HM Institute’s Holistic Alzheimer’s Disease Protocol

Bredesen…naturopathic…improved with other

 

In order to determine a satisfactory course of remedial action, it is necessary to know Alzheimers’ etiology (causes). In Alzheimer’s disease, a peptide called amyloid beta forms aggregates (oligomers), which accumulate in the brain and form deposits known as amyloid plaques. (Source) Inflammation and oxidative damage are also associated with the progession of Alzheimer’s disease. (Source). Recent research at the Brown University in Rhode Island and elsewhere (Source), suggests that the development of Alzheimers is connected to lifestyle assaults, in particular to that which causes diabetes, the lack of insulin sensitivity. To read more, click here….

Non-invasive brain stimulation. Few studies have demonstrated that transcranial direct current stimulation (tDCS), a method of neuromodulation with consecutive robust excitability changes within the stimulated cortex area, is beneficial in AD. There is also evidence that tDCS enhances memory function in cognitive rehabilitation in depressive patients, Parkinson’s disease, and stroke. tDCS improves working and visual recognition memory in humans and object-recognition learning in the elderly. AD’s neurobiological mechanisms comprise changes in neuronal activity and the cerebral blood flow (CBF) caused by altered microvasculature, synaptic dysregulation from ß-amyloid peptide accumulation, altered neuromodulation via degenerated modulatory amine transmitter systems, altered brain oscillations, and changes in network connectivity. tDCS alters (i) neuronal activity and (ii) human CBF, (iii) has synaptic and non-synaptic after-effects (iv), can modify neurotransmitters polarity-dependently, (v) and alter oscillatory brain activity and (vi) functional connectivity patterns in the brain. It thus is reasonable to use tDCS as a therapeutic instrument in AD as it improves cognitive function in manner based on a disease mechanism. Moreover, it could prove valuable in other types of dementia. Future large-scale clinical and mechanism-oriented studies may enable us to identify its therapeutic validity in other types of demential disorders” .Front Psychiatry. 2012;3:48. doi: 10.3389/fpsyt.2012.00048. Epub 2012 May 15. Action mechanisms of transcranial direct current stimulation in Alzheimer’s disease and memory loss. Hansen N. Source Department of Neurophysiology, Ruhr University Bochum Bochum, Germany. (Source). There are 13 studies in pub med on tDCS and Alzheimier like conditions (source) and source a.  Clinical trial ongoing. For Israel research, see source. For technique modalities, source. This technique is also good for pain source and source b and source c

 

In this talk, we will thus show how to avoid Alzheimer’s as well as other neurological risks by over 90 percent. Reversal of most of these mental disorders has also been established, including for Alzheimer’s Disease via the Bredensen protocol. Because toxemia also affects the gastro-intestinal system as much as the brain, safe and efficient holistic gut restoration techniques will also be examined including, but not limited to PH correction, bile & digestive enzyme secretion, insuline (glycemic variability) regulation, microbiota diversity, liver optimization, tastebuds sensitization, nose receptors activation, neurogenesis and, among other gut-brain issues, mastication, saliva balance, bowel movement, cellular detox, wine medicine, coconut therapy, hyperthermia, smokeless cannabis, clinical nutrition, leaky gut & leaky brain fixing, colon cleaning and, among other holistic techniques, the often forgotten circadian element, known as chronobiology,  a medical speciality which is popular in both Chinese and French medicine. (8)

 

Holy basil….depree see amen

 

protocol has been tested in over 250 subjects to effectively reverse cognitive decline in neurodegenerative diseases such as Alzheimer’s Disease and Dementia.

Food Chem Toxicol. 2008 Aug;46(8):2881-7. doi: 10.1016/j.fct.2008.05.030. Epub 2008 Jun 4.

Curcumin protected PC12 cells against beta-amyloid-induced toxicity through the inhibition of oxidative damage and tau hyperphosphorylation.

Park SY1, Kim HS, Cho EK, Kwon BY, Phark S, Hwang KW, Sul D.

Author information

Abstract

One of the pathological hallmarks of Alzheimer’s disease is the progressive accumulation of beta-amyloid (Abeta) in the form of senile plaques, and Abeta insult to neuronal cells has been identified as one of the major causes of the onset of the disease. Curcumin, the major and most active antioxidant of Curcuma longa, protects neuronal cells against Abeta-induced toxicity. Therefore, in this study, we investigated the neuroprotective mechanisms by which curcumin acts against Abeta (25-35)-induced toxicity in PC12 cells. Following the exposure of PC12 cells to 10 microM Abeta (25-35) for 24h, significant increases in the level of antioxidant enzymes, and DNA damage were observed, and these increases were accompanied by a decrease in cell viability, and an increase in intracellular calcium levels and tau hyperphosphorylation. In addition, pretreatment of PC12 cells with 10 microg/ml curcumin for 1h significantly reversed the effect of Abeta, by decreasing the oxidative stress, and DNA damage induced by Abeta, as well as attenuating the elevation of intracellular calcium levels and tau hyperphosphorylation induced by Abeta. Taken together, these data indicate that curucmin protected PC12 cells against Abeta-induced neurotoxicity through the inhibition of oxidative damage, intracellular calcium influx, and tau hyperphosphorylation.

https://www.ncbi.nlm.nih.gov/pubmed/18573304

FASEB J. 2015 Jul;29(7):2681-9. doi: 10.1096/fj.14-264218. Epub 2015 Mar 24.

