L-Serine, hope for Alzheimers and ALS

Misshapen proteins that collect in the brains of patients who eventually are diagnosed with Alzheimer’s dementia or in patients with ALS may be due to a substitution being made by BMAA a toxin in some types of cyanobacteria (a blue-green algae) in place of the amino acid L-serine.

Trials have begun with dietary intake of L-serine amino acid powder. The powder is readily available for purchase and is non toxic, (available online from bulk supplement companies that may market to weight lifters). Varying doses have been tried and 30 grams per day, slightly more than an ounce, have been found helpful. See: Alzheimer’s Disease – Could New Approach Lead to Breakthrough? (fortune.com).

The main researcher, Dr. Paul Cox, has a team or researchers involved now and has been focused on Alzheimer’s or ALS, however this is a breakthrough that might also help patients with autism as similar misshapen proteins are often found to be involved in that condition too. A review of research on levels of certain amino acid that have brain neurotransmitter roles in patients with autism diagnoses had some mixed results as there is a D-serine and L-serine form and levels of each can vary and whether a research study measured them separately of together was inconsistent, but several did find lower levels for patients with autism compared to the control group without an autism diagnosis.

See: Zheng HF, Wang WQ, Li XM, Rauw G, Baker GB. Body fluid levels of neuroactive amino acids in autism spectrum disorders: a review of the literature. Amino Acids. 2016;49(1):57-65. ncbi.nlm.nih.gov/PMC5241332/.

More recent research has not replicated or reinforced the theory that BMAA is involved in development of Alzheimer’s disease.

The role of the non-essential amino acid BMAA as a causal agent of Alzheimer’s or ALS may involve other factors in addition to chronic buildup of BMAA over time as a review of research about the topic did not conclude a causal relationship of the amino acid with neurodegenerative disorders.

  • See: A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans. Chernoff, et al, 2017, (ncbi.nlm.nih.gov).
  • Reanalysis of samples of the suspected source of BMAA from the initial research did not find significant amounts, see: The analysis of underivatized β-Methylamino-L-alanine (BMAA), BAMA, AEG & 2,4-DAB in Pteropus mariannus mariannus specimens using HILIC-LC-MS/MS. Foss et al, 2018, (ncbi.nlm.nih.gov).
  • β- N-Methylamino-l-alanine (BMAA) Not Involved in Alzheimer’s Disease. Rauk, 2018, (ncbi.nlm.nih.gov).

The prevailing theory that Beta amyloid protein is a causal agent in Alzheimer’s disease is now being questioned as almost 200 experimental drugs designed to decrease levels of the protein have been found ineffective as treatments for the disease. The protein is involved but likely isn’t the initial problem — regarding Beta amyloid in Alzheimer’s disease: “Brain amyloid is therefore generally accepted as being essential for disease progression but not sufficient on its own to drive disease. The next observable change in brain is impaired glucose metabolism within AD brain,” … “Based on these imaging and biomarker studies it is emerging that brain glucose
(reduced glucose metabolism) and tau toxicity (increased phosphorylation of the Tau protein making it malfunction) likely reflect central events in the progression of AD (1,2,8).”  – Zhu et al, 2014, The emerging link between O-GlcNAc and Alzheimer’s disease, (jbc.org/content/early/2014/full.pdf)

So if BMAA is not a causal agent and Beta amyloid itself also isn’t the primary factor in development of Alzheimer’s disease – that leaves us asking what is involved? The answer is likely multifactorial – multiple issues that may vary somewhat for different patients.

Causal Agent versus Multifactorial Disorder.

Causal roles of a toxin traditionally look at toxins individually and as a toxin that would have the same risk for all people or animals if an animal study. Multifactorial disorders however may involve increased risk for some people based on genetic differences from average, or also require nutrient deficiencies to be present or other infectious or inflammatory conditions to also be present chronically.

Cyanotoxins including BMAA and a metabolite, DAB, have been analyzed for risk of cell death or inflammation in murine (aquatic rather than land based species) brain cells. Low doses of some of the cyanobacteria toxins were found to be a concern but not the BMAA or DAB.

  • See: Cyanotoxins at low doses induce apoptosis and inflammatory effects in murine brain cells: Potential implications for neurodegenerative diseases. Takser, et al, 2016 (ncbi.nlm.nih.gov).

