Alzheimer's Disease - RCF NuernbergRCF Nuernberg

Alzheimer’s Disease

New und Updates
Alzheimer's Disease

Alzheimer’s Disease

For Biochemistry we had to write a 10-page paper on a disease associated with a metabolic pathway and list possible nutritional recommendations for that disease.  I chose Alzheimer’s Disease, and was astounded to read the latest research by Dr. Dale Bredesen documenting (with MRI brain scans, etc) how his protocol has reversed cognitive decline in hundreds of patients leading in many cases to complete regression and no signs of the disease.  Improvements in all cases have been maintained from the time of implementation of the protocol up until the present time, meaning around 5 years for a few patients.  This has gotten a tiny bit of media coverage in America, but I don’t know if it is being discussed in Germany:  The subject is really complex, & this is really just an overview, but all the topics are cited in my reference section if you’d like to dive deeper.

If you’ve been confused about all the buzz over the future of Functional Medicine and its potential in combatting chronic disease, research into Dale Bredesen’s protocol will get you excited too.  So far 99% of his protocol involves no drugs – only lifestyle modifications and nutrition.

Maybe this information might encourage you to get your DNA genotyped from an organization like 23andme:  Certainly, knowing if you are ApoE4 homozygous or heterozygous is useful information in any prevention program.


Part I. What the disease is:  symptoms, & in which type of population it’s most prevalent

Alzheimer’s Disease is still considered by most practitioners as a progressive neurodegenerative disease, where symptoms of dementia including memory and thinking skills worsen gradually and unstoppably over time5,12.  Survival after diagnosis averages 8 years, rendering patients by the end vacant-eyed and unable to respond to visitors or their environment12.  Alzheimer’s in 2016, was considered “the third leading cause of death in the United States, following only cardiovascular disease and cancer,” but another recent research review determined that many deaths from Alzheimer’s go unreported, meaning the total number of deaths significantly exceeds CDC’s estimations2,5.   Of the 318 million Americans living, it is estimated that 45 million (15% of the population) will get Alzheimers during their lifetime37.  But the incidence of Alzheimer’s has reached almost 50% in people over 85 years of age46.  Although it is the elderly population over 65 that generally gets a diagnosis of Alzheimer’s, clear symptoms of the disease’s predecessors including mild cognitive impairment (MCI) and subjective cognitive impairment (SCI) can be observed 20 years previously, and can be successfully addressed and often reversed at that time31

There is a very recent model of Alzheimer’s Disease promoted by Dale E. Bredesen, PhD who describes it not as “a progressive and…irreversible neurodegenerative disease” (like most research papers in the last decade describe it), but as “the body’s protective response to several metabolic and toxic insults”, which can mechanistically be reversed, especially when caught in its early stages1,7.  Due to the fact that Dr. Bredesen’s group is the only group showing documented, objective, and peer-reviewed success in treating Alzheimers, this report focuses on theories he supports from causal microbiome vulnerability to the molecular mechanism behind neurodegeneration, and multifaceted therapies for treatment.  The peer-reviewed research that backs up Dr. Bredesen’s theories that are cited following this report’s conclusion, represent only a small fraction of a massive volume performed on Alzheimer’s in the last two decades. 

Dr. Bredesen is currently the Director, Mary S. Easton Center for Alzheimer’s Research  and founder/CEO of the Buck Institute for Research on Aging, and champions the metabolic enhancement for neurodegeneration (MEND) therapeutic approach (allied with Functional Medicine ideals), which has achieved radical success in not only halting the progress of Alzheimer’s, but in reversing its destruction and bringing in many cases normal cognitive function back not only to individuals experiencing Mild Cognitive Impairment (MCI) and Subjective Cognitive Impairment (SCI) pre-Alzheimer’s conditions, but also to individuals in early stages of Alzheimer’s Disease2.  MEND is now in version 3.0, has been actively healing Alzheimer’s patients for nearly 5 years, and involves personalized solutions for a myriad of categories following identification of the etiology behind an individual’s diagnosis: with the cumulative result, that over 500 individuals who have gone through the MEND program (as Bredesen reported early this year) have not only stopped Alzheimer’s progression, but have reversed cognitive decline1,2,31