ω-3 Supplementation increases amyloid-β phagocytosis and resolvin D1 in patients with minor cognitive impairment.

Fiala M1, Halder RC2, Sagong B2, Ross O2, Sayre J2, Porter V2, Bredesen DE2.

Author information

Abstract

We investigated the effects of 4-17 month supplementation with ω-3 fatty acids and antioxidants (Smartfish drink; Smartfish AS, Oslo, Norway) in 12 patients with minor cognitive impairment (MCI) [minimental state examination (MMSE) ≥19], 2 patients with pre-MCI (normal MMSE), and 7 patients with Alzheimer disease (AD) (MMSE <19). We measured the phagocytosis of amyloid-β 1-42 (Aβ) by flow cytometry and microscopy, the transcription of inflammatory genes by RT-PCR, the production of resolvin D1 (RvD1) by enzyme immunoassay, and the cognitive status by MMSE. In patients with MCI and pre-MCI, phagocytosis of Aβ by monocytes increased from 530 to 1306 mean fluorescence intensity units (P = 0.016). The increase in patients with AD was not significant (N.S.). The lipidic mediator RvD1, which stimulates Aβ phagocytosis in vitro, increased in macrophages in 80% of patients with MCI and pre-MCI (mean increase 9.95 pg/ml) (N.S.). Transcription of inflammatory genes’ mRNAs was increased in a subgroup of patients with low transcription at baseline, whereas it was not significantly changed in patients with high transcription at baseline. The mean MMSE score of patients with MCI and pre-MCI was 25.9 at baseline and 25.7 after 4-17 months (N.S.). Our study is the first to show significant immune and biochemical effects of ω-3 fatty acids with antioxidants in patients with MCI. Cognitive benefits of ω-3 supplementation in patients with MCI should be tested in a clinical trial.

KEYWORDS:

https://www.ncbi.nlm.nih.gov/pubmed/25805829

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Neurochem Int. 2017 May;105:64-79. doi: 10.1016/j.neuint.2017.01.008. Epub 2017 Jan 23.

Coconut oil protects cortical neurons from amyloid beta toxicity by enhancing signaling of cell survival pathways.

Nafar F1, Clarke JP1, Mearow KM2.

Author information

Abstract

Alzheimer’s disease is a progressive neurodegenerative disease that has links with other conditions that can often be modified by dietary and life-style interventions. In particular, coconut oil has received attention as having potentially having benefits in lessening the cognitive deficits associated with Alzheimer’s disease. In a recent report, we showed that neuron survival in cultures co-treated with coconut oil and Aβ was rescued compared to cultures exposed only to Aβ. Here we investigated treatment with Aβ for 1, 6 or 24 h followed by addition of coconut oil for a further 24 h, or treatment with coconut oil for 24 h followed by Aβ exposure for various periods. Neuronal survival and several cellular parameters (cleaved caspase 3, synaptophysin labeling and ROS) were assessed. In addition, the influence of these treatments on relevant signaling pathways was investigated with Western blotting. In terms of the treatment timing, our data indicated that coconut oil rescues cells pre-exposed to Aβ for 1 or 6 h, but is less effective when the pre-exposure has been 24 h. However, pretreatment with coconut oil prior to Aβ exposure showed the best outcomes. Treatment with octanoic or lauric acid also provided protection against Aβ, but was not as effective as the complete oil. The coconut oil treatment reduced the number of cells with cleaved caspase and ROS labeling, as well as rescuing the loss of synaptophysin labeling observed with Aβ treatment. Treatment with coconut oil, as well as octanoic, decanoic and lauric acids, resulted in a modest increase in ketone bodies compared to controls. The biochemical data suggest that Akt and ERK activation may contribute to the survival promoting influence of coconut oil. This was supported by observations that a PI3-Kinase inhibitor blocked the rescue effect of CoOil on Aβ amyloid toxicity. Further studies into the mechanisms of action of coconut oil and its constituent medium chain fatty acids are warranted.