The research by Dr. Paul Cox with BMAA in Alzheimer’s found that the risk association was with concentrated doses over decades,
(fortune.com), so lower doses may not be a significant risk or possibly risk may also require other factors to be present such as a chronically low intake of L-serine.

Many factors have been associated with increased risk for autism spectrum disorder some involving the early prenatal time of conception and implantation of the fetus and later stages of fetal development. Infants may seem to be developing typically and develop symptoms later as a toddler when rapid changes generally occur in the number of connections between brain cells. Genetic and environmental and nutrient deficiencies may also increase risk for the child later developing symptoms of autism or other cognitive conditions such as Attention Deficit/Hyperactive Disorder (ADHD).

  • For more information see: Causal Agent versus Multifactorial Disorder, which I am modifying into an easier to use format from a long series of posts on another of my sites, Believing is the First Step Towards Change.
  • An excerpt from that earlier document – Mice bred to be genetically defective in their ability to produce L-serine, a component of sphingolipids, all died as embryos – they never made it to birth. And: “As expected, all brain L-serine-derived lipids such as phosphatidylserine, phosphatidylethanolamine, sphingomyelin, and GD3 ganglioside are greatly reduced in Phgdh knockout mice.” – See: Hirabayashi Y. A world of sphingolipids and glycolipids in the brain–novel functions of simple lipids modified with glucose. Proc Jpn Acad Ser B Phys Biol Sci. 2012;88(4):129-43.   ncbi.nlm.nih.gov/pmc/articles/PMC3406307/
  • Sphingolipid and serine synthesis are somewhat dependent on each other – inhibiting or increasing one or the other can inhibit or increase production of the other. This may help in treatment of cancer and help with better understanding of intellectual disability conditions as sphingolipid is important for a type of cell common to both. “Sphingolipid levels are tightly linked to serine synthesis, and inhibiting either serine or sphingolipid synthesis can specifically impair the fitness of aneuploid cells “– “Deciphering these mechanisms is important because aneuploidy is associated with diseases including intellectual disability and cancer.” — Hwang S, Gustafsson HT, O’Sullivan C, et al. Serine-Dependent Sphingolipid Synthesis Is a Metabolic Liability of Aneuploid CellsCell Rep. 2017;21(13):3807-3818. ncbi.nlm.nih.gov/pmc/articles/PMC5747309/

So is metabolic problems in serine metabolism or lack of protein in the diet an initial problem? or O-GlcNAc?

Serine is considered a non-essential amino acid because it can be made out of the amino acid glycine in normal health, or it can be converted back into glycine. (ScienceDirect/serine) Both glycine and serine are used in large amounts within myelin, the protein used to form the white fatty coating around the connecting channels between nerve cells. There are 18 molecules of serine within a molecule of myelin protein (172 amino acids long per an older source). See: Amino Acid Sequence of the Basic Protein of the Myelin Membrane, Eylar, 1970, (ncbi.nlm.nih.gov/page=3). – an old source but the graphic is viewable.

O-GlcNAc is a type of sugar/amino acid linkage that may have protective effects against Tau protein, another type of protein that seems to collect in the brain tissue of patients with Alzheimer’s disease. “O-GlcNAcylation is a dynamic form of protein glycosylation which involves the addition of β-d-N-acetylglucosamine (GlcNAc) via an O-linkage to serine or threonine residues of nuclear, cytoplasmic, mitochondrial and transmembrane proteins.” – Wani, et al, 2017, O-GlcNAcylation and neurodegeneration, (sciencedirect.com).

(*N-Acetylglucosamine is a type of monosaccharide that can be formed from a molecule of glucose in times of normal health. It is available as a supplement marketed for arthritis pain as glucosamine, generally derived from chitin found in shellfish. It is not typically found in common foods in the human diet.)(Health is a miracle of complex chemistry, in my opinion.)

Food Sources of L-Serine.

The research on BMAA and trials providing extra L-serine as a possible treatment for ALS (Amyotrophic lateral sclerosis, also known as Lou Gehrig’s Disease, a degenerative nerve condition which causes muscle paralysis) is discussed on another site in an article that includes a list of food sources of L-serine. Animal products such as dairy foods and a variety of meats are good sources but sesame, sunflower, and pumpkin and squash seeds are also sources along with hemp kernels, soy products and other beans, and peanuts and pistachio nuts. See: What is L-Serine and What is Research Telling Us? (naturalhealthyconcepts.com).