Part II: Epidemiology/etiology Molecular mechanism of the disease

One of the mentors of Dale E. Bredesen, PhD is Stanley Prusiner who received a Nobel Prize for his discovery of the prion, or mutant form of infectious protein found to be responsible for many neurodegenerative diseases including Creutzfelt-Jakob Disease1.  Prions are what is responsible screen-shot-2017-05-01-at-9-57-59-pmfor shifting of balance among proteins involved in synaptic reorganization (forgetting) and synaptic maintenance (remembering).  Bredesen argues that Alzheimer’s is a molecular cancer, where the amplification occurs at the biochemical (protein) level instead of the cellular level, which is possibly driven by prion replication and resultant imbalance31, 38

It was Bredesen’s group in 1993 that discovered “dependence receptors”, so named because they created states of dependence on their respective ligands23,31,39.  Bredesen’s group found that in vitro when they transfected any gene associated with neurodegeneration into neural cells, the probability that they commit suicide increases31.  Looking into the cause of this programmed cell death, Bredesen’s group found that dependence receptors induce the death of cells when they don’t get appropriate trophic support31.  Amyloid precursor protein (APP) that lies at the heart of Alzheimer’s Disease is one of these receptors31.  This is where Bredesen’s conception of a plasticity balance at the heart of the pathology arises2,42.  Depending on where APP is cleaved, it will either support neurite extension or neurite retraction2,42.  Two types of lesions in the brain characterize screen-shot-2017-05-01-at-1-53-57-pmAlzheimer’s: “extracellular senile plaques consisting primarily of amyloid precursor protein (APP)-derived amyloid-β (Aβ) peptide and intracellular neurofibrillary tangles consisting largely of hyper-phosphorylated microtubule-associated tau protein42.

Synapse loss and neuronal cell death represent the basis for cognitive impairment in AD, and the C-terminal caspase cleavage of APP resulting in release of a 31 amino acid C-terminal fragment has been shown to be a likely contributor to neuronal death in AD42.


Amyloid-β (Aβ) peptide is the main component of Alzheimer’s Disease plaques and is derived from Amyloid Precursor Protein (APP).

Dr. Bredesen’s own research argues that amyloid is a protective response to three categories of threat; he explains that organisms make amyloid for three reasons31:

  1. Infection or Inflammation.  Senile plaques were actually found to consist of colonies of Spirochetes, bacteria commonly found in oral cavities which are associated with gum disease28.  See a video of them here:  A-beta is a very good indigenous anti-biofilm28.  It binds metals with an ability comparable to ethylenediaminetetraacetic acid (EDTA) used in chelation therapy, & it is toxic to bacteria (antibiotic effect)28.
  2. Trophic withdraw.  Neurons from which Nerve Growth Factor (NGF) is withdrawn, will make beta amyloid protein as part of their programmatic downsizing process29.
  3. Toxic assault.  When bacteria is challenged with toxins, it makes amyloid as a protective response, with the ability to bind and sequester the toxins,28,30.

Dr. Bredesen believes that there are many different causes of Alzheimers and many routes for problematic substances to take to our brain31.  Diversity in non-pathologenic microbial communities at crucial sites on the body including oral, nasal, otic cavities, GI tract, skin and urogenital tracts is critical toward avoiding disease36.  Where Alzheimer’s is concerned, there are clear links with imbalance & inflammation in our oral microbiome, our sinonasal bacterial microbiome as well as gut microbiome.  The relationship between the health and diversity of our gut bacteria with our brain health and disease resistance was decisively established by a recent double-blind placebo controlled trial where just in 12 weeks, patients on probiotics were observed to have decreased levels of inflammatory marker hs-CRP by 18%, with a substantial improvement in brain function mini-mental status exam (MMSE) score, while patients not on probiotic therapy increased hs-CRP by 45% and experienced a huge reduction in brain function capability.34  “Decreased bacterial richness and diversity” in the sinonasal bacterial microbiome has been shown to have links to chronic disease35,36.  An estimated 500,000 of the 5.2 million Americans currently diagnosed with and suffering from Alzheimer’s disease symptoms actually may have Inhalational Alzheimer’s Disease (IAD), which is curable37.  Those patients tend to display lab biomarkers of Chronic Inflammatory Response Syndrome (CIRS) and fall under Dr. Bredesen’s Type3AD definition explained below37.  Oral inflammation is heavily associated with Alzheimer’s, notably that involving p.gingivalis, Oral Herpes Simplex Virus (HSV-1), or Spirochetes microorganisms31,46.  Periodontitis and gingivitis have both been linked to Alzheimer’s31,46.

