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Genes & common infections (herpes & candida) linked to Alzheimer’s/dementia

Content reviewed by Donna Gates
Written by Body Ecology on January 28th, 2021

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What causes Alzheimer’s and dementia? The APOE4 gene variant has been associated with a higher risk of Alzheimer’s disease (AD), but it’s not the only factor thought to contribute to this type of neurological decline.1 Increasingly, researchers are investigating the damaging effects of microbial infection of the central nervous system and even the toxins produced by fungi, such as Candida albicans.

What does APOE have to do with Alzheimer’s and dementia?

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The APOE is a gene that creates a protein called apolipoprotein E (APOE). This protein binds to fat to create lipoproteins (fats bound to proteins), which help carry cholesterol around the bloodstream and are mainly responsible for carrying fats to and from the brain and central nervous system.

Research in mice has shown that Candida albicans can cross the blood-brain barrier and enter the brain.

As you know, good fats play a vital role in brain function. Basically, we all have a fatty brain.

So, why all the fuss about APOE4? Large studies show that of the three major forms of the APOE gene, two are associated with a greater risk of certain diseases and conditions.

The three variants are:

  • APOE2
  • APOE3
  • APOE4

APOE3 is the most common form of the gene and is considered neutral in terms of health risks. You are fortunate if you have this version of the APOE gene. We won’t say much about E3 here.

Having variants in the APOE2 gene is a risk factor for high triglycerides.2 If you have variants in APOE2, then it’s very important to avoid sugars in your diet. Sugars are inflammatory and may also promote brain inflammation, which may contribute to Alzheimer’s.

APOE2 is linked to a higher risk of cardiovascular disease, which may be because this variant of the gene seems to limit how dietary fat is filtered from the blood.3 While not directly related to Alzheimer’s disease risk, carrying the APOE2 gene variant may indirectly increase the risk of neurological disease by interfering with blood flow in the brain.

For those with APOE2, certain foodstuffs could be beneficial, such as nattō, made from fermented soybeans.

This contains an enzyme called nattokinase that is synthesized by the bacteria that ferment the soybeans. Nattokinase is a very powerful clot-buster — helping to break up fibrin blood clots, which could offset some of the cardiovascular risks associated with the APOE2 gene.4 If finding and eating nattō is highly unlikely for you, nattokinase is also available as a dietary supplement in your health food store.

Finally, APOE4 is the variant most associated with an increased risk of Alzheimer’s disease and other neurological conditions.1 It isn’t, however, at all clear why this variant increases a person’s risk of AD. Potentially, this variant might affect the development of neurites, part of the brain’s neural network.5

There is certain agreement within the scientific community that those with the APOE4 genotype may fare badly on a diet high in the processed fats and inflammatory seed oils that are so pervasive in our diets today. These may cause a dramatic increase in brain inflammation.

This genotype should strictly avoid these inflammatory foods and may do best on a diet higher in anti-inflammatory dark green and root vegetables, obtaining their animal protein from grass-fed animals. Grass-fed animals have a higher ratio of omega-3 fats.

The top 5 risk factors that could cause Alzheimer’s disease

The APOE gene is just one genetic factor in the development of AD and may have the most impact later in life as the risk of AD doubles every five years after the age of 65. For those with early-onset AD/dementia, however — which is considered a diagnosis before the age of 65 — three other genes may be significant.

These are:

  • APP
  • PSEN1
  • PSEN2

APP is the gene that encodes amyloid precursor protein, which influences the formation of amyloid plaques in the brain.

Aside from genetics, though, there are five key risk factors thought to contribute to around a third of all cases of AD. These are:

1. Smoking

2. Physical inactivity (being sedentary)

3. Obesity

4. Diabetes

5. High blood pressure (hypertension)

We all know that getting regular, daily exercise and avoiding being sedentary has a range of benefits for health, but research also suggests that this can reduce amyloid plaque formation, even in those carrying an APOE4 variant.6

Another potential risk factor is also under investigation: microbial infection.

How much do you know about what’s hiding in your genes? Listen in on these incredible interviews from the Genius of Your Genes Summit for free.

Could Alzheimer’s be linked to candida? It’s likely.

A paper published in 2015 in the journal Nature revealed that samples of brain tissue from people who had died from Alzheimer’s disease contained fungal cells and hyphae.7 In the study, all samples of brain tissue from AD patients showed fungal infection, whereas samples from control patients without AD were not infected. The researchers also found fungal infection in blood cells, which they linked to the vascular damage seen in people with AD.

Research in mice has shown that Candida albicans can cross the blood-brain barrier and enter the brain, where it triggers inflammatory processes and leads to the formation of abnormal structures similar to the plaques seen in AD. These changes and inflammation were linked to spatial memory impairments in the mice infected with Candida albicans in this study.8

Candida albicans and other opportunistic pathogens, such as the mold Aspergillus fumigatus, are known to produce gliotoxin, a substance that has immunosuppressive properties.9 Glutathione can partially counteract these effects.