KEYWORDS:

Amyloid toxicity; Coconut oil; Cortical neurons; Neural protection; Signaling pathways

PMID: 28126466 DOI: 10.1016/j.neuint.2017.01.008

https://www.ncbi.nlm.nih.gov/pubmed/28126466

 

Cannabis reverses aging processes in the brain, study suggests

Researchers restore the memory performance of Methuselah mice to a juvenile stage

Date:
May 8, 2017
Source:
University of Bonn
Summary:
Memory performance decreases with increasing age. Cannabis can reverse these ageing processes in the brain. This was shown in mice by scientists at the University of Bonn with their colleagues at The Hebrew University of Jerusalem (Israel). Old animals were able to regress to the state of two-month-old mice with a prolonged low-dose treatment with a cannabis active ingredient. This opens up new options, for instance, when it comes to treating dementia.
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Prof. Dr. Andreas Zimmer (left) and the North Rhine-Westphalia science minister Svenja Schulze (centre) in the lab of the Institute of Molecular Psychiatry at University of Bonn.
Credit: © Photo: Volker Lannert/Uni Bonn

Memory performance decreases with increasing age. Cannabis can reverse these ageing processes in the brain. This was shown in mice by scientists at the University of Bonn with their colleagues at The Hebrew University of Jerusalem (Israel). Old animals were able to regress to the state of two-month-old mice with a prolonged low-dose treatment with a cannabis active ingredient. This opens up new options, for instance, when it comes to treating dementia. The results are now presented in the journal Nature Medicine.

Like any other organ, our brain ages. As a result, cognitive ability also decreases with increasing age. This can be noticed, for instance, in that it becomes more difficult to learn new things or devote attention to several things at the same time. This process is normal, but can also promote dementia. Researchers have long been looking for ways to slow down or even reverse this process.

Scientists at the University of Bonn and The Hebrew University of Jerusalem (Israel) have now achieved this in mice. These animals have a relatively short life expectancy in nature and display pronounced cognitive deficits even at twelve months of age. The researchers administered a small quantity of THC, the active ingredient in the hemp plant (cannabis), to mice aged two, twelve and 18 months over a period of four weeks.

Afterwards, they tested learning capacity and memory performance in the animals — including, for instance, orientation skills and the recognition of other mice. Mice who were only given a placebo displayed natural age-dependent learning and memory losses. In contrast, the cognitive functions of the animals treated with cannabis were just as good as the two-month-old control animals. “The treatment completely reversed the loss of performance in the old animals,” reported Prof. Andreas Zimmer from the Institute of Molecular Psychiatry at the University of Bonn and member of the Cluster of Excellence ImmunoSensation.

Years of meticulous research

This treatment success is the result of years of meticulous research. First of all, the scientists discovered that the brain ages much faster when mice do not possess any functional receptors for THC. These cannabinoid 1 (CB1) receptors are proteins to which the substances dock and thus trigger a signal chain. CB1 is also the reason for the intoxicating effect of THC in cannabis products, such as hashish or marihuana, which accumulate at the receptor. THC imitates the effect of cannabinoids produced naturally in the body, which fulfil important functions in the brain. “With increasing age, the quantity of the cannabinoids naturally formed in the brain reduces,” says Prof. Zimmer. “When the activity of the cannabinoid system declines, we find rapid ageing in the brain.”

To discover precisely what effect the THC treatment has in old mice, the researchers examined the brain tissue and gene activity of the treated mice. The findings were surprising: the molecular signature no longer corresponded to that of old animals, but was instead very similar to that of young animals. The number of links between the nerve cells in the brain also increased again, which is an important prerequisite for learning ability. “It looked as though the THC treatment turned back the molecular clock,” says Zimmer.

Next step: clinical trial on humans

A low dose of the administered THC was chosen so that there was no intoxicating effect in the mice. Cannabis products are already permitted as medications, for instance as pain relief. As a next step, the researchers want to conduct a clinical trial to investigate whether THC also reverses ageing processes in the brain in humans and can increase cognitive ability.

The North Rhine-Westphalia science minister Svenja Schulze appeared thrilled by the study: “The promotion of knowledge-led research is indispensable, as it is the breeding ground for all matters relating to application. Although there is a long path from mice to humans, I feel extremely positive about the prospect that THC could be used to treat dementia, for instance.”

Story Source:

Materials provided by University of BonnNote: Content may be edited for style and length.