Dr. Bredesen has put Alzheimer’s Disease patients in different groups according to their metabolic profiling data45:

Type 1AD:  Inflammatory (hot).  Includes sterile inflammation or infection-related inflammation.  Inflammation stimulates amyloid secretion.  External drivers & Internal drivers include sugars in our diet, high transfats – inflammatory processes31,45.

Type 1.5AD: Glycotoxic (sweet). Internal drivers of inflammation include insulin resistance (gives you the atrophic portion & type 2AD) & glycated proteins (cause the inflammation that gives you the type 1AD31,45.

Type 2AD: Atrophic (cold). Signs of trophic support withdraw, and amyloid is being produced as part of a programmatic downsizing. Patients observed to be deficient in trophic support biomarkers including Nerve Growth Factor, Brain Derived Neurotrophic Factor, estradiol, testosterone, thyroid hormone, vitD, vitB12, folate, estradiol, and have a high copper to low zinc ratio.  Other telltale biomarkers for this version of Alzheimer’s Disease indicate methylation defects, and high homocysteine.  Dr. Bredesen said they use the George Brewer protocol to correct zinc deficiency (zinc picolinate, small amount of Manganese, vitB6, N-Acetyl Cysteine, high dose of ascorbate)31,33,45.

Type 3AD: toxic (vile): external drivers of inflammation include chemical exposure (like pesticides and BPA), heavy metals (like mercury, lead, cadmium and arsenic),  and biotoxins (like mold spores, mycobacteria, fungi, endotoxins, inflammagens, and microbial volatile organic compounds).  Almost all Dr. Bredesen’s patients with the HLA-DRDQ haplotype are highly sensitive to biotoxins31.  Many different microorganisms are associated with Alzheimers, especially in biofilms (p.gingivalis, Oral Herpes Simplex Virus (HSV-1), Spirochetes, Borelia burgdorferi, etc)31,45.

Since the time Dr. Bredesen published his research paper on 3 types of Alzheimer’s, he has in lectures described 5 types, the last two being related to Type 2AD, and they are Type 4AD which is “vascular” (pale) with atherosclerotic/cardiac risk symptoms, and Type 5AD which is “traumatic” (dazed) with previous history of head trauma31,45.

Part III: Assessment of Risk Factors, and Nutritional Deficiencies of the Disease


There are 60 different things measured in Dr. Bredesen’s MEND 3.0 protocol31.  He includes diagnostic testing of these variables as well as a functional medical assessment, and puts them in a computer algorithm to determine proper Alzheimer’s type and treatment31.  Here are a collection of the top indices mentioned by Dr. Bredesen collectively representing high risk for Alzheimers:

1.ApoE4 homozygous. 

ApoE4 is present in 95% of late-onset Alzheimer’s Disease cases, and as such is considered a screen-shot-2017-05-01-at-9-35-16-pmmajor genetic risk factor for Alzheimer’s Disease.1,40.  ApoE3 is the dominant gene worldwide, representing 75% of Americans, and this majority has a 9% risk of contracting Alzheimer’s1,31.  75 million Americans have 1 copy of ApoE4, and they have a 30% risk of contracting Alzheimer’s as a result1,31.  The unfortunate 7 million with 2 copies have a 90% chance1,31.

Interestingly, all Hominids were ApoE4 homozygous up until the discovery of fire.

Apolipoprotein E (ApoE) is a glycoprotein that consists of 299 amino acids, which is the major protein component of very low-density lipoproteins (VLDL) as well as the major apolipoprotein present in our brain26. ApoE assists in regulating cholesterol and lipid metabolism, as well as in cellular repair25.  The ApoE gene is positioned on chromosome 19, and has three isoforms, Apo2, 3, & 425.


