Health and Disease

Can Humans Use Smell to Detect Cancer?


Olfactory receptors (ORs) are specialised proteins that detect volatile chemicals that are common odorants in the environment.  Discovered in 1991 by Buck and Axel, these chemicals constitute for the largest gene family in humans with approximately four hundred genes [10].  Most ORs are not exclusively expressed or located in the olfactory sensory neurons, however. They have been found in all other human tissues tested to date, yet they’re poorly understood [11].  ORs are highly expressed in different cancer tissues and thus, has been found to possibly be conceivable when it comes to treating specific types of cancer [11]. 

ORs being nerve cells are most often directly connected to the brain.  The olfactory system simply works by scent molecules being detected and recognized by ORs embedded in the ciliary membrane.   

Odour recognition firstly involves the binding of odorant molecules to ORs, where once bound, a biochemical chain reaction occurs in the OR cell, which results in a shift of the cell’s electrical charge [12].  This shift causes the cell to set off electrical impulses that are sent to the brain along axons from the olfactory epithelium, the primary region in which signals are successfully processed at neurological level [13].  When this process reaches a critical level, the receptor cells send more signals to the olfactory bulb (OB), which is the part of the brain that processes odour information [14,15].  The OB is situated in the forebrain and relays the olfactory stimuli to transmit them to the olfactory cortex, where the conscious awareness of a smell takes place, and to the limbic system, which is the part of the brain heavily involved with memory and emotion [11,16-19].  


Colorectal is one of the most pertinent types of cancer amongst humanity.  With approximately 1.8 million cases in 2018 alone, according to the WHO, this cancer causes much burden and pain for patients.  The symptoms can range from rectal bleeding, to change in bowel habits and anaemia [20].  Colorectal cancer affects the digestive system, and depending on where the primary tumour originated, it can be referred to as bowel cancer, colon cancer, or rectal cancer.  This form of cancer typically spreads via the bloodstream and the lymph nodes to other parts of the body, particularly the liver, lungs and the peritoneum, and sometimes even bones, as metastatic or stage IV colorectal cancer.  Generally, colorectal cancers have been found to be relatively slow growing however they are still very aggressive. 

Colorectal cancer develops through multistage processes, involving accumulation of genetic, epigenetic and environmental factors and alterations [21].  In many cases, colorectal cancer is linked with physical inactivity, excess body weight, and the overconsumption of energy, which is especially prominent in Western countries [22]. 

In recent years, the investigation on how olfactory receptors are linked to the pathogenesis of colorectal cancer has increased, but it is still very scarce and not in depth.  Due to the very diverse nature of many ORs, it appears that many have different and versatile functions. Sailem et al. most recently used AI to find that specific ORs being “turned on” can cause worse colon cancer outcomes [23]. Li et al. found that OR1D2, OR4F15 and OR1A1 also disrupted colorectal cancer cases [24]. Xu et. Al also found that OR8D2 acts as a predictor of recurrence risk and prognosis for colon cancer patients [25].  Some ORs seem to have been slightly more researched than others with their involvement in colorectal cancer, one of them being 0R51B4. 

OR51B4 is found to be highly expressed primarily in the colon cancer cell line HCT116, and in native human colon cancer tissues.  Weber et al. Found that by stimulating the OR with its ligand, Troenan, cell proliferation and growth were inhibited as well as inducing apoptosis, cell death [26].  Lee et al. seems to further agree and find that the regulation of OR51B4 via Troenan can inhibit cancer in the cells thus may be able to be a possible novel target for colon cancer [27]. As colon cancer is accessible from the lumen, the rectal or oral ingestion of Troenan could be plausible to use for a potential treatment. 

OR7C1 is another example of a more commonly studied OR in the involvement of colorectal cancer.  It has been found to play a crucial role in the physiology of cancer, initiating cells in the colon as an increased expression of OR7C1 correlates to a higher tumorigenicity [28]. In addition, immunohistochemical staining revealed that OR7C1 high expression was correlated with poorer prognosis in CRC patients, thus could also be a viable target for treating colon cancer [29]. 


