Does hygiene lead to a higher risk of Alzheimer’s Disease?

As a student who is passionate about studying psychology, I came across an article on the University of Cambridge’s research site that talks about Alzheimer’s disease, which can be defined as “a progressive disease that destroys memory and other important mental functions”. The article, titled “Better hygiene in wealthy nations may increase Alzheimer’s risk,” argues that there is a strong positive correlation between clean, industrialized countries and the prevalence of Alzheimer’s disease in the countries’ population. (Fox, 2013) While I was initially fascinated by this claim, I knew that I needed to be a little more objective when trusting these relatively one-sided claims. In doing so, then, I formulated the following question: To what extent does hygiene actually contribute to the development of Alzheimer’s disease? In other words, is there a direct cause-effect relationship between cleanliness and Alzheimer’s or is there simply a correlation between the two?

To me, the article seems to suggest that Alzheimer’s Disease (AD) is caused by high sanitation levels within a country because of limited contact with certain bacteria, viruses, and other microorganisms. Deficiency of contact with these microorganisms, they claim, can lead to an insufficient amount of T-cells, which are a form of white blood cells that effectively counteract “foreign substances and disease” (Apple dictionary). The resulting inflammation that occurs from a lack of T-cells is linked to the inflammation that is commonly found in the brains of Alzheimer’s patients. (Better hygiene in wealthy nations may increase Alzheimer’s risk, 2013) So in searching for a clearer answer to my question, I knew that I needed to understand the differences between the brain of an AD patient and a healthy brain, and break them down to their elemental, molecular level to understand exactly what could be the root cause of AD.

The brains of Alzheimer’s patients are characterized by 3 “hallmarks”: an abundance of amyloid plaques, an increase in neurofibrillary tangles, and the destruction of and loss of connection between the nerve cells. (National Institutes of Health, 2011) From this, I thought that perhaps the excess of amyloid plaques could be linked to the lack of T-cells in an Alzheimer’s brain. From here I came across a scientific study that related T-cells to the amyloid-beta proteins (that make up the plaques), and I found that “chronic stimulation by the amyloid-beta protein present in the blood” could be the cause of changes in the T-cells of AD patients that otherwise make us immune to bacteria and other microorganisms. (Mariavaleria et al., 2011) I then came across a second scientific study that claimed that T-cell immunity to bacteria and other microorganisms in AD patients decreased significantly in comparison to the T-cell immunity of healthy patients. (Giubilei et al., 2003) This research seemed to tell me that hygiene may not be the direct cause of AD, but rather that the build-up of amyloid-beta proteins in our brain could be a biological cause.

I followed through with this prediction – that the build-up of amyloid-beta proteins in our body causes AD – by trying to find out where the amyloid-beta protein comes from. Interestingly, I found that there are actually three types of amyloid-beta proteins that are processed from what is called the amyloid precursor protein (APP), which is found widely within the cells of our own bodies. Two types of amyloid-beta proteins (amyloid-beta 38 and amyloid-beta 40) are benign while the third type of amyloid-beta protein (amyloid-beta 42) is toxic and seems to be the one that causes brain damage in AD patients. (Khan) After identifying the type of amyloid-beta protein, then, I came across its chemical structure:

(chemBlink)
(chemBlink)

The molecular formula for amyloid-beta 42 is C203H311N55O60S (chemBlink); clearly, I can see that the molecular structure is quite large. It is also characteristic of a protein, as evidenced by the presence of primary, secondary, and tertiary amides that are part of the molecule. I found that this protein may actually be responsible for damaging the blood-brain barrier by making it more permeable. (Sharma et al., 2012)

From this, I thought that maybe the increase in permeability of the BBB could be linked to a less immune brain, which could connect back to the “hygiene hypothesis.” So I then decided to go back to investigating the immune system’s role in AD pathology by connecting it to its relation with the amyloid-beta 42. I found that the amyloid-beta 42 activates the production of one type of T-cells that “secrete pro-inflammatory cytokines, which cross the BBB and directly activate microglia and astrocytes in the brain, as well as indirectly induce inflammation by activating dendritic cells.” (Town et al., 2005 as cited in Fox et al., 2013) Microglia and astrocytes are “cellular components of the brain’s immune network” (Cohen, 2009); hence, I observe that T-cells modify the performance of these components in the immune system, which fosters the development of AD.