Plasticity Imbalance:  When a cell is in a ApoE4 dominant state, the cell turns on an inflammatory cascade that involves RelA (phosphorylation of which regulates NF-kappaB activation)27.  ApoE4 binds to 1700 genes in their promoter regions, many of which involve microtubule disassembly, glucose homeostasis, synaptic dysfunction, and inflammation.  If a cell is in an ApoE3 dominant state, the cell will put more resources into recycling and longevity.

Plasticity Imbalance:  Of the three isoforms, “only screen-shot-2017-05-01-at-1-52-47-pmApoE4 significantly reduces the ratio of soluble amyloid precursor protein alpha (sAPPa) to Amyloid beta, reduces Sirtuin T1 (SirT1) expression [up to 80%], resulting in markedly differing ratios of neuroprotective SirT1 to neurotoxic SirT2, triggers Tau phosphorylation (p-Tau) and APP phosphorylation ((p)-APP), and induces programmed cell death”24.  You may recall (I explained earlier in this report) that Alzheimer’s Disease “tangles” consist largely of hyper-phosphorylated tau protein.  You also may recall that amyloid-β (Aβ) peptide is the main component of Alzheimer’s Disease “plaques” and is derived from Amyloid Precursor Protein (APP).  All of these ratio shifts are favoring propensity for synaptoclastic activity instead of synaptoblastic activity.

2. Homocysteine greater than 7.  Elevated homocysteine levels and oxidative stress are directly linked to Alzheimer’s Disease risk20,21.

3. Vitamin B12 less than 5001,31.  Low B-vitamin intake is linked to Alzheimer’s risk17, 18.  Other vitamins and minerals Dr. Bredesen routinely measures low in Alzheimer’s patients include VitC, VitK2, folate, magnesium, and zinc31,44.  Vitamin D intake is especially critical, with blood levels under 30 linked to Alzheimer’s risk19.

4. hs-CRP greater than 1.01,31

5. Total Protein and Albumin/Globulin (A/G) ratio less than 1.81,31

6. Hemoglobin A1c (HbA1c) greater than 5.61,31

7. Fasting insulin greater than 6 uIU, and Fasting Blood Sugar greater than 901,31.  Dr. Bredesen remarks that “as metabolism goes, so goes the cognition”31.  Metabolic Syndrome, Type 2 Diabetes, and Prediabetes all carry greater risk for Alzheimer’s Disease1,31.

8. Simple carbs in diet.  Frequent simple carbohydrate ingestion has been linked to risk of Alzheimer’s6.

9. Thyroid: TSH greater than 2.0, Free T3 less than 3.2, Reverse T3 greater than 20, and Free T4 less than 1.3.1,31

10. Post-menopausal1,31

11. Sleep apnea or hypopnea.  Little (< 6 hours) or poor quality sleep is linked to Alzheimer’s31,41.

12. Low androgen levels: Total Testosterone (T) less than 500, and Free T less than 6.51,31.

13. Low estradiol: E2 less than 100, hysterectomy at under 41 years old1,31.

14. Low pregnenolone: under 201,31.

15. History of head trauma1,31.  Retired National Football League players are 4-times more likely to die of Alzheimer’s than the general US population43.