Olfactory receptors, their involvement, and their potential to act as targets for treating colon/colorectal cancer, more so than many other types of cancer, seems to be promising as being efficacious.  Nevertheless, whether humans would be able to find a way to consciously recognise the scent of specific cancer directly is heavily questionable.  ORs have very little research to back up any statements and prospects, particularly to administer clinically as of yet, thus it would need much heavier investigation. 


[1] Williams, H., & Pembroke, A. (1989). Sniffer dogs in the melanoma clinic?. The Lancet, 333(8640), 734. 

[2] Ehmann, R., Boedeker, E., Friedrich, U., Sagert, J., Dippon, J., Friedel, G., & Walles, T. (2012). Canine scent detection in the diagnosis of lung cancer: revisiting a puzzling phenomenon. European respiratory journal, 39(3), 669-676. 

[3] Bushdid, C., Magnasco, M. O., Vosshall, L. B., & Keller, A. (2014). Humans can discriminate more than 1 trillion olfactory stimuli. Science, 343(6177), 1370-1372. 

[4] Shepherd, G. M. (2004). The human sense of smell: are we better than we think?. PLoS Biol, 2(5), e146. 

[5] Siegel, R. L., Miller, K. D., & Jemal, A. (2016). Cancer statistics, 2016. CA: a cancer journal for clinicians, 66(1), 7-30. 

[6] Blackadar C. B. (2016). Historical review of the causes of cancer. World journal of clinical oncology, 7(1), 54–86. 

[7] Coyle Y. M. (2009). Lifestyle, genes, and cancer. Methods in molecular biology (Clifton, N.J.), 472, 25–56. 

[8] Hassanpour, S. H., & Dehghani, M. (2017). Review of cancer from perspective of molecular. Journal of Cancer Research and Practice, 4(4), 127-129. 

[9] Loeb, K. R., & Loeb, L. A. (2000). Significance of multiple mutations in cancer. Carcinogenesis, 21(3), 379–385. 

[10] Buck, L., & Axel, R. (1991). A novel multigene family may encode odorant receptors: a molecular basis for odor recognition. Cell, 65(1), 175–187. 

[11] Maßberg, D., & Hatt, H. (2018). Human olfactory receptors: novel cellular functions outside of the nose. Physiological reviews, 98(3), 1739-1763. 

[12] Malnic, B., Gonzalez-Kristeller, D. C., & Gutiyama, L. M. (2010). Odorant receptors. The neurobiology of olfaction, 181-202. 

[13] Sharma, A., Kumar, R., Aier, I., Semwal, R., Tyagi, P., & Varadwaj, P. (2019). Sense of Smell: Structural, Functional, Mechanistic Advancements and Challenges in Human Olfactory Research. Current neuropharmacology, 17(9), 891–911. 

[14] DeMaria, S., & Ngai, J. (2010). The cell biology of smell. The Journal of cell biology, 191(3), 443–452. 

[15] Su, C. Y., Menuz, K., & Carlson, J. R. (2009). Olfactory perception: receptors, cells, and circuits. Cell, 139(1), 45–59. 

[16] Hatt, H. (2004). Molecular and cellular basis of human olfaction. Chemistry & biodiversity, 1(12), 1857-1869. 

[17] Antunes, G., & Simoes de Souza, F. M. (2016). Olfactory receptor signaling. Methods in cell biology, 132, 127–145. 

[18] Lodovichi, C., & Belluscio, L. (2012). Odorant receptors in the formation of the olfactory bulb circuitry. Physiology (Bethesda, Md.), 27(4), 200–212. 

[19] Strotmann J. (2001). Targeting of olfactory neurons. Cellular and molecular life sciences : CMLS, 58(4), 531–537. 

[20] Schlussel, A. T., Gagliano, R. A., Jr, Seto-Donlon, S., Eggerding, F., Donlon, T., Berenberg, J., & Lynch, H. T. (2014). The evolution of colorectal cancer genetics-Part 1: from discovery to practice. Journal of gastrointestinal oncology, 5(5), 326–335. 