Journal Reference:

  1. Andras Bilkei-Gorzo, Onder Albayram, Astrid Draffehn, Kerstin Michel, Anastasia Piyanova, Hannah Oppenheimer, Mona Dvir-Ginzberg, Ildiko Rácz, Thomas Ulas, Sophie Imbeault, Itai Bab, Joachim L Schultze, Andreas Zimmer. A chronic low dose of Δ9-tetrahydrocannabinol (THC) restores cognitive function in old miceNature Medicine, 2017; DOI: 10.1038/nm.4311

 

 

Published online 2008 Nov 8. doi:  10.1016/j.neuint.2008.10.008

PMCID: PMC2892907

NIHMSID: NIHMS196020

PMID: 19041676

Dietary supplementation with resveratrol reduces plaque pathology in a transgenic model of Alzheimer’s Disease

Saravanan S. Karuppagounder,a John T. Pinto,b Hui Xu,a Lian H. Chen,a M. Flint Beal,c and Gary E. Gibsona,*

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The publisher’s final edited version of this article is available at Neurochem Int

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Abstract

article-meta

Resveratrol, a polyphenol found in red wine, peanuts, soy beans, and pomegranates, possesses a wide range of biological effects. Since resveratrol’s properties seem ideal for treating neurodegenerative diseases, its ability to diminish amyloid plaques was tested. Mice were fed clinically feasible dosages of resveratrol for forty-five days. Neither resveratrol nor its conjugated metabolites were detectable in brain. Nevertheless, resveratrol diminished plaque formation in a region specific manner. The largest reductions in the percent area occupied by plaques were observed in medial cortex (−48%), striatum (−89%) and hypothalamus (−90%). The changes occurred without detectable activation of SIRT-1 or alterations in APP processing. However, brain glutathione declined 21% and brain cysteine increased 54%. The increased cysteine and decreased glutathione may be linked to the diminished plaque formation. This study supports the concept that onset of neurodegenerative disease may be delayed or mitigated with use of dietary chemo-preventive agents that protect against β-amyloid induced neuronal damage.

Keywords: Oxidative stress, mitochondria, Alzheimer’s disease, Aβ peptide, Stilbenes

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Introduction

Mitochondrial dysfunction and oxidative stress have been implicated in multiple neurodegenerative diseases including Alzheimer’s disease (AD) (Balaban et al., 2005; Beal, 2005; Gibson et al., 2005), and the changes can be plausibly linked to plaque and tangle formation. Studies on postmortem tissues from AD patients reveal reductions in key thiamine-dependent enzymes of the pentose shunt (transketolase), the tricarboxylic acid cycle (TCA) (i.e., the α-ketoglutarate dehydrogenase complex; KGDHC) and the link of glycolysis and the TCA cycle (i.e., the pyruvate de

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892907/

 

 

 

 

 

 

 

 

 

 

Basics

 

This protocol used to be called the MEND protocol, but now is called ReCODE. R

Aging (Albany NY). 2016 Jun; 8(6): 1250–1258.

Published online 2016 Jun 12. doi:  10.18632/aging.100981

PMCID: PMC4931830

PMID: 27294343

Reversal of cognitive decline in Alzheimer’s disease

Dale E. Bredesen,1,2 Edwin C. Amos,3 Jonathan Canick,4 Mary Ackerley,5 Cyrus Raji,6 Milan Fiala,7 and Jamila Ahdidan8

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Abstract

article-meta

Alzheimer’s disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer’s disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), was published [1]. The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Patients who had had to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co-workers all reported clear improvements. Here we report the results from quantitative MRI and neuropsychological testing in ten patients with cognitive decline, nine ApoE4+ (five homozygous and four heterozygous) and one ApoE4−, who were treated with the MEND protocol for 5-24 months. The magnitude of the improvement is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. These results have far-reaching implications for the treatment of Alzheimer’s disease, MCI, and SCI; for personalized programs that may enhance pharmaceutical efficacy; and for personal identification of ApoE genotype.

Keywords: neurodegeneration, cognition, biomarkers, dementia, neuropsychology, imaging, Alzheimer’s disease, Apolipoprotein E

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INTRODUCTION

Alzheimer’s disease is now the third leading cause of death in the United States, following only cardio-vascular disease and cancer [1]. There are approximately 5.2 million Americans with AD, but this estimate ignores the many young Americans destined to develop AD during their lifetimes: given the lifetime risk of approximately 15% when including all ApoE genotypes, as many as 45 million of the 318 million Americans now living may develop AD during their lifetimes if no prevention is instituted [2].

Effective treatment of Alzheimer’s disease has been lacking, but recently a novel programmatic approach involving metabolic enhancement was described, with promising anecdotal results [3]. This treatment is based on connectomic studies [4] and previous transgenic findings [5] as well as epidemiological studies of various monotherapeutic components of the overall program [6]. The approach is personalized, responsive to suboptimal metabolic parameters that reflect a network imbalance in synaptic establishment and maintenance vs. reorganization, and progressive in that continued optimization is sought through iterative treatment and metabolic characterization.

Here we report the initial follow-up of ten patients who were treated with this metabolic programmatics approach. One patient had well documented mild cognitive impairment (MCI), with a strongly positive amyloid-PET (positron emission tomography) scan, positive FDG-PET scan (fluorodeoxyglucose PET scan), abnormal neuropsychological testing, and hippocampal volume reduced to 17th percentile; after 10 months on the MEND protocol, his hippocampal volume had increased to 75th percentile, in association with a reversal of cognitive decline. Another patient had well documented early Alzheimer’s disease, with a positive FDG-PET scan and markedly abnormal neuro-psychological testing. After 22 months on the MEND protocol, he showed marked improvement in his neuropsychological testing, with some improvements reaching three standard deviations from his earlier testing.