16. DHEA intake.  Low DHEA intake is solidly linked to Alzheimer’s risk7,9,10,11, 18

17. Cholesterol measured greater than 255 or less than 150 carries a greater risk for Alzheimer’s Disease1,31.

18.  Prescription & nonprescription drugs also notably raise Alzheimer’s risk, including:

    • Statins:  In 2011 a study was published coauthored by Dr. Bredesen, reviewing all the drugs the FDA had approved for their effects on Alzheimer’s, and the drugs that had the highest negative effect on Alzheimer’s progression were statin drugs13.   Statins and lipophilic statins like simvastatin and cerivastatin in particular were found to stimulate Abeta production42. Dr. Bredesen refers to statins as “dementegens”, and believes just like we currently name some substances “carcinogens” the same type labeling should arguably apply to warn of the increased risk for neurodegenerative disease31.
    • PPIs:  Beta-amyloid (Aß) plaque increases in the brains of mouse models when PPIs are used:  “Aß aggregation leads to formation of fibrillar b-pleated sheet structures that are major components of extracellular senile plaques which are found in the brains of AD patients”14  Acidic lysosomes located within phagocytic microglia play a critical role  in their digestion of fibrillar Aß (fAß)14.  When these lysosomes become less acidic, they can no longer degrade & clear fAß, a major step in the pathogenesis of Alzheimers14. Studies have shown that clearing fibrillar Alzheimer amyloid-ß peptide (fAß) is effective Treatment for Alzheimers, at least in murine models14.  PPIs suppress the secretion of gastric acid “by inhibition of the H+/K+ ATPase present on the plasma membrane of the gastric parietal cells”, but have been demonstrated by several studies to both penetrate the blood-brain barrier, and to block V-ATPases on macrophages’ lysosomal membrane14.  It is a reasonable hypothesis that PPIs also inhibit V-ATPases on microglia’s lysosomal membranes, lowering lysosome acidification and reducing fAß clearance14. Dr. Bredesen commented that when he sees an Alzheimer’s patient with a low zinc level, he usually asks them if they are on PPIs, and they usually are. 
    • Neuroactive medications have been solidly linked to Alzheimer’s disease risk15.
    • Illicit Drugs.  Use of illicit drugs has been linked to Alzheimer’s risk1,31.

Part IV: Interventions

Typical medical treatment for the disease:  

Conventional treatment for Alzheimer’s usually includes prescription of cholinesterase inhibitors (donepezil, rivastigmine and galantamine), or the NMDA antagonist memantinemedication.  Cholinesterase inhibitors (like often prescribed Donepezil (Aricept) HCL 5mg) prevents acetylcholine breakdown in brain tissue though its inhibition of cholinesterase, and is often used in treating dementia symptoms47.  But the prognosis is bleak:   out of 244 drugs approved for Alzheimers in the last decade, all but one have failed to treat the pathology, and the one that avoided abject failure has very minimal advantageous effects1.

Dr. Bredesen’s Nutritional & Lifestyle Management for Alzheimer’s Disease


Intervention that has seen progress (even reversal of cognitive decline and regrowth of brain tissue) with Alzheimer’s patients is Dr. Bredesen’s 36-point MEND 3.0 personalized therapy program.  Dr. Bredesen describes his MEND 3.0 intervention as always starting with optimal Nutrition, and puts an emphasis on its involvement not only in the initial intervention, but in continued management of the disease1.  He directs patients to convert from high-carb diets to good-fat diets, and directs that all simple carbohydrate food-sources (highly-processed) should be completely cut out1.  His own and others’ empirical evidence shows these changes assist patients with managing their fasting insulin levels and regaining insulin sensitivity6,8,31.  Both the ketogenic diet and the real-food Mediterranean Diet have shown reduced risk of Alzheimer’s in research8,16.  Bredesen also administers food sensitivity/allergy testing to his patients in order to determine which foods cause them gut dysfunction, chronic inflammation, and impaired nutrient absorption1.  His participants are given prebiotics and probiotics to avoid inflammation and autoimmunity34.  Bredeson also uses targeted herbs shown to reduce inflammation and Abeta including curcumin and ashwagandha1,31.  He prescribes high-dose antioxidants like glutathione and vitC, cod liver oil for DHA/EPA, vitamin A, D, and additional K2 supplementation for healthy bones1,31.  Dr. Bredeson administers an Organic Acids Test to rule out CIRS, toxins, and infections including yeast or bacterial dysbiosis and to get an initial determination of metal homeostasis1,31.  He initiates adrenal support and hormone optimization for patients’ (usually) hypothyroid symptoms, and prescribes supplementation of nutrients such as 5-HTP, melatonin, and L-theanine to support participant’s sleep quality1,31,41.  He also looked for drugs that would help put his patients on the correct side of APP processing and found one called FO3 that is now currently in clinical trial in Australia31.