[21] Femia, A. P., Luceri, C., Toti, S., Giannini, A., Dolara, P., & Caderni, G. (2010). Gene expression profile and genomic alterations in colonic tumours induced by 1, 2-dimethylhydrazine (DMH) in rats. Bmc Cancer, 10(1), 194. 

[22] Giovannucci E. (2002). Modifiable risk factors for colon cancer. Gastroenterology clinics of North America, 31(4), 925–943. 

[23] Sailem, H. Z., Rittscher, J., & Pelkmans, L. (2020). KCML: a machine‐learning framework for inference of multi‐scale gene functions from genetic perturbation screens. Molecular systems biology, 16(3), e9083. 

[24] Li, Z., Yu, D., Gan, M., Shan, Q., Yin, X., Tang, S., Zhang, S., Shi, Y., Zhu, Y., Lai, M., & Zhang, D. (2015). A genome-wide assessment of rare copy number variants in colorectal cancer. Oncotarget, 6(28), 26411–26423. 

[25] Xu, G., Zhang, M., Zhu, H., & Xu, J. (2017). A 15-gene signature for prediction of colon cancer recurrence and prognosis based on SVM. Gene, 604, 33-40. 

[26] Weber, L., Al-Refae, K., Ebbert, J., Jägers, P., Altmüller, J., Becker, C., Hahn, S., Gisselmann, G., & Hatt, H. (2017). Activation of odorant receptor in colorectal cancer cells leads to inhibition of cell proliferation and apoptosis. PloS one, 12(3), e0172491. 

[27] Lee, S. J., Depoortere, I., & Hatt, H. (2019). Therapeutic potential of ectopic olfactory and taste receptors. Nature Reviews Drug Discovery, 18(2), 116-138. 

[28] Maßberg, D., & Hatt, H. (2018). Human olfactory receptors: novel cellular functions outside of the nose. Physiological reviews, 98(3), 1739-1763. 

[29] Morita, R., Hirohashi, Y., Torigoe, T., Ito-Inoda, S., Takahashi, A., Mariya, T., … & Kubo, T. (2016). Olfactory receptor family 7 subfamily C member 1 is a novel marker of colon cancer–initiating cells and is a potent target of immunotherapy. Clinical Cancer Research, 22(13), 3298-3309. 

[30]Penttila, N. (2019, September 19). The Senses: Smell and Taste. Retrieved August 07, 2020, from

Health and Disease

What is Antibiotic Resistance?

Antibiotics are medicines that fight infections in human beings and animals. They work by killing the bacteria or by making it difficult for bacteria to multiply and grow. Antibiotic medicines have revolutionized drugs and influence our everyday life, as they are used in a wide range of places. They are used to promote growth in farms, to protect building materials from contamination, or to treat growth issues in orchards. Although they have a multitude of uses, overuse threatens their effective nature due to the existence of antibiotic resistant bacteria. Dealing with resistance bacterium is not easy, but there are many ways to prevent antibiotic resistance.

Bacteria that resides in organisms may alter over time. They reproduce and unfold quickly and efficiently, and can adapt to their environment and change in ways that promote their survival. Once confronted with an antibiotic that hinders their ability to breed, genetic changes (mutations) will occur that allow the bug to thrive. 

Tests can be performed to confirm that bacteria is resistant and cannot be killed by an antibiotic. However, diagnostic tests can take days or weeks to produce results as sometimes several of the tests need the bacteria to grow over a set period of time before it will be known.

A provider could use another antibiotic that may fight the infection. However, it can have an array of drawbacks. There could be multiple side effects such as feelings of drowsiness and nausea. Also, there is a risk of promoting a new resistance. In many cases, the supplier won’t have another choice of an antibiotic. So, to prevent a situation like this, there are several measures one can take to maintain good health. Preventing overuse is a major method and the following info will clearly establish why that’s the case. 