The initial results for these patients show greater improvements than have been reported for other patients treated for Alzheimer’s disease. The results provide further support for the suggestion that such a comprehensive approach [3] to treat early Alzheimer’s disease and its precursors, MCI and SCI, is effective. The results also support the need for a large-scale, personalized clinical trial using this protocol.

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RESULTS

Case studies

Patient 1

A 66-year-old professional man presented with what he described as “senior moments” (for example, forgetting where his keys were or forgetting appointments) of two-years duration, and difficulty performing his work. There was a positive family history of dementia in both parents. He was an ApoE4 heterozygote (3/4), his amyloid PET scan was markedly positive, and his fluorodeoxyglucose (FDG) PET scan showed temporoparietal reduced glucose utilization indicative of Alzheimer’s disease. An MRI showed hippocampal volume at only 17th percentile for his age. His neuropsychological testing was compatible with a diagnosis of MCI. His hs-CRP was 9.9mg/l, albumin: globulin ratio was 1.6, homocysteine 15.1μmol/l, fasting glucose 96mg/dl, hemoglobin A1c 5.5%, fasting insulin 32mIU/l, 25-hydroxychole-calciferol 21ng/ml, TSH 2.21mIU/l, and testosterone 264ng/dl.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4931830/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4931830/

 

 

 

 

 

 

 

 

 

 

 

 

 

The overall goal of this protocol is to fix the following (which in turn reverses cognitive decline and helps with Alzheimer’s and Dementia):

  • Insulin resistance
  • Inflammation/infections
  • Hormone, nutrient, and trophic factor optimization
  • Toxins (chemical, biological, and physical)
  • Restoration and protection of lost (or dysfunctional) synapses

Protocols like this may never reach global recognition or even FDA consideration for further evaluation.

The problems with most FDA-based studies is that they only look at one aspect of the disease – X causes Y.

Unfortunately, AD is complex and there are many root causes to it.

The ReCODE protocol looks at 45 factors (metabolic markers) that have to be simultaneously optimized

Amyloid Plaques

Amyloid Precursor Protein

Amyloid precursor protein (APP) is naturally occurring in the brain and depending on how it is cut (either by netrin-1 or other molecules) it can either turn into:

  1. Something healthy for the brain (such as sAPPα and αCTF)
    OR
  2. Something toxic such as amyloid-beta (as well as Jcasp and C31). R
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221920/

If APP is cut to produce amyloid-beta, then amyloid-beta can continue to cut APP into more amyloid-beta plaques.

This creates a positive feedback loop, thus creating more and more amyloid-beta plaques in the brain, instead of creating healthy molecules for the brain.

app cut.jpg

This positive feedback loop creates a clastic (destructive) effect on the synapses, instead of a blastic (protective) response.

Amyloid-Beta Plaque

The dogma behind amyloid plaque (the sticky plaque that builds up in the brain of Alzheimer’s patients) as the main evil in Alzheimer’s Disease (AD) is actually incorrect.

In fact, it may be protective: R

FASEB J. 2015 Jul;29(7):2681-9. doi: 10.1096/fj.14-264218. Epub 2015 Mar 24.
ω-3 Supplementation increases amyloid-β phagocytosis and resolvin D1 in patients with minor cognitive impairment.

Abstract

We investigated the effects of 4-17 month supplementation with ω-3 fatty acids and antioxidants (Smartfish drink; Smartfish AS, Oslo, Norway) in 12 patients with minor cognitive impairment (MCI) [minimental state examination (MMSE) ≥19], 2 patients with pre-MCI (normal MMSE), and 7 patients with Alzheimer disease (AD) (MMSE <19). We measured the phagocytosis of amyloid-β 1-42 (Aβ) by flow cytometry and microscopy, the transcription of inflammatory genes by RT-PCR, the production of resolvin D1 (RvD1) by enzyme immunoassay, and the cognitive status by MMSE. In patients with MCI and pre-MCI, phagocytosis of Aβ by monocytes increased from 530 to 1306 mean fluorescence intensity units (P = 0.016). The increase in patients with AD was not significant (N.S.). The lipidic mediator RvD1, which stimulates Aβ phagocytosis in vitro, increased in macrophages in 80% of patients with MCI and pre-MCI (mean increase 9.95 pg/ml) (N.S.). Transcription of inflammatory genes’ mRNAs was increased in a subgroup of patients with low transcription at baseline, whereas it was not significantly changed in patients with high transcription at baseline. The mean MMSE score of patients with MCI and pre-MCI was 25.9 at baseline and 25.7 after 4-17 months (N.S.). Our study is the first to show significant immune and biochemical effects of ω-3 fatty acids with antioxidants in patients with MCI. Cognitive benefits of ω-3 supplementation in patients with MCI should be tested in a clinical trial.