Part V:  Discussion

Dr. Bredesen describes Alzheimer’s as your roof having 36 holes in it.  His multifaceted therapy involves plugging as many holes as possible, whereas every single drug currently on trial for Alzheimers is a monotherapy drug1.  For such a a complex pathology with a variety of potential causes and presenting with a range of symptoms, is it any wonder that plugging one or two holes has little effect on Alzheimer’s progression?  Naturally a patient presenting with Type1AD-causes calls for vastly different therapeutic targets than one presenting with type3AD-causes.  The source of Alzheimer’s (& there are many!!) needs to be understood in order to stop the progression of neurodegenerative decline, and then needs to be addressed on an individualized basis using a multifaceted method.  This chronic disease like many others needs to be addressed through a Functional Medicine approach.  Being that this is currently the only viable approach, Alzheimer’s treatment could signal a paradigm shift in medical practice where Functional Medicine gets integrated into conventional medicine.  It is an amazing, exciting time to be a student of Human Nutrition!  We can prove with documented, objective, and peer-reviewed evidence that progressive memory loss has been reversed and disease markers have disappeared in a chronic, hopeless disease with no pharmaceutical solution.  These paradigms will hopefully serve as a wrecking ball to obliterate a conventional model which clings to pharmaceutical solutions being the only option when it comes to chronic disease. 


1. Bredesen, Dale E. (24 Feb 2016). Insights from Metagenics PreConference. Cognitive Health: Dawn of the Era of Treatable Alzheimer’s Disease. Integrative Healthcare Symposium Pre-Conference. Midtown, New York City

2. Bredesen, D. E., Amos, E. C., Canick, J., Ackerley, M., Raji, C., Fiala, M., & Ahdidan, J. (2016). Reversal of cognitive decline in Alzheimer’s disease. Aging (Albany NY), 8(6), 1250–1258.

3. European Commission’s Scientific Committee on Consumer Safety (SCCS) Opinion On the safety of aluminium in cosmetic products (27 Mar 2014).

4. Tomljenovic, Lucija. “Aluminum and Alzheimer’s disease: after a century of controversy, is there a plausible link?.” Journal of Alzheimer’s Disease 23.4 (2011): 567-598.

5. James, B. D., Leurgans, S. E., Hebert, L. E., Scherr, P. A., Yaffe, K., & Bennett, D. A. (2014). Contribution of Alzheimer disease to mortality in the United States. Neurology, 82(12), 1045–1050.

6. Tay, J., Zajac, I. T., Thompson, C. H., Luscombe-Marsh, N. D., Danthiir, V., Noakes, M., … & Brinkworth, G. D. (2016). A randomised-controlled trial of the effects of very low-carbohydrate and high-carbohydrate diets on cognitive performance in patients with type 2 diabetes. British Journal of Nutrition, 116(10), 1745-1753.

7. Belkouch, M., Hachem, M., Elgot, A., Van, A. L., Picq, M., Guichardant, M., … & Bernoud-Hubac, N. (2016). The pleiotropic effects of omega-3 docosahexaenoic acid on the hallmarks of Alzheimer’s disease. The Journal of Nutritional Biochemistry, 38, 1-11.

8. Gasior, M., Rogawski, M. A., & Hartman, A. L. (2006). Neuroprotective and disease-modifying effects of the ketogenic diet. Behavioural Pharmacology, 17(5-6), 431–439.

9. Bazan, N. G., Molina, M. F., & Gordon, W. C. (2011). Docosahexaenoic Acid Signalolipidomics in Nutrition: Significance in Aging, Neuroinflammation, Macular Degeneration, Alzheimer’s, and Other Neurodegenerative Diseases. Annual Review of Nutrition, 31, 321–351.

10. Tremblay, M.-E., Zhang, I., Bisht, K., Savage, J. C., Lecours, C., Parent, M., … Maysinger, D. (2016). Remodeling of lipid bodies by docosahexaenoic acid in activated microglial cells. Journal of Neuroinflammation, 13, 116.

11. Esfahani, A., Somi, M. hossein, Ayromlou, H., Nikanfar, A., Jafarabadi, M. A., Sadat, B. E., & Ghoreishi, Z. (2016). The effect of n-3 polyunsaturated fatty acids on incidence and severity of oxaliplatin induced peripheral neuropathy: a randomized controlled trial. Biomarker Research, 4, 13.