So in answering my question, I find that the amyloid-beta protein and the immune system of the brain are bidirectional in developing AD, and both play significant roles in the pathology of AD. That means that our immune system’s response to different levels of hygiene, along with our genetic predisposition (the presence of APP) both can contribute to increase risk in Alzheimer’s disease.

What are the implications, then, of my findings about AD? Well, since AD is the 5th leading cause of death for those aged 65 and older (Alzheimer’s Association, 2013), understanding the causes of AD can help us better find cures for this disease, which are not entirely ready as of yet. For example, realizing that the blood-brain barrier has increased permeability in AD patients tells drug developers that treating AD involves strengthening the blood-brain barrier so it does not allow toxic substances (such as cytokines) to enter and trigger inflammatory responses. (Sharma et al., 2012) In addition, after researching more thoroughly into the claims of the initial reading on AD, I now understand that certain claims can often turn out to be monochromatic and therefore they must be taken with a grain of salt. The health and diet claims that are so prevalent on the web must be, in my opinion, scrutinized and considered comprehensively in order to be trusted, especially since our well-being is directly at risk.

All in all, my investigation on AD has taught me more than just causes or effects of the disease. My findings have led me to understand that critical evaluation and rational judgment (the weighing of pros and cons) is often necessary when we are faced with decisions to make the best choices, both for ourselves and for our society.

Resources:

Alzheimer’s facts and figures. (2013). Retrieved from http://www.alz.org/alzheimers_disease_facts_and_figures.asp

Alzheimer’s disease: Unraveling the mystery. (2008, September). Retrieved from http://www.nia.nih.gov/alzheimers/publication/part-2-what-happens-brain-ad/hallmarks-ad

Brown, C., & Ford, M. (n.d.). Medicine and drugs. In Higher Level Chemistry: Developed specifically for the IB Diploma Pearson Baccalaureate.

Cohen, R. M. (2009). The role of the immune system in alzheimer’s disease. The journal of lifelong learning in psychiatry, 7(1), 28-35. Retrieved from http://psychiatryonline.org/data/Journals/FOCUS/1837/foc00109000028.pdf

Fox, M. (2013, September 04). Better hygiene in wealth nations may increase alzheimer’s risk. Research at Cambridge. Retrieved from http://www.cam.ac.uk/research/news/better-hygiene-in-wealthy-nations-may-increase-alzheimers-risk

Fox, M., Knapp, L.A., Andrews, P.W., & Fincher, C.L. (2013). Hygiene and the world distribution of alzheimer’s disease. Evolution, medicine, & public health, 2013(1), doi: 10.1093/emph/eot015

Giubelei, F., Antonini, G., Montesperelli, C., Sepe-Monti, M., Cannoni, S., Pichi, A., & Tisei, P. et al., US National Library of Medicine, National Institutes of Health. (2003). T cell response to amyloid-beta and to mitochondrial antigens in alzheimer. Retrieved from PubMed.gov website: http://www.ncbi.nlm.nih.gov/pubmed/12714798

Khan, A. (n.d.). The amyloid hypothesis and potential treatments for alzheimer’s disease. The Journal of Quality Research in Dementia, (4), Retrieved from http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=383&pageNumber=6

Mayo Clinic staff. (n.d.). Alzheimer’s: Causes. Retrieved from http://www.mayoclinic.com/health/alzheimers-disease/DS00161/DSECTION=causes

Pellicano, M., Larbi, A., Goldeck, D., Colonna-Romano, G., Buffa, S., Bulati, M., Rubino, G., Iemolo., F., Candore, G., Caruso, C., Derhovanessian, E., & Pawelec, G. (2012). Journal of neuroimmunology, 242(1), 52-59. Retrieved from http://www.jni-journal.com/article/S0165-5728(11)00305-5/abstract

Sharma, H. S., Castellani, R.J., Smith, M.A., Sharma, A., US National Library of Medicine, National Institutes of Health. (2012). The blood-brain barrier in alzheimer’s disease: Novel therapeutic targets and nanodrug delivery (10.1016/B978-0-12-386986-9.00003-X). Retrieved from PubMed.org website: http://www.ncbi.nlm.nih.gov/pubmed/22748826

Image Resources:

Beta-Amyloid (1-42) human [Web Graphic]. Retrieved from http://www.chemblink.com/products/107761-42-2.htm

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