Other studies have also found that:

  • There’s evidence that bacterial and viral infections that are present in the body of someone with AD trigger amyloid plaque formation, possibly as a defense mechanism.10-12 In other words, the brain is forming these plaques to protect itself. Indeed, amyloid beta peptide has antimicrobial activity and is especially good at inhibiting Candida albicans.13
  • Common infections found in people with AD include Lyme disease; any of the herpes family viruses, such as herpes simplex type 1 virus (HS-#1); another common virus called CMV Cytomegalovirus (HS-#5); and Chlamydophila pneumoniae, a bacterial infection in the lungs.
  • The APP and APOE4 genes appear to be affected by the herpes simplex HSV-1, with strong evidence accumulating that reactivation of HSV-1 in the brain tissue of people with the APOE4 variant could lead to AD.11 Specifically, latent HSV-1 may be reactivated by other infections, immunosuppression, and inflammation, with cumulative damage to brain tissue amounting to AD in later years.14
  • Several pathogens have also been associated with changes in the brain characteristic of AD. These include the human immunodeficiency virus (HIV) and the measles virus.15 The latter can lead to a very serious disease called subacute sclerosing panencephalitis, for instance.16 Thankfully, this is now rare due to successful worldwide measles vaccination programs.

All these connections aren’t particularly surprising when we think about how microbial infections affect the entire body and, logically, would also affect the brain.

Aside from cognitive decline, most people with AD/dementia have elevated levels of inflammation, damage to blood vessels, changes in how and when brain cells multiply and die, and the formation of plaques in the brain. Researchers have found higher levels of several cytokines involved in inflammation, including interleukins 1 and 6, tumor necrosis factor alpha, and interferon gamma, in people with AD.17

Take action: What can you do to reduce risk of Alzheimer’s/dementia?

Given what we know about the causes of Alzheimer’s and dementia, there are many steps we can all use right away to reduce the risk of developing the condition.

In addition to stopping smoking, achieving a healthy body weight, and getting regular exercise, it can help to:

  • Manage your blood sugar; keep it well controlled. Stave off diabetes or manage the condition well if already diagnosed. The same goes for hypertension. Cutting down on refined salt (especially if you have a salt-sensitive gene), exercising, reducing or eliminating alcohol consumption, and practicing healthy stress management can all help stabilize blood pressure.
  • Reduce stress and the impact of unavoidable stress on the body. Stress elevates cortisol, and this elevates blood sugar. Stress causes unresolved and ongoing inflammation in every cell in the body. Managing stress — which is not easy to do today — also supports a healthy immune function, which is essential for fighting off viruses and other microbial infections!
  • Make balanced lifestyle and dietary choices. Healthy habits can also help control inflammation and provide antioxidant nutrients, such as glutathione, which may help reduce any negative impacts of latent viral, fungal, and bacterial infections on brain tissue.
  • Focus — always — on gut health. A healthy gut is absolutely essential for a healthy brain and a healthy immune system too. If you have any digestive problems at all, focus on the 3 Rs: Remove, Repair, and Replace. Remove all the toxic foods and microbes causing inflammation in the gut. Remove infections in the small intestine, like SIBO (small intestine bacterial overgrowth) and SIFO (small intestine fungal overgrowth — mold and candida). Repair the gut lining, and Replace the dysbiotic inner ecosystem with a diversity of beneficial microbes instead.

And finally, including probiotic-rich, fermented foods and liquids into your diet on a daily basis will help ensure a wide diversity of these beneficial microbes in your colon.

While this is not yet an area of research that’s directly linked to Alzheimer’s, it’s logical that they may be shown to have an important role in keeping cognitive decline at bay. Not only does a healthy microbiome help to control pathogenic organisms. It can help to better manage whole-body inflammation, maintain your immune system, and support a functional gut-brain axis, helping to benefit cognitive wellbeing for life.18

REFERENCES:

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  2. 2. Kuhel DG, Konaniah ES, Basford JE, et al. Apolipoprotein E2 accentuates postprandial inflammation and diet-induced obesity to promote hyperinsulinemia in mice. Diabetes. 2013;62(2):382-391. doi:10.2337/db12-0390.
  3. 3. Weisgraber KH, Innerarity TL, Mahley RW. Abnormal lipoprotein receptor-binding activity of the human E apoprotein due to cysteine-arginine interchange at a single site. J Biol Chem. 1982 Mar 10;257(5):2518-21. PMID: 6277903.
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  6. 6. Head D, Bugg JM, Goate AM, et al. Exercise Engagement as a Moderator of the Effects of APOE Genotype on Amyloid Deposition. Arch Neurol. 2012;69(5):636-643. doi:10.1001/archneurol.2011.845.
  7. 7. Pisa, D., Alonso, R., Rábano, A. et al. Different Brain Regions are Infected with Fungi in Alzheimer’s Disease. Sci Rep 5, 15015 (2015). https://doi.org/10.1038/srep15015.
  8. 8. Wu, Y., Du, S., Johnson, J.L. et al. Microglia and amyloid precursor protein coordinate control of transient Candida cerebritis with memory deficits. Nat Commun 10, 58 (2019). https://doi.org/10.1038/s41467-018-07991-4.
  9. 9. Bertling A, Niemann S, Uekötter A, Fegeler W, Lass-Flörl C, von Eiff C, Kehrel BE. Candida albicans and its metabolite gliotoxin inhibit platelet function via interaction with thiols. Thromb Haemost. 2010 Aug;104(2):270-8. doi: 10.1160/TH09-11-0769. Epub 2010 Apr 29. PMID: 20431851.
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