This very exciting as there is no shortage of L-serine, it is non-toxic commonly available in foods or as a bulk powder supplement, there would be no wait for a drug approval process. The clinical trials help prove efficacy, safety, and dosage recommendations.

Pumpkin seed kernels, raw, unsalted, with a standard size teaspoon.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.

Glutathione, Nrf2, Autism and glyphosate

Glyphosate use has escalated (1) at a similar rate and overlapping time frame to the increase in autism in children. The rate of autism in Japanese children is even greater than in U.S. children. The Japanese children may be consuming a larger percent of GMO soy from the U.S. as the country is a significant importer of the crop. (4)Testing has shown that basically all GMO soy, Roundup Ready, has residue of glyphosate. (1) Glyphosate residue has been found in all foods tested by the FDA except for broccoli. (6)

The herbicide Roundup has been shown to induce oxidative stress in animal studies (5), and children with autism have been shown to have an increase in oxidative stress and reduced levels of an antioxidant, glutathione, (2), that is made within our bodies during normal health.

Use of Nrf2 promoting foods might help increase our own production of glutathione. (3) Broccoli is one food that may help promote our own supply of Nrf2 which then helps us make the antioxidant glutathione.

Glyphosate may be metabolized into other chemicals within the body and it or the metabolites may inhibit enzymes important for a variety of functions throughout the body. (7) Radioactive labeling of glyphosate in animal studies by the company Monsanto showed that bioaccumulation of the chemical does occur, particularly in blood cells found in bone and bone marrow, also in the testes and ovaries, see slide 11 for a copy of the table of data: (8).

A thorough overview of the theoretical and known health risks of glyphosate is available by a personal fitness coach from Australia, Alex Fergus, (9), in part two of a three part series on his website. Part one covers the history of the synthetic chemical’s discovery and patent history and increased agricultural use in the U.S. and globally, (10), and his list of tips on how to protect yourself and try to reduce exposures through diet and supplements, (11). The list is comprehensive however doesn’t include Epsom salt/magnesium sulfate as an additional source of bioactive sulfate. Baths or footsoaks provide a topical absorption route that would bypass any problems with malabsorption in the digestive system or problems with sun exposure to bioactivate other forms of sulfur into the bioactive sulfate form.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.

  1. John Peterson Myers, Michael N. Antoniou, Bruce Blumberg, Lynn Carroll, Theo Colborn, Lorne G. Everett,Michael Hansen, Philip J. Landrigan, Bruce P. Lanphear, Robin Mesnage, Laura N. Vandenberg, Frederick S. vom Saal,Wade V. Welshons, and Charles M. Benbrook,

    Concerns over use of glyphosate-based herbicides and risks associated with exposures: a consensus statement.  Environ Health. 2016; 15: 19. Pub. online 2016 Feb 17,  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4756530/?utm_content=buffere016d&utm_medium=social&utm_source=twitter.com&utm_campaign=buffer

  2. S. Rose, S MelnykO PavlivS BaiT G NickR E Frye,  S J James, Evidence of oxidative damage and inflammation associated with low glutathione redox status in the autism brain, Translational Psychiatry Vol. 2, page 134 (2012), nature.com, https://www.nature.com/articles/tp201261
  3. Megan L. Steele, Stacey Fuller, Mili Patel, Cindy Kersaitis, Lezanne Ooi, and Gerald Münch, Effect of Nrf2 activators on release of glutathione, cysteinylglycine and homocysteine by human U373 astroglial cellsRedox Biol. 2013; 1(1): 441–445. Published online 2013 Sep 12, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3814960/