12. Nehls, M. (2016). Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy. Journal of Molecular Psychiatry, 4, 3.

13. Descamps, O., Zhang, Q., John, V., & Bredesen, D. E. (2011). Induction of the C-terminal proteolytic cleavage of AβPP by statins. Journal of Alzheimer’s disease: JAD, 25(1), 51.

14. Fallahzadeh, M. K., Borhani Haghighi, A., & Namazi, M. R. (2010). Proton pump inhibitors: predisposers to Alzheimer disease?. Journal of clinical pharmacy and therapeutics, 35(2), 125-126.

15. de Gage, S. B., Moride, Y., Ducruet, T., Kurth, T., Verdoux, H., Tournier, M., … & Bégaud, B. (2014). Benzodiazepine use and risk of Alzheimer’s disease: case-control study. Bmj, 349, g5205.

16. Pérez-López, F. R., Chedraui, P., Haya, J., & Cuadros, J. L. (2009). Effects of the Mediterranean diet on longevity and age-related morbid conditions. Maturitas, 64(2), 67-79.

17. Douaud, G., Refsum, H., de Jager, C. A., Jacoby, R., Nichols, T. E., Smith, S. M., & Smith, A. D. (2013). Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. Proceedings of the National Academy of Sciences, 110(23), 9523-9528.

18. Smith, D., Refsum, H., Oulhaj, A., de Jager, C. A., & Jerneren, F. (2016). Beneficial Interactions Between B Vitamins and Omega-3 Fatty Acids in the Prevention of Brain Atrophy and of Cognitive Decline in Early Stage Alzheimer’s Disease. The FASEB Journal, 30(1 Supplement), 407-6.

19. Pludowski, P., Holick, M. F., Pilz, S., Wagner, C. L., Hollis, B. W., Grant, W. B., … & Soni, M. (2013). Vitamin D effects on musculoskeletal health, immunity, autoimmunity, cardiovascular disease, cancer, fertility, pregnancy, dementia and mortality—a review of recent evidence. Autoimmunity reviews, 12(10), 976-989.

20. Miwa, K., Okazaki, S., Yagita, Y., Sakaguchi, M., Mochizuki, H., & Kitagawa, K. (2015). Increased Total Homocysteine Levels Are Associated With the Risk of Dementia Independently of Cerebral Small-vessel Disease. Stroke, 46(Suppl 1), A224-A224.

21. Cankurtaran, M., Yesil, Y., Kuyumcu, M. E., Oztürk, Z. A., Yavuz, B. B., Halil, M., … & Arıoğul, S. (2013). Altered levels of homocysteine and serum natural antioxidants links oxidative damage to Alzheimer’s disease. Journal of Alzheimer’s Disease, 33(4), 1051-1058.
22.  Poksay, K. S., Sheffler, D. J., Spilman, P., Campagna, J., Jagodzinska, B., Descamps, O., … & Cosford, N. D. (2017). Screening for small molecule inhibitors of statin-induced APP C-terminal toxic fragment production. Frontiers in Pharmacology, 8.
23.  Zhong, N., Scearce-Levie, K., Ramaswamy, G., & Weisgraber, K. H. (2008). Apolipoprotein E4 domain interaction: synaptic and cognitive deficits in mice. Alzheimer’s & Dementia, 4(3), 179-192.
24.  Theendakara, V., Patent, A., Libeu, C. A. P., Philpot, B., Flores, S., Descamps, O., … & John, V. (2013). Neuroprotective Sirtuin ratio reversed by ApoE4. Proceedings of the National Academy of Sciences110(45), 18303-18308. 
25.  Raichlen, D. A., & Alexander, G. E. (2014). Exercise, APOE genotype, and the evolution of the human lifespan. Trends in neurosciences37(5), 247-255. 
26.  Puglielli, L., Tanzi, R. E., & Kovacs, D. M. (2003). Alzheimer’s disease: the cholesterol connection. Nature neuroscience6(4), 345-351.
27.  Lawrence, T. (2009). The nuclear factor NF-κB pathway in inflammation. Cold Spring Harbor perspectives in biology1(6), a001651.
28. Miklossy, J. (2016). Bacterial amyloid and DNA are important constituents of senile plaques: further evidence of the spirochetal and biofilm nature of senile plaques. Journal of Alzheimer’s Disease53(4), 1459-1473.
29.  Capsoni, S., & Cattaneo, A. (2006). On the molecular basis linking nerve growth factor (NGF) to Alzheimer’s disease. Cellular and molecular neurobiology26(4-6), 617-631.   
30.  Kumar, D. K. V., Choi, S. H., Washicosky, K. J., Eimer, W. A., Tucker, S., Ghofrani, J., … & Moir, R. D. (2016). Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease. Science translational medicine, 8(340), 340ra72-340ra72. 
31. Bredesen, Dale E. “Reversing Alzheimer’s Disease” (17 Nov 2016) Silicon Valley Health Institute presentation.
32. Theendakara, V., Peters-Libeu, C. A., Spilman, P., Poksay, K. S., Bredesen, D. E., & Rao, R. V. (2016). Direct transcriptional effects of apolipoprotein E. Journal of Neuroscience, 36(3), 685-700.