Appropriate use of antibiotics is important to prevent drug-resistant microorganism infections and to stop any microorganism resistance from rising. One should solely take antibiotics as they are required and should not take more than prescribed in order to prevent antibiotic resistance. Antibiotic resistance happens once the bacteria is able to resist the strength of an antibiotic. In other words, the bacteria will not be killed/ fail to be killed and still grow and multiply. Antibiotic overuse and overprescribing can be attributed to clinicians prescribing antibiotics before taking a look at lab results to make sure there is a microorganism infection present. Also, patient pressure to receive an antibiotic from their supplier is another significant issue. It has been said that patients who believe they need antibiotics and consume them by purchasing them online or in another country can easily develop antibiotic resistance. Self-diagnosing a sickness could be a major part of developing antibiotic resistance. It is never a good idea to use or share left over antibiotics. There are many ways to stop resistance and these methods are quite easy to follow and abide by. 

Primarily, always follow the directions given by your doctor and do not stop taking them as prescribed even if you are feeling better. If you stop taking them accordingly, some bacteria could survive and re-infect you. Do not save your antibiotics for later or share them with others. Also, Never try and take antibiotics prescribed for somebody else. This might delay the most effective treatment for you, cause you to even sicker, or cause other uncomfortable side effects. Not all infections  can be cured by antibiotics. Work together with your provider to make sure you’re obtaining the proper antibiotic, at the proper quantity, for the right amount of time. Do not demand antibiotics if your provider says they’re unnecessary. Overall, stop infections by frequently washing hands, making proper food with good hygiene in mind, avoiding shut contact with sick folks, and keeping track of yearly vaccinations. 

While there are some new antibiotics in development, none of them are expected to be effective against the most dangerous types of antibiotic-resistant bacteria. Antibiotics do not seem to be effective against contagious agent infections like respiratory infections or contagious diseases like the stomach flu. Abuse of antibiotics after they don’t seem to be required contributes to antibiotic resistance and unwanted facet effects. Many have been led to believe that antibiotics will be a fast fix to any illness, however that is certainly not the case.

In recent years, antibiotics have become less effective and therefore the increase in antibiotic resistance has skyrocketed. It is conjointly vital to notice that the number of staple antibiotics being discovered is decreasing. This poses a danger wherever antibiotics that have seemingly been exhausted by infections are currently troubled to combat waves of resistant bacteria. The  message here is to take care of oneself and follow your providers instructions accordingly. Antibiotics should be taken fully and should be finished even if you feel better. Antibiotics must not be taken if you’re simply feeling under the weather and need to accelerate the recovery. If you remain responsible and aware, you will not fall victim to the effects of antibiotic resistance.

Works Cited

“Antibiotic / Antimicrobial Resistance.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 20 July 2020,

“Stock Photo.” 123RF Stock Photos,

Health and Disease

How Pesticides Increase the Transmission Rate of Schistosomiasis 

Both pesticides and fertilizers have had their dark history of harming the environment, yet it is still commonplace today.  The continuous usage of agrochemicals carries far more unintended consequences than we expected.  Recent discoveries from the University of California, Berkeley research team has revealed that the rising water developmental projects such as dams have allowed a rise in the freshwater snail population, while dispersing its predators which are necessary for keeping its numbers in check.  In addition, agrochemicals we utilize today are polluting the environment, therefore increasing our exposure and vulnerability to infectious diseases, particularly schistosomiasis.  

What is Schistosomiasis?

Schistosomiasis, known as bilharzia or snail fever, derives from parasitic worms (In this case, Schistosoma haematobium) in tropical and subtropical freshwater environments.  This disease earned the moniker “snail fever” due to the schistosome parasites’ use of snails as their hosts.  As a result, the freshwater becomes contaminated, when humans make contact with these waters parasites burrow into their bodies.  The worms travel through the bloodstream to vital organs such as the liver, kidney, and intestines.  Meanwhile, females lay their eggs which are passed through human urine and feces.  If these excretions reach freshwater sources, they will repeat the process to inhabit snails and grow before infecting another human. Without this trend, the parasitic eggs remain in the body and are attacked by the immune system.  There are different symptoms as they pertain to the infected area.  For example, one might experience seizures, headaches, and loss of balance if their nervous system is infected.  If not treated properly, short-term or acute schistosomiasis can lead to long-term or chronic schistosomiasis.  In this state, females will continue to reproduce and infected organs can be critically damaged.  