KEYWORDS:

https://www.ncbi.nlm.nih.gov/pubmed/25805829

  • Acts as an anti-microbial
  • Binds to toxins (like heavy metals)
  • Protects against inflammation

If you have been shot, would you just patch up the wound and not remove the bullet?

No, you would treat the underlying problems (remove the bullet) and replace the blood loss.

The Bredesen Protocol first targets the underlying problem.

3 Types Of Alzheimer’s Disease

There are 3 types of Alzheimer’s disease described in the ReCODE protocol.

You can develop one of these or a combination:

1. Inflammation

 http://journal.frontiersin.org/article/10.3389/fnins.2014.00315/full

Anything that causes inflammation to the brain (low chronic inflammation can do this as well) can contribute to Alzheimer’s Disease (AD):

  • AGEs
  • ApoE4 (and ApoE3R
  • Diet High in Lectins
  • Imbalances in fatty acids (omegas)
  • Infections
  • Insulin Resistance
  • Leaky Gut or Leaky Blood Brain Barrier
  • Neuroinflammation
  • Toxins (incl metals)

1.5 Glycotoxic

Glycotoxicity comes form an imbalance of glucose/insulin usage in the brain.

The pancreas produces Insulin-Degrading Enzyme (IDE, the enzyme that breaks down insulin) to break down amyloid beta.

If IDE is used up by a diet too high in sugar (like someone with insulin resistance), then there is none left to break down amyloid beta.

This type of AD is called 1.5 because it is a combination of AD 1, inflammation and AD 2, trophic loss.

For example, having high amounts of glucose in the blood creates inflammation, and having improper usage of insulin, degrades insulin’s ability to act as a neurotrophic (brain growth) promoter.

Intranasal insulin may help with this type.

2. Metabolic/Trophins Loss

This type of AD is usually caused by imbalances in the endocrine system (hormones) and nutrient depletion, as well as neurotrophic loss (brain breaking down faster than it can regrow).

This includes:

  • ApoE4R
  • Hormone Imbalances (Vitamin D, Sex and Neuro Steroids, Thyroid)
  • Insulin Resistance
  • Methylation Problems
  • Mitochondrial Damage
  • Neurotrophic Loss (atrophy in brain)
  • Nutrient Depletion

3. Toxins

The toxin/infectious type of AD is more environmental and can be caused by:

  • ApoE3 (more common)
  • Heavy Metals (including amalgams)
  • Hormonal Imbalances
  • HPA-Axis Imbalances
  • Infections (such as mold, Lyme, HSV, active EBV, oral/nasal/gut dysbiosisR
  • Low Zinc/high copper ratio R
  • Psychiatric disorders (correlation)
  • Toxins (including haptens, pesticides, NSAIDSPPIs, statins, and other drugs) R

This usually occurs after 80 y/o.

Testing/Biomarkers

All the labs and tests for the Bredesen Protocol can be ordered here (does not include MRI/PET scan).

Blood tests:

  • Albumin/Globulin Ratio (A:G Ratio)
    • ≥ 1.8
    • >4.5 (albumin)
  • Alpha-MSH
    • 35–81 pg/ml
  • Arsenic
    • <7 mcg/L
  • Cadmium
    • <2.5 mcg/L
  • Calcium
    • 8.5-10.5 mg/dl
  • Cholesterol
    • 150
  • Complement C4a
    • < 2830 ng/ml
  • Copper
    • 90-110 mcg/dL
  • Copper:Zinc Ratio (also look at ceruloplasmin ≤ 30)
    • 0.8-1.2
  • Cortisol (morning)
    • 10-18 mcg/dL
  • DHEA
    • 350-430 (women) mcg/dL
    • 400-500 (men) mcg/dL
  • Estradiol (Estrogen)
    • 50-250 pg/ml
  • Folate
    • 10-25 ng/ml
  • Glucose (fasting)
    • 70-90 mg/dL
  • Glutathione
    • 5-5.5 micromolar
  • HbA1C
    • ≤5.6%
  • HDL
    • >50
  • HLA-DR/DQ
    • negative
  • Hs-CRP
    • ≤0.9ng/dL
  • Il-6
    • ≤3pg/ml
  • Insulin (fasting)
    • ≤4.5 microIU/ml
  • LDL-p
    • 700-1000
  • Lead
    • <2 mcg/dL
  • Leptin
    • 0.5-13.8 ng/mL (male)
    • 1.1-27.5 ng/mL (female)
  • Mercury
    • <5 mcg/L
  • MMP9
    • 85-332 ng/mL
  • Omega 6:3 Ratio
    • 0.5-3.0
  • Osmoality
    • 280-300 mosmol
  • Oxidized LDL
    • <60 U/l
  • Pregnenolone
    • 50-100 ng/dL
  • Progesterone
    • 1-20 ng/ml
  • Potassium
    • 4.5-5.5 mEq/L
  • RBC Magnesium
    • 5.2-6.5 mg/dL
  • RBC Thiamine Pyrophosphate
    • 100-150 ng/ml
  • sdLDL
    • <20 mg/dL
  • Selenium
    • 110-150 ng/ml
  • T3
    • 3.2-4.2 pg/ml (free)
    • <20 ng/dL(reverse)
  • T4
    • 1.3-1.8 ng/dL (free)
  • TSH
    • <2 microIU/ml
  • Testosterone 
    • 500-1000 ng/dL (total)
    • 6.5-15 ng/dL (free)
  • TGF-β1
    • < 2380 pg/ml
  • TNF-alpha
    • ≤6pg/ml
  • Triglycerides
    • <150
  • Vasopressin
    • 1.0-13.3 pg/ml
  • VEGF
    • 31-86 pg/mL
  • VIP
    • 23-63 pg/mL
  • Vitamin B6
    • 60-100 mcg/L
  • Vitamin B12 (MMA test can complement, but isn’t a replacement)
    • 500-1500 pg/ml
  • Vitamin C
    • 1.3-2.5 mg/dL
  • Vitamin D
    • 50-80 ng/ml
  • Vitamin E (as Alpha-Tocopherol)
    • 12–20 mcg/ml
  • Zinc
    • 90-110 mcg/mL