  4. Zen Honeycutt, Shockingly Higher Rates of Autism and Developmental Delays in Asia, Report from Japan speaking tour, March 1-10, March 21, 2017, MomsAcrossAmerica.com, https://www.momsacrossamerica.com/shockingly_higher_rates_of_autism_and_developmental_delays_in_asia
  5.  Low toxic herbicide Roundup induces mild oxidative stress in goldfish tissuesChemosphere, Vol. 76, Issue 7, Aug 2009, pp 932-937
    ScienceDirect,  https://www.sciencedirect.com/science/article/pii/S0045653509005256
  6. Toxic Weed Killer Glyphosate Found in Most Foods Sold in the U.S., wakeup-world.com, https://wakeup-world.com/2018/05/24/toxic-weed-killer-glyphosate-found-in-most-foods-sold-in-the-u-s/
  7. Ford et al., Mapping Proteome-wide Targets of Glyphosate in Mice, Cell Chemical Biology (2016), http://dx.doi.org/10.1016/
    j.chembiol.2016.12.013 https://www.cell.com/cell-chemical-biology/pdf/S2451-9456(16)30474-3.pdf
  8. Anthony Samsel, Glyphosate Herbicide Pathways To Modern Diseases Synthetic Amino Acid And Analogue of Glycine Mis-incorporation Into Diverse Proteins , Slides 2016,,   https://people.csail.mit.edu/seneff/DC2016/AnthonySamsel_DC2016.pdf (8)
  9. Alex Fergus, Glyphosate: Why You Need to Eat Organic,   https://www.alexfergus.com/blog/glyphosate-why-you-need-to-eat-organic (9)
  10. Alex Fergus, Glyphosate: The Weed Killer Found in Our Food & Water, https://www.alexfergus.com/blog/glyphosate-the-weed-killer-found-in-our-food-water (10)
  11. Alex Fergus, How to Protect Yourself from Glyphosate, https://www.alexfergus.com/blog/how-to-protect-yourself-from-glyphosate (11)

Average Autism and Alzheimer’s Rates Differ by Gender

Autism is more of a risk for boys than girls by a factor of four boys for every one girl or three boys for every one girl diagnosed with autism depending on the type of study and diagnostic criteria. There is some speculation that autism in girls presents with less obvious symptoms than in boys. Girls with autism may have less repetitive behavior and be able to fit in socially better than boys with autism and may have less obvious focus on one main topic of interest. (1)

At the other end of the age spectrum females have a greater rate of Alzheimer’s Disease than males. (13)

The difference has been shown to be significant, not just a difference in diagnostic criteria. Estrogen is a female hormone that may be protecting girls from the risk of developing autism but then in menopause is no longer protecting older females from the risk of developing Alzheimer’s Disease. Patients with Autism and Alzheimer’s have been shown to have a tendency to have increased amounts of protein clusters (amyloid beta) in the brain which in normal health would be cleared away. An animal based study found a genetic strain of mice with a clear gender and age difference. Young male mice developed autism like symptoms and older female mice developed Alzheimer’s like symptoms.

A different study found a gender difference in the amount of a protective protein (ADNP) in young male mice with autism like symptoms and older female mice with Alzheimer’s like symptoms. (6) Complete lack of the protective protein leads to very early death with neural tube defects in animal studies.  (7) The neuroprotective protein (ADNP) seems to promote autophagy (our body’s recycling method, it makes us more energy efficient and helps detoxify/remove old cells or material such as the beta-amyloid protein for reuse, read more:  14) and the deficit of it may also be involved in schizophrenia. (8) The protein is involved with control of the dendritic branching of brain cells which is typically found to be  different in children with autism. The protein also plays a role in regulating over 400 genes involved in embryo development including ApoE and the tau protein which is found to collect in the brains of patients with Alzheimer’s Disease in addition to beta-amyloid protein. (9)

The role of apoE involves membranes, cholesterol, cannabinoid receptors and lipid rafts – chemistry geeks have fun, three dimensional drawings and a discussion of cholesterol within the brain and its role in several neurodegenerative diseases is available online in full text, the brain includes 25% of the body’s cholesterol even though the brain only accounts for 2% of the total body weight, on average. (10).  A briefer description of the role apoE plays in the brain and with estrogen and Alzheimer’s risk is available with a discussion of the gene differences that are known to increase but not guarantee risk of developing Alzheimer’s Disease. (11)

Disclosure: a genetic screening suggests I do have one of the higher risk differences in the ApoE gene. (rs2254958)

Strategies to help increase autophagy may help reverse some of the risk factors associated with reduced ApoE/reduced ADNP levels –

  1. vigorous exercise,
  2. a ketosis promoting, low carbohydrate diet, regularly or occasionally,
  3. fasting for a day or a partial day occasionally. (14)

The activity of the apoE protein on other genes can be affected by cannabinoids, too little cannabinoids may be a problem or too much.