Researchers have found that the utilization of agrochemicals has accelerated the transmission process of schistosomiasis.  Some effects of agrochemical pollution include eliminating snail predators, increasing algae which are a main food source for the snails, as well as impacting the schistosome parasites’ survival directly.  The insecticides, chlorpyrifos, and profenofos are toxic to the predators that hunt these snails which allows the freshwater snail population to increase dramatically, activating a top-down trophic cascade.  Atrazine, an agricultural herbicide, was discovered to indirectly aid the growth of the algae which these snails consume, causing a bottom-up trophic cascade.  The snail population expanded, allowing more snails to serve as intermediate hosts for the parasites. Sub-Saharan Africa, where over 90% of schistosomiasis cases originate, has been exponentially increasing its application of agrochemicals in hopes for efficient and less arduous methods of farming.  With an ever-increasing freshwater snail population, the waterborne parasite population grows as well, resulting in a rise in the human infection rate.

This diagram from The Lancet Planetary Health shows the use of different agrochemicals and their effects in relation to the study.

In addition, researchers input their data into a complex mathematical model in order to have a general form of structure for the situation.  Then, they could easily approximate the R0 (basic reproduction number) of the schistosomes.  The R0 of S haematobium was about 1.65 while in an agrochemical-free environment.  However, the R0 has increased triple the amount when affected by agrochemicals.  The model was also capable of estimating the number of DALYs (disability-adjusted life-years) lost per 100,000 people from the altered schistosomiasis.  This represents about how many years are lost due to the disease they have.  It has been approximated that there have been 142 additional DALYs lost per 100,000 people.  By discovering the effects of individual chemicals within the pesticides, the research team could estimate both the R0 and DALYs that each caused.


This isn’t the first time we’ve witnessed the ramifications of using agrochemicals.  One notable instance was the widespread usage of the insecticide, DDT, which leaked into waterways, poisoning fish and other aquatic life.  When bald eagles consumed these toxic fish, they lost the ability to produce sturdy eggshells for their offspring.  As a result, the eggs often did not survive due to its lackluster protection which led to a massive decline in the bald eagle population.  

There are countless chemical compounds used in pesticides, all harboring dangerous side effects that can greatly impact the ecosystem.  Justin Remais, a leading figure in UC Berkeley’s School of Public Health, explains that reducing agrochemical pollution will not only reduce risk of schistosomiasis, but other infectious diseases as well.  Now that we know agrochemicals cause both unwanted direct and indirect effects, it is especially crucial that we find alternative methods to lower the risk of transmission by eliminating agrochemical pollution in regions where schistosomiasis is endemic.  


  • Effects of agrochemical pollution on schistosomiasis transmission: a systematic review and modelling analysis,The Lancet Planetary Health, July 2020

  • “Schistosomiasis”, World Health Organization, March 2020,where%20the%20females%20release%20eggs.

  • “Pesticide use can speed the transmission of schistosomiasis”, News Medical Life Sciences, July 2020

  • “Schistosomiasis (bilharzia)”, National Health Service, November 2018

Health and Disease

Parry-Romberg: The Face Deflating Disease


Parry-Romberg syndrome is an incredibly rare disorder characterized by the slow, progressive deterioration of the skin and soft tissues of half of the face (hemifacial atrophy) and, in very rare cases, the entire face. In some cases, Parry-Romberg will not only affect the face of a patient but certain limbs as well. Neurological abnormalities, or abnormalities with the subject’s teeth and/or eyes, are other side effects from Parry-Romberg syndrome. Though it can affect males, Parry-Romberg is more common in females. The severity of symptoms in people varies greatly from patient to patient. Currently, the cause of Parry-Romberg syndrome is unknown and seems to appear sporadically in patients.