It’s also a good idea to test for leaky gut, leaky brain, and food sensitivities:

Infections can travel to the brain (via a leaky brain) through the nose, vagus nerve, or eye such as:

  • Aspergillus
  • CIRS
  • Gingivitis
  • Lyme (Borrelia)
  • HSV
  • Syphilis (neurosyphhilus)

This can also cause meningitis.

For mitochondrial function testing, use an organic acids test or look at 8-oxo-dg.

A urine culture should be free of mycotoxins.

All microbiomes shouldn’t have dysbiosis or infections.

Imaging can be done with:

  • PET (FDG-PET, Amyloid PET, or Tau PET)
  • MRI with volumetrics (Neuroreader or NeuroQuant).

Body mass index (BMI) should be 18–25; waistline < 35 inches (women) or < 40 inches (men).

Here are some cognitive tests:

  • MMSE (Mini-Mental State Examination)
  • MoCA (Montreal Cognitive Assessment) – A normal MoCA score is 26 to 30
  • SAGE (Self-Administered Gerocognitive Examination)

Genetics

ApoE4 (epsilon 4) is the most common genetic variable for predicting Alzheimer’s.

What does ApoE4 do?

  • Reduces the clearance of amyloid-beta plaques
  • Regulates over 1,700 different genes (1/20 of human genome)
  • Shuts down the gene that makes SirT1, which helps with gene regulation (resveratrol would help this)
  • Activates NF-κB, thus promoting inflammation.

ApoE4 (14% of the population) is the worst, followed by ApoE3 (78%), then ApoE2 (8%). R

Read more about ApoE here and see if you are ApoE4.

It’s also a good idea to check any mutations or polymorphisms in APP, PS1, PS2, CD33, TREM2, CR1, and NLRP1.

Treatment

Treatment is different for everyone, but simply goes like this:

  1. Fixing the underlying cause (infections, toxin exposure, chronic inflammation)
  2. Changing lifestyle to increase neurotrophic factors and proper autophagy
  3. Using diet and treatments to restore biomes and insulin sensitivity in the brain/body
  4. Optimizinghormones and other biomarkers using bioidentical hormones, supplements, and herbs

Infections

Treat MARCoNs if positive.

Inactivate/excrete pathogens using:

Here are some other useful tools to help remove infections or toxins:

Lifestyle

 https://www.ncbi.nlm.nih.gov/pubmed/25405649

These are lifestyle requirements for the ReCODE protocol that help reverse AD:

Sleep:

Brain Stimulation:

  • Do brain training games
  • Exercise
  • Increase neurotrophic factors (BDNF and NGF, but I recommend CNTFGDNFCDNF andMANF as well)

Psychological:

  • Keep stress low (for reduced atrophy)

Oral Hygiene:

Diet (Ketoflex 12/3)

The ReCODE diet, called “Ketoflex 12/3”, consists of being in ketosis, eating high amounts of fiber, eating within a 12 hour window, and stop eating at least 3 hours before bed.