The take home point – magnesium and adequate cannabinoids seem to be involved in helping clear the protein clusters during normal health.

  • Nutritional strategies recommended to help prevent Alzheimer’s disease include increasing intake of magnesium. Research has found that low levels of magnesium promoted build up of  beta amyloid protein while high levels of magnesium promoted breakdown of the misshapen proteins.

“Lab studies show that magnesium modulates enzymes involved in amyloid beta production; at low levels, magnesium favors amyloid beta buildup, while at higher levels it favors amyloid beta breakdown.101,102″ [2]  (from a  2014 post)

Certain genetic conditions and chronic health conditions or older age can make the body less able to make cannabinoids endogenously/internally. External sources of cannabinoids have been shown to be helpful for clearing the protein clusters involved in Alzheimer’s Disease. (https://www.sciencedaily.com/releases/2016/06/160629095609.htm)

An underlying infection with bacteria or yeast may be involved in the buildup of the protein clusters as they have a protective effect against some types of infection, so addressing low grade chronic infection may be needed to help stop the over production of the amyloid beta protein clusters in addition to providing adequate magnesium and cannabinoids. Note that there are non-euphoric cannabinoids and legal food sources in addition to medical marijuana. Pumpkin seeds are a good source, $200 billion per year is estimated to be spent on Alzheimer’s care annually at our current rate of the disease prevalence – that would buy a lot of pumpkin seeds. (15 )

That article also mentions that 192 pharmaceutical chemicals have been anticipated and tested in hope of a cure or effective treatment for Alzheimer’s Disease but which have ultimately not been found to be successful. One hundred and ninety two chemicals tested, one hundred and ninety two chemicals found ineffective – magnesium and cannabinoids however have been found effective at helping the body to naturally break down the tau and  beta-amyloid protein clumps that lead to brain damage and later symptoms of dementia in Alzheimer’s Disease and a few other neurological conditions including traumatic brain injuries and autism. (15 ) (links re tau/amyloid in autism & Alzheimers) (links re tau/amyloid protein in traumatic brain injury)

Ibuprofen is a pharmaceutical that is no longer covered by a patent and it has been found to be beneficial in protecting against Alzheimer’s Disease (link: 16) and the underlying reason is likely that ibuprofen prevents the break down of cannabinoids (17)(Search term: “ibuprofen prevents break down of cannabinoids”) – but you need cannabinoids first and some people might no longer be able to make them after a certain age or state of health or may never have been able to make them as well due to genetic differences.

So celebrate protecting your brain today by eating pumpkin seeds, cardamom spice, the herb rosemary, chocolate, or leafy green vegetables. – and the brightly colored tiny inner part of a piece of corn that you can see when eating corn on the cob is also a good source.

  • The misshapen tau/amyloid-beta proteins have a protective effect against bacteria and the yeast Candida albicans so a chronic lowgrade infection may be an underlying cause of the accumulation of beta amyloid placques. [3] [4] (from a  2014 post)

There are many more legal food sources of cannabinoids or a precursor available, a longer list is included below. The progression of Alzheimer’s Disease can take twenty years before symptoms are obvious, so getting an early start on protecting against the tau/beta-amyloid protein build-up makes sense to me (Disclosure, I have a direct family history of the disease in older relatives and a genetic screening suggests that I am more at risk, so I am biased towards preventing the disease in my own brain or other family members.)

Phospholipids are part of cannabinoids and other phosphorus containing nutrients are important in energy production. The phospholipids and cannabinoids are important for the health and function of skin and other membranes lining cells and organs, and/or if you care more about having a good hair day than whether you might get Alzheimer’s Disease in several decades, then the phospholipids are also important for hair growth: *The phospholipid mixture in this animal-based study was applied on the skin surface for hair loss associated with inflammatory skin dermatitis: (18)

(Additional Discloure: I am also genetically at risk for Male Pattern Baldness which became visibly apparent when my autoimmune disease was more severe, however with my switch to phospholipid rich foods my hair has since grown back and my autoimmune condition is in remission as long as I continue with my new health habits).

