD or Wilson's alleles, they will show up.



#343 lancebr

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Posted 08 November 2018 - 04:28 AM

I heard about this recent study (PMC6194148) titled: "Phenylindanes in Brewed Coffee Inhibit Amyloid-Beta and Tau Aggregation"

 

The study finds that they indentified "phenylindane as a dual-inhibitor of Aβ and tau aggregation, and propose that it is the

phenylindane component of coffee that is responsible for the observed aggregation inhibition activity of the coffee extracts

toward Aβ and tau."

 

It also stated that "Inhibition of Aβ and tau aggregation by phenylindanes in coffee can be considered as a plausible

mechanism of neuroprotection in AD pathologies for individuals who consume coffee beverages."

 

They found that the highest source of this component was in dark roasted coffee.

 

So based upon this study, is dark roasted coffee something that would be useful for this protocol?

 

https://www.ncbi.nlm...les/PMC6194148/


Edited by lancebr, 08 November 2018 - 04:30 AM.

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#344 Turnbuckle

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Posted 08 November 2018 - 09:57 AM

I heard about this recent study (PMC6194148) titled: "Phenylindanes in Brewed Coffee Inhibit Amyloid-Beta and Tau Aggregation"

 

The study finds that they indentified "phenylindane as a dual-inhibitor of Aβ and tau aggregation, and propose that it is the

phenylindane component of coffee that is responsible for the observed aggregation inhibition activity of the coffee extracts

toward Aβ and tau."

 

It also stated that "Inhibition of Aβ and tau aggregation by phenylindanes in coffee can be considered as a plausible

mechanism of neuroprotection in AD pathologies for individuals who consume coffee beverages."

 

They found that the highest source of this component was in dark roasted coffee.

 

So based upon this study, is dark roasted coffee something that would be useful for this protocol?

 

https://www.ncbi.nlm...les/PMC6194148/

 

 

While coffee extracts do have some apparent positive effects in vitro, these are somewhat sketchy in vivo. As the paper says--

 

A 2010 systematic review and meta-analysis by Santos et al. (2010) suggests that a positive correlation between coffee consumption and dementia prevention is apparent, but inconsistencies in study design and methodology make interpretation of experimental results complicated (Costa et al., 2010). A more recent study by Mirza et al. (2014) claim that there is no correlation between coffee consumption and incident dementia...

 

 

Bottom line, drinking coffee is not a problem re AD, but is not a useful treatment by itself. Used with the protocol it might help, but not sufficiently to recommend it to people who don't already drink it. Caffeine is seriously addictive. I've been drinking it for more than 50 years. I've tried to stop in the past, but was unable to.


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#345 Hebbeh

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Posted 08 November 2018 - 01:03 PM

Good points but they did infer decaf was as beneficial as regular.  I've been drinking decaf for a long time for the many benefits various studies have indicated.  IMHO it couldn't hurt.


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#346 ceridwen

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Posted 08 November 2018 - 01:37 PM

I think it works-a bit

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#347 Empiricus

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Posted 13 November 2018 - 08:13 AM

Finland has both the world's highest rate of coffee consumption (over 9kg per capita) and the world's highest dementia death rate (170 per 100,000).  

 

The typical Finn drinks 8-9 cups of coffee/day drip-brewed and lightly roasted.  Now, if dark roast is most protective, there's no surprises here. 

 

Interestingly, Finns didn't always drink lightly roasted coffee: "…Finnish coffee with light roast tastes like what it tastes like....  Finns used to drink very dark roasted coffee. Then, when the post-war depression period was finally over and coffee finally was available, the demand was so great that the roasteries realized that the folk would drink any mud they would deliver, and they left toasting half-way, just to be able to supply enough coffee through the whole country. After that, our country has been dominated by the tyranny of that light slop.” https://lacocinadesm...malainen-ruoka/

 

As it happens, Finland's death rate from dementia rose from only 20 per 100,000 in 1980 to 170 per 100,000 by 2016.  Who knows if the switch to light roast explains the rise, but the "light slop" probably isn't helping!

 

 


Edited by Empiricus, 13 November 2018 - 08:22 AM.

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