Symptoms and Diagnosis:

Parry-Romberg is extremely rare and seemingly affects 1 in 250,000 people. The syndrome is usually diagnosed early in life between the ages of 5 and 15. It is much more common for people to have mild cases of Parry-Romberg rather than severe cases. The defining symptom of Parry-Romberg syndrome is the atrophy of various tissues on the whole or half of someone’s face. The progression of the facial atrophy usually lasts from 2 to 10 years, then the process usually enters a phase of stability. Though, due to the shrinkage of fat, skin, connective tissues, and muscle on the face, the subject develops asymmetry, with one half of their face appearing to be “sunken in.” When the disease surrounds the eye, problems with the retina and optic nerve may occur. Frequently, the facial atrophy progresses slowly for several years before stopping. In extremely rare cases, the atrophy will resume later in life. In other cases, the atrophy progressed indefinitely. Cases in which the Parry-Romberg syndrome started earlier in life had the atrophy accelerate faster than those who had it later.

In terms of the progression of Parry-Romberg, the shrinkage usually starts in the middle portion of the face with the cheeks and upper jaw area or between the nose and the upper corner of the lip. The disease then usually affects the upper part of the face (eye, eyebrow, and ear area) as well as the lower jaw bone and sometimes the chin. Individuals may exhibit an unusually bony or hollow appearance in the forehead, the bony cavity that accommodates the eye, and/or the lower jawbone. Some cases even develop a distinct line down the center of their face where the unharmed portion meets the portion going through atrophy. The abnormal skin on half the face is thickened and hardened (sclerosis). This condition is referred to as linear scleroderma “en coup de sabre” or LSCS. LSCS does not always accompany Parry-Romberg and can occur by itself. According to the medical literature, LSCS is either a separate disorder that commonly overlaps with Parry-Romberg syndrome or essentially the same disorder. Though the relationship between LSCS and Parry-Romberg is not fully understood, the two do frequently co-exist with about one third of people with Parry-Romberg also having LSCS.

Another area that Parry-Romberg does sometimes affect is the ear area. Some people’s ears become small, misshapen, and/or protrude abnormally due to the shrinkage of supporting tissue. In about 20% of cases, limbs such as the arms, and legs of a patient go through the same atrophy as the face. Usually this happens on the same side of the body that the facial atrophy happens on, but in some cases it has happened on the opposite side. Additionally, subjects with Parry-Romberg syndrome develop bald patches, lose eyelashes, lose the middle section of their eyebrow, and/or develop white hair on the affected side of their face. As said before, Parry-Romberg has been known to lead to abnormalities in the mouth and teeth of some people as well. Subjects have also been known to develop dermatological abnormalities such as hyperpigmentation and vitiligo. These lead to abnormal darkening or skin fading, and/or white patches on those affected with Parry-Romberg. Lastly, Parry-Romberg can affect the eyes with the loss of tissue creating a sunken in look in the eye area. Additional ocular symptoms include displacement of the eyeball farther back in the eye socket, drooping of the upper eyelid, different colored eyes, and difficulty closing the eye.

Neurological side effects in some cases of Parry-Romberg are migraine headaches that are more sensitive and prolonged than those seen in the normal person. About 10% of subjects with Parry-Romberg experience epiliptic seizures, which are characterized by jerky movements on the side of the body not affected by hemifacial atrophy. Additional neurological symptoms include abnormal sensations (e.g., prickling or burning sensations called paresthesia) in the facial area and/or episodes of severe pain in the facial areas. Jaw spasms sometimes occur in Parry-Romberg syndrome, usually on the same side as the hemiatrophy. In some cases, people experience weakness on the side of the body opposite the hemiatrophy.


The cause of Parry-Romberg syndrome is unknown and believed to happen sporadically, though there are multiple theories on what starts it. Some of the theories include viral or bacterial infections, autoimmune diseases, nervous system abnormalities, inflammation of the brain or meninges (lining of the skull), and physical trauma. Scientists do not believe it is genetic due to the fact that it is extremely rare for someone with Parry-Romberg to have a relative with the same condition.

In recent years, studies have highlighted the possibility of the “somatic mutation” of genes causing the disease. Somatic mutations are genetic problems that occur after the sperm has fertilized the egg, but when the developing human being is still a “ball of cells.” At this stage, one of the cells can develop a spontaneous genetic mutation, which can cause problems later on. It is not known if this is the cause of Parry-Romberg, but it is a hypothesis.