33. Brewer, G. J. (2016). Alzheimer’s disease causation by copper toxicity and treatment with zinc. Frontiers in aging neuroscience, 6.

34. Akbari, E., Asemi, Z., Kakhaki, R. D., Bahmani, F., Kouchaki, E., Tamtaji, O. R., … & Salami, M. (2016). Effect of probiotic supplementation on cognitive function and metabolic status in Alzheimer’s disease: a randomized, double-blind and controlled trial. Frontiers in Aging Neuroscience, 8.

35. Ramakrishnan, V. R., Hauser, L. J., & Frank, D. N. (2016). The sinonasal bacterial microbiome in health and disease. Current opinion in otolaryngology & head and neck surgery, 24(1), 20.

36. Bhattacharjee, S., & Lukiw, W. J. (2013). Alzheimer’s disease and the microbiome.     

37. Bredesen, D. E. (2016). Inhalational Alzheimer’s disease: an unrecognized—and treatable—epidemic. Aging, 8(2), 304-313.

38. Goedert, M. (2015). Alzheimer’s and Parkinson’s diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein. Science, 349(6248), 1255555.

39. Bredesen, Dale E (2016) Prionic Loops, Anti-Prions, and Dependence Receptors in Neurodegeneration Buck Institute for Research on Aging, Novato, California.

40. Theendakara, V., Peters-Libeu, C. A., Spilman, P., Poksay, K. S., Bredesen, D. E., & Rao, R. V. (2016). Direct transcriptional effects of apolipoprotein E. Journal of Neuroscience, 36(3), 685-700.

41. Nesse, R. M., Finch, C. E., & Nunn, C. L. (2017). Does selection for short sleep duration explain human vulnerability to Alzheimer’s disease?. Evolution, Medicine, and Public Health, 2017(1), 39.

42. Poksay, K. S., Sheffler, D. J., Spilman, P., Campagna, J., Jagodzinska, B., Descamps, O., … & Cosford, N. D. (2017). Screening for small molecule inhibitors of statin-induced APP C-terminal toxic fragment production. Frontiers in Pharmacology, 8.
43. Lehman, E. J., Hein, M. J., Baron, S. L., & Gersic, C. M. (2012). Neurodegenerative causes of death among retired National Football League players. Neurology, 79(19), 1970-1974. 

44.  Hoogenraad, T. U. (2011). Paradigm shift in treatment of Alzheimer’s disease: zinc therapy now a conscientious choice for care of individual patients. International Journal of Alzheimer’s Disease, 2011. 

45. Bredesen, D. E. (2015). Metabolic profiling distinguishes three subtypes of Alzheimer’s disease. Aging (Albany NY), 7(8), 595-600.

46.  Abbayya, K., Puthanakar, N. Y., Naduwinmani, S., & Chidambar, Y. S. (2015). Association between periodontitis and Alzheimer’s disease. North American journal of medical sciences, 7(6), 241

47. National Institute on Aging. National Institutes of Health. “Alzheimer’s” (2015)

There are no comments yet, but you can be the first

Leave a Reply

The Healthy Baby Code

Personal Paleo

Paleo Products