The goals:

  • Increases ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) and BDNF
  • MCT oil (caprylic acid is the strongest form) is a must for ApoE4until insulin sensitivity is restored, then must switch to MUFAs (like avocado) and PUFAs predominantly (such as olive oil)
  • Lots of uncooked veggies
  • Fasting 12 hours/day
  • Stop eating 3 hours before bed
  • Increase insulin sensitivity

Foods

Eat frequently:

  • Avocados
  • Artichokes
  • Beets
  • Cilantro
  • Cruciferousvegetables (such as cauliflower, broccoli/broccoli sprouts, various types of cabbage, kale, radishes, Brussels sprouts, turnips, watercress, kohlrabi, rutabaga, arugula, horseradish, maca, rapini, daikon, wasabi, and bok choy)
  • Dandelions
  • Garlic
  • Ginger
  • Grapefruit
  • Jicama
  • Kimchi
  • Leafy greens (such as kale spinach, and lettuce)
  • Leeks
  • Lemons
  • Mushrooms
  • Olive oil
  • Onions
  • Pasture raised eggs
  • Resistant starches (such as sweet potatoes, rutabagas, parsnips, and green bananas)
  • Saurkraut
  • Seaweed
  • Tea (oolongblack, and green)
  • Wild-caught fish (SMASH fish such as salmon, mackerel, anchovies, sardines, and herring)

Eat less frequently:

  • Coffee (such as super coffee)
  • Grass-fed beef
  • Legumes (such as peas and beans)
  • Nightshades (such as eggplant, peppers, and tomatoes)
  • Nontropical fruits (low glycemic, such as berries)
  • Pasture raised chicken
  • Starchy veggies (such as corn, peas, squash, but sweet potatoes are an exception)
  • Wine (1 glass/wk)

Avoid:

  • Dairy (occasional cheese or plain yogurt is okay, I recommend A2-based dairy)
  • Fruits (high glycemic ones especially)
  • Gluten
  • Grains
  • High mercury fish (such as tuna, shark, and swordfish)
  • Processed foods
  • Sugar and simple carbs (including breads, wheats, rice, cookies, cakes, candies, sodas, etc)

Some important notes about the diet:

  • Avoid overheating foods (as it creates AGEs)
  • Fish is good, but don’t do too much meat.
  • Remove all inflammatory lectins. R
  • If you do eat fruits, make sure they are higher in fiber and not as juice.
  • Include lots good fats in your diet (such as avocadosolive oilMCT oils like caprylic acid, and if non-lectin sensitive then nuts and seeds oils are okay)
  • Use digestive enzymes

MicroBiome

Include probiotics and prebiotics:

If you have any infections with biofilms, you must take care of those as well (may use Bactroban/MupirocinSinuClenz, or Xlear).

For the nasal microbiome:

Insulin Resistance

Here are some supplements recommended for decreasing insulin resistance:

Supplements And Herbs

Supplements on the ReCODE program that help with cognition and inflammation:

Herbs on the ReCODE program that help with cognition and inflammation: R

https://www.ncbi.nlm.nih.gov/pubmed/28236613

Also, pro-resolving mediators (like SPM Active), such as resolvinsprotectins, and maresins will also help against inflammation. R

Mechanism Of Action

Here are all the functions that the ReCODE protocol aims to accomplish:

  • Increase α-cleavage
  • Increase ADNP
  • Increase autophagy
  • Improve axoplasmic transport
  • Increase BDNF
  • Increase cAMP
  • Increase GABA
  • Increase glutathione
  • Increase IDE
  • Increase insulin sensitivity
  • Improve LTP
  • Increase NGF
  • Increase microglial clearance of 
  • Increase netrin-1
  • Increase neprilysin
  • Increase PPAR-γ 
  • Increase phagocytosis index
  • Increase PP2A
  • Increase resolvins
  • Increase SirT1
  • Increase synaptoblastic signaling
  • Increase telomere length
  • Improve vascularization
  • Increase VIP
  • Increase vitamin D signaling
  • Optimize all metals
  • Optimize cholinergic neurotransmission
  • Optimize cortisol
  • Optimize detoxification
  • Optimize DHEA
  • Optimize E2:P (estradiol to progesterone) ratio
  • Optimize estradiol
  • Optimize free T3
  • Optimize free T4
  • Optimize insulin secretion and signaling
  • Optimize leptin
  • Optimize mitochondrial function and biogenesis
  • Optimize pregnenolone
  • Optimize progesterone
  • Optimize stem-cell-mediated brain repair
  • Optimize synaptic components
  • Optimize testosterone
  • Optimize TSH
  • Reduce amyloid-beta oligomerization
  • Reduce APPβ-cleavage
  • Reduce caspase-6 cleavage
  • Reduce caspase-3 cleavage
  • Reduce γ-cleavage
  • Reduce glial scarring
  • Reduce homocysteine
  • Reduce inflammation
  • Reduce mTOR activation R
  • Reduce NF-κB
  • Reduce phospho-tau
  • Reduce oxidative damage and optimize ROS
  • Reduce synaptoclastic signaling

 

 

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