There is no treatment or cure to stop Parry-Romberg syndrome. Surgery may help repair tissue, but it cannot stop the disease altogether. Even then, people are generally advised to wait until after the atrophy has ceased or reached a stable period to receive the surgery. Unfortunately for some, this can take up to 10 years. Muscle or bone grafts have also been known to help people with Parry-Romberg.


Parry-Romberg is a fascinating, rare disease that causes atrophy in different parts of someone’s face and body. It affects mostly women, and can have a slew of side effects that target not only the physical body but also the brain. The cause of Parry-Romberg is unknown, and although there are no known treatments to cure Parry-Romberg, there are various institutions dedicating time and effort to understanding this rare disease. The hope is that sometime in the future, people will no longer have to suffer from what is known as the face deflating disease.


“Parry Romberg Syndrome.”, National Association for Rare  Diseases, Accessed 21 July 2020. 

“Parry-Romberg Syndrome Information Page.”, National Institute of  Neurological Disorders and Stroke, 27 Mar. 2019, Disorders/All-Disorders/Parry-Romberg-information-page. Accessed 21 July 2020. 
“Symptoms & Causes of Parry-Romberg Syndrome.”, Boston  Children’s Hospital, conditions/p/parry-romberg-syndrome/symptoms-and-causes. Accessed 21 July 2020.

Health and Disease

Nystagmus: Types, Causes, and Treatments

Nystagmus is an involuntary shaking of the eye, or both eyes, similar to a twitch. They can move in different directions: vertical, horizontal, and in circular motions. Typically, nystagmus is a sign of another underlying eye or neurological condition. If someone has nystagmus, it can be picked up using special equipment and tests, one being the caloric reflex. The caloric reflex test is when a doctor, or nurse, gently runs either hot or cold water, or air, down one ear canal. If the patient has nystagmus, this test will stimulate it because of the temperature gradient.

One cause of nystagmus is an inner ear infection. Infections, such as labyrinthitis and vestibular neuritis, are known to cause nystagmus due to the eye attempting to compensate for the lack of balance. This is a similar effect as travel sickness; if the fluid in the ear is unstable due to an infection, you will feel as if you are constantly in motion, and the eyes and ears will be receiving different sensory messages. The eyes then overwork to attempt to regain equilibrium and balance, causing nystagmus. This particular type of nystagmus should resolve itself once the inner ear infection has been fought off. To diagnose this nystagmus, an ophthalmologist may get you to follow their finger up and down and side to side to check which direction triggers the shuddering of the eye.

Another type of nystagmus can be brought on by conditions such as albinism and develop in infants aged 2-3 months. This nystagmus, due to ocular albinism, is more common in male babies and early signs of it may include them tilting or “bobbing” their head to get a clearer vision. Other symptoms of albinism, which are likely to coincide with the nystagmus, are a lack of pigmentation in the iris and abnormal connection between the nerves on the retina and the brain. Treatment for ocular albinism includes glasses, which can improve vision greatly, as well as sun shields and rimmed headgear to reduce the effects of light sensitivity related to albinism.

One of the most common causes of nystagmus is a neurological condition, usually present since birth. Some conditions which can cause nystagmus include multiple sclerosis, Meniere’s disease, and strokes. Nystagmus due to multiple sclerosis is most often a result of the disease-causing damage to the cerebellum and affecting muscles, vision, and balance. In addition, certain medications for epilepsy can cause nystagmus due to how they interact with the brain. To diagnose what the root cause of the nystagmus is, a neurologist or ophthalmologist may suggest for you to get a CT scan or MRI of the brain to rule out any more sinister causes.

Being diagnosed with nystagmus can impact individuals’ lives. Not only could nystagmus be the first indicator of a more invasive disease, but it can also cause a decline in eyesight and make it uncomfortable to do normal things. Many people that suffer from nystagmus say that it is an unpleasant feeling and twitching can strain the muscles in the eye. Getting a thorough consultation with an ophthalmologist is the first step in improving your nystagmus related symptoms; they can consider whether you need glasses or other methods to control the symptoms.