Other nutrients including the B vitamins, vitamin E, and zinc are also important for healthy hair growth (read more) but many of the following list would also be good sources of B vitamins, vitamin E, zinc and other trace minerals and essential omega 3 and omega 6 fatty acids. Pumpkin seeds are a good vegetarian source of zinc, otherwise the mineral is more commonly available in meats.

  • Food Sources of Phospholipids and other phospho-nutrients: Hemp seed kernels and oil; Artemisia turanica/wormwood leaf; amaranth seed; asparagus; avocado fruit or the inner kernel, dried and powdered; beans/legumes; cardamom seeds and powder; carrots; celery stalks and leaves; cocoa beans and cocoa powder, baker’s chocolate, dark chocolate and to a lesser amount milk chocolate and chocolate syrup; coconut; cumin seed/powder; fennel seed, flax seed, pine nuts; sesame seeds, pumpkin seed kernels, squash seeds; butternut squash and pumpkin; gingko leaf; grapefruit and orange juice with the pulp; Jerusalem artichoke (this is a root vegetable rather than a green artichoke); lettuce, spinach and mustard leaves and other leafy green vegetables and herbs; nuts/peanuts, cashews, walnuts; oats; okra seeds; onion root, leek leaves, garlic;  parsnip root; pomegranate seeds and pomegranate peel extract;rice, white or brown but the bran is the best source; rosemary; sorghum;  sweet potato or yam; buckwheat (a seed botanically that is not wheat and is gluten free); wheat. (G.26)

That topic took a walk around the block and picked some daisies along the way but the important message might be that eating well and exercising regularly may promote healthy hair, a fit body right now while helping maintain healthy brain function into the future. Genetic susceptibility may be involved in the rate of young males with autism and older females with autism and prevention might include more magnesium and phospholipid rich foods in the diet with a diet that is moderate in carbohydrates and regular vigorous exercise to promote autophagy to help promote the natural recycling of tau and beta-amyloid protein that tends to accumulate in the brains of people with autism and Alzheimer’s Disease. Lack of ADNP protein may lead to lack of ApoE or a genetic difference may cause reduced ApoE and the deficiency may lead to a reduced level of autophagy.

Fasting for a day or partial day occasionally or a low carbohydrate diet, even just a diet balance as low as 30% of calories, and vigorous exercise are three natural ways that may help promote autophagy – our body’s natural method for removing and reusing old cellular material. (14) Those strategies might help a woman with Alzheimer’s risk but for an infant or toddler may need to be adapted to simply allowing vigorous, safe play, and a diet that with a greater percentage of healthy fats than average. The list of phosphonutrient rich foods are generally healthy and safe for prenatal diets or other stages of life and would likely promote a fit body and healthy hair for a person of any age and gender – and what is good for the hair is good for other membranes throughout the body and is also good for the brain. The hair is a protein that is a modified form of skin tissue and so is fingernail protein – beauty is more than skin deep.

Some daisies.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes. Thanks.

  1. Sarah Deweerdt,  Estimate of autism’s sex ratio reaches new low, April 27, 2017,  spectrumnews.org https://www.spectrumnews.org/news/estimate-autisms-sex-ratio-reaches-new-low/ 
  2. Liam Hawkins, Nutritional Strategies and Alzheimers, March 2013 lifeextension.com, http://www.lifeextension.com/magazine/2013/3/Nutritional-Strategies-to-Combat-Alzheimers/Page-02
  3. Lisa Conrick, What is Causing Beta-Amyloid Production in Alzheimer’s and Autism?, Oct. 23, 2012, ageofautism.com, http://www.ageofautism.com/2012/10/what-is-causing-beta-amyloid-production-in-alzheimers-and-autism.html
  4. Molnar Mark, Alzheimer’s Disease Emerging Role of Infection,  http://miklossy.ch/
  5. Why women have more Alzheimer’s disease than men: gender and mitochondrial toxicity of amyloid-beta peptide. J Alzheimers Dis. 2010;20 Suppl 2:S527-33. https://www.ncbi.nlm.nih.gov/pubmed/20442496
  6. Activity-dependent neuroprotective protein (ADNP) exhibits striking sexual dichotomy impacting on autistic and Alzheimer’s pathologies. Transl Psychiatry. 2015 Feb 3;5:e501. https://www.ncbi.nlm.nih.gov/pubmed/25646590
  7. Shmuel Mandel, Gideon RechaviIllana Gozes, Activity-dependent neuroprotective protein (ADNP) differentially interacts with chromatin to regulate genes essential for embryogenesis. Developmental Biology, Volume 303, Issue 2, 15 March 2007, Pages 814-824. https://www.sciencedirect.com/science/article/pii/S0012160606013960

