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ALZHEIMER’S DISEASE (AD) TREATMENT
The widespread belief that there is no cure or effective treatment for Alzheimer’s disease is wrong. It can be prevented, and it can be cured in the early stages, with symptoms resolving surprisingly quickly. Even in later stages it can be usefully treated. The following treatment will reverse symptoms, remove the causative plaques, and restore functional deficits that aren’t due to irreversible neuronal loss. While it doesn’t have FDA approval, it has been trialed by a number of people with AD symptoms since I posted it 3 years ago on a website for self-experimenters, with good results.
Who should use it While not making any medical recommendation, those with symptoms can benefit, and those with at least one APOE ε4 allele — one of 3 common variants of the APOE gene. Everyone is at risk, but this varies enormously. With just one ε4 variant, the risk of AD goes up 3-fold. With two ε4 variants, the risk goes up 12 fold. 15% of the population have one, and 2-3% of the population have two. I have two, thus I found it necessary to design a treatment, as the pharmaceutical industry had failed to do so.
The presence of the APOE ε4 alleles and other genes involved in AD can be found through an inexpensive genetic test, such as available from 23andMe. These aren’t the only risk factors, just the most important. Other potential factors include concussions and chemo, and certain prescription and OTC drugs can raise the odds slightly.
The cause of AD Amyloid beta (Aβ) is the initiator of AD, which also involves hyperphosphorylated-tau (p-tau) as a secondary aspect. They propagate in prion-like fashion and form plaques. These plaques are damaging in themselves, and they also result in inflammation that recruits microglia, making it worse.
The treatment In the following treatment protocol, HEPPS (a biological buffer) is used to dissolve Aβ, along with antioxidants to render the dissolved portion non-toxic. Nicotinamide is used to dephosphorylate p-tau. P-tau and Aβ are sticky, toxic, and can redeposit. It is important to detox them as the half-life of the cerebral spinal fluid that carries the dissolved debris is around 11 hours, so without taking measures, a portion could redeposit for a day or two afterward.
Where to get the ingredients All items are available from Amazon in the US, and most from other sources, such as iHerb. HEPPS is available to residential addresses through Amazon. If you have a commercial or educational address, it can be obtained through Research Products International (RPI) more cheaply, and also from Granger. It is moisture sensitive, so should be sealed in a ziplock bag with silica gel packets after opening. As all of it is sourced from China, a war could interrupt the supply.
Alzheimer’s treatment protocol The following is taken as pills and/or dissolved in fruit juice once a day. Suggested frequency is three times a week until function is restored (and preferably longer), then once a week. Improvement may be noted quickly, but that doesn’t mean the plaques are gone. Any residual Aβ will act as seeds proliferating more of it in prion-like fashion.
Removing plaques ● *HEPPS (200-500 mg initially, increasing to 1g) ● *Taurine (6 g) ● Nicotinamide (500 mg)
Detox ● Hydroxytyrosol (100 mg) ● Sulforaphane glucosinolate (50 mg) ● Astaxanthin (24 mg) ● *Vitamin C (500 mg)
Optional ● *L-Serine (0.5-1 g), for memory ● *Glutathione, reduced (0.5-1g), master antioxidant ● *Melatonin (3-5 mg), only if taken at night
*Can be mixed into fruit juice
Notes
Taurine alone will not do the job. It requires HEPPS (also called EPPS). Do not use the similarly named HEPES. It is remarkably close to HEPPS chemically, but does the exact opposite. It compacts plaques rather than dissolving them.
For prevention or for early symptoms, 1 gram of HEPPS can be used initially. If there is a lot of plaque, removing too much at once can cause headaches and redeposition. So in that case, begin with a lower dose and increase it incrementally.
References
1. Amyloid-β and tau: the trigger and bullet in Alzheimer disease pathogenesis. Aβ is upstream of tau in AD pathogenesis and triggers the conversion of tau from a normal to a toxic state, but there is also evidence that toxic tau enhances Aβ toxicity via a feedback loop. Because soluble toxic aggregates of both Aβ and tau can self-propagate and spread throughout the brain by prionlike mechanisms, successful therapeutic intervention for AD would benefit from detecting these species before plaques, tangles, and cognitive impairment become evident and from interfering with the destructive biochemical pathways that they initiate. https://www.ncbi.nlm...pubmed/24493463
2. EPPS [HEPPS] reduces Aβ-aggregate-induced memory deficits in mice Previously, we reported a series of small ionic molecules that could accelerate the formation of Aβ aggregates in vitro. Unexpectedly, in addition to the compounds facilitating Aβ aggregation, we identified six small molecules that inhibited the formation of Aβ oligomers and fibrils13... Among the six orally administered molecules, only 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid (EPPS) ameliorated AD-like phenotypes in our mouse model. https://www.nature.com/articles/ncomms9997
3. Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease We orally administered taurine via drinking water to adult APP/PS1 transgenic mouse model for 6 weeks. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice. https://www.nature.com/articles/srep07467
4. Nicotinamide Restores Cognition in Alzheimer's Disease Transgenic Mice via a Mechanism Involving Sirtuin Inhibition and Selective Reduction of Thr231-Phosphotau These preclinical findings suggest that oral nicotinamide may represent a safe treatment for AD and other tauopathies, and that phosphorylation of tau at Thr231 may regulate tau stability. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2617713/
5. Preventive and therapeutic potential of ascorbic acid in neurodegenerative diseases. Ascorbic acid acts mainly by decreasing oxidative stress and reducing the formation of protein aggregates, which may contribute to the reduction of cognitive and/or motor impairments observed in neurodegenerative processes. https://www.ncbi.nlm.nih.gov/pubmed/28980404
6. Astaxanthin Ameliorated Parvalbumin-Positive Neuron Deficits and Alzheimer’s Disease-Related Pathological Progression in the Hippocampus of AppNL-G-F/NL-G-F Mice The results indicated that astaxanthin ameliorated memory deficits and significantly reversed AD pathological processes (Aβ42 deposition, pTau formation, GSH decrease, and PV-positive neuronal deficits). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7078363/
7. The neuroprotective mechanisms and effects of sulforaphane In the brains of transgenic mouse models of Alzheimer’s disease, SFN [sulforaphane] reduces the amount of amyloid beta (Aβ) and phosphorylated tau proteins as well as their aggregation. It also reduces memory deficits in mouse models... The oxidative stress that the aggregated proteins cause in Alzheimer's disease is also reduced with SFN supplementation. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6611193/
8. Diet Supplementation with Hydroxytyrosol Ameliorates Brain Pathology and Restores Cognitive Functions in a Mouse Model of Amyloid-β Deposition We found that HT supplementation significantly improved cognitive functions of TgCRND8 mice and significantly reduced Aβ42 and pE3-Aβ plaque area and number in the cortex; in the hippocampal areas of HT-fed TgCRND8 mice, we found a significant reduction in the pE3-Aβ plaque number together with a tendency toward a reduction in Aβ42 load and pE3-Aβ plaque area, associated with a marked reduction of TNF-α expression and astrocyte reaction. https://pubmed.ncbi.nlm.nih.gov/29710709/
The above methods and compositions are patented and available for licensing.
© 2023 Lou Dischler
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