  8. Shlomo Sragovich, Avia Merenlender‐Wagner, Illana Gozes, ADNP Plays a Key Role in Autophagy: From Autism to Schizophrenia and Alzheimer’s Disease. BioassaysVolume39, Issue 11, November 2017, Pages 1700054 https://onlinelibrary.wiley.com/doi/pdf/10.1002/bies.201700054

  9. Gozes Illana, (2015) Activity-dependent neuroprotective protein (ADNP): from autism to Alzheimer’s disease. SpringerPlus. 4. L37. 10.1186/2193-1801-4-S1-L37.  https://www.researchgate.net/publication/282802744_Activity-dependent_neuroprotective_protein_ADNP_from_autism_to_Alzheimer’s_disease
  10. M Maccarrone, G Bernardi, A Finazzi Agrò, and D Centonze, Review: Cannabinoid receptor signalling in neurodegenerative diseases: a potential role for membrane fluidity disturbance. British Journal of
    Pharmacology, Themed Issue: Cannabinoids in Biology and Medicine, Part I, Nov. 16, 2010. http://files.iowamedicalmarijuana.org/petition/2012/bjp-aug-2011-1379-1390.pdf
  11. Hilary Lampers, ND, 5 Reasons to Know Your APOE:  Understanding Your Alzheimer’s Disease Risk. June 13, 2016 thenatpath.com
  12. http://thenatpath.com/body/5-reasons-to-know-your-apoe/
  13. Maxwell A. Ruby, Daniel K. Nomura, Carolyn S. S. Hudak, Lara M. Mangravite, Sally Chiu, John E. Casida, and Ronald M. Krauss, Overactive endocannabinoid signaling impairs apolipoprotein E-mediated clearance of triglyceride-rich lipoproteins. Proc Natl Acad Sci U S A. 2008 Sep 23; 105(38): 14561–14566. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2567196/

  14. Nick English, Autophagy: The Science-Backed Way to Cleanse Your Body, July 4, 2016, greatist.com, https://greatist.com/live/autophagy-fasting-exercise
  15. Stuart W Titus, PhD, Dr. Titus’ Insights: Alzheimer’s Research and the Work of Dr. Schubert, Aug. 5, 2016, medicalmarijuanainc.com,  https://www.medicalmarijuanainc.com/dr-titus-insights-alzheimers-research-work-dr-schubert/
  16.  Neuroscientists say daily ibuprofen can prevent Alzheimer’s disease., March 26, 2018, sciencedaily.com,   https://www.sciencedaily.com/releases/2018/03/180326140239.htm

  17. K. D. Rainsford, IbuprofenDiscovery, Development and Therapeutics. 
    John Wiley & Sons, June 25, 2015, page 134, https://books.google.com/books?id=CAcLCgAAQBAJ&pg=PA134&lpg=PA134&dq=ibuprofen+prevents+break+down+of+cannabinoids&source=bl&ots=oJ_cjSrWXr&sig=yQgwSrdZOkA1MNDkbf7EF7waItY&hl=en&sa=X&ved=0ahUKEwjf7ZKPrcnaAhVlneAKHeDyAuAQ6AEIlQEwCA#v=onepage&q=ibuprofen%20prevents%20break%20down%20of%20cannabinoids&f=false
  18. Seong-Hyun Choi, Jeong-Su Moon, Byung-Suk Jeon, Yeon-Jeong Jeon, Byung-Il Yoon, and Chang-Jin Lim, Hair Growth Promoting Potential of Phospholipids Purified from Porcine Lung Tissues. Biomol Ther (Seoul). 2015 Mar; 23(2): 174–179. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354319/
  19. ADNP related syndrome FTNW, *lack of ADNP genetically leads to reduced muscle tone and can cause eating problems in children. https://www.rarechromo.org/media/information/Chromosome%2020/ADNP%20related%20syndrome%20FTNW.pdf