A lot of sufferers, especially teenagers, may feel quite self-conscious about their nystagmus due to it being visible to other people. Stress and fatigue can also exacerbate nystagmus so sufferers must try to stay away from tense environments and keep good sleep hygiene. Anyone with nystagmus must remember that it is not anything to be embarrassed about or hide, it is involuntary and nothing to be ashamed of. Sufferers need to speak to their medical team to get more support with their condition and to ensure it is monitored for any signs of regression or progress.


“Labyrinthitis and Vestibular Neuritis.” NHS , NHS, 11 Feb. 2020,

“Nystagmus.” American Optometric Association, American Optometric Association,,What%20causes%20nystagmus%3F,stroke%2C%20multiple%20sclerosis%20or%20trauma.

“Nystagmus.” American Optometric Association,,or%20in%20a%20circular%20pattern.

Wachler, Brian S. Boxer. “Nystagmus: Symptoms, Causes, Diagnosis, Treatment.” WebMD, WebMD, 7 Nov. 2019,

Health and Disease

MicroRNA-146a: A Potential Target for Treating Neurological Disease


Neurological diseases, though having significant impact on individuals, thoroughly lack in knowledge and insight of epidemiology due to their complex nature. As of current research, neurological diseases are classified as the gradual functional deterioration and loss of neurons.  Various neurological diseases have been recognised to have mutual aspects such as pathological nature, nervous mechanisms but also inflammatory responses in the nervous system.  MicroRNAs (MiRNAs) are small non-coding RNAs that regulate the expression of most of the genes in humans.  MiRNAs have been discovered to hold significant roles, many known and yet to find, in the pathogenesis of many diseases and conditions.  This review depicts the potential for MicroRNAs, more specifically, MiRNA-146a as a potential target and biomarker for the treatment of neurological diseases, focusing on its involvement within Alzheimer’s disease (AD) in particular.


Initially identified in 1993 under the lab of Victor Ambrose, the discovery of MicroRNAs (MiRNAs) has paved the way for many possibilities and prospective insights to combating diseases and conditions; some having been looked into, and others completely unexplored [1].  MiRNAs are 21- to 23-oligonucleotide non-coding RNAs processed from longer transcripts, which regulate gene expression in most human genes.  Conserved in many species alike, MiRNAs have widespread, conserved targets, and at some point, in development most genes have been regulated by these MiRNAs, providing a possibility of efficacy for treating diseases [2]. 

MiRNAs act through inhibition of protein expression of messenger RNA (mRNA) at post-transcription level within Argonaute proteins in order to regulate gene expression [3].  It is critical for many biological processes and animal development for MiRNAs to be expressed at a normal rate as dysregulated MiRNAs have been associated with multiple diseases [4].  A number of MiRNAs have been found to function for biologically diverse processes including that of cell death, neuronal patterning, immunity, and cell proliferation, just to state a few [5,6].  They can be secreted by living neurons and other cells within the CNS into extracellular vesicles (EVs) packaged in microvesicles, lipoprotein complexes and exosomes, thus carves the way for many neurological diseases to be linked to aberrant MiRNA expression and distribution [4, 7]. 

Amongst recent literature on potential targets for the treatment of diseases, MiRNAs are one of the most extensively characterized, yet heavily require more experimental confirmation [6].  As MiRNAs are a potential novel class of therapeutic targets, advances in research, particularly in its involvement within central nervous system (CNS) disease, would be beneficial, due to the CNS being the least accessible of all tissues [4]. 

A plethora of MiRNAs have been identified as having significant roles within processes in neurological diseases, and with the growing collection of literature on MicroRNAs, MiRNA-146a is often highlighted in its involvement with neurological diseases [8]. 


MiRNA-146a is a small, non-coding, regulatory RNA that pertains to crucial roles in physiological and pathophysiological processes such as negatively regulating antiviral pathways, immune, and neuroinflammatory responses [5].  It is one of the most abundant MiRNAs that can be expressed in the CNS, and its polymorphisms are found to be closely associated to a majority of major neurological disorders not limited to but including: neuro autoimmune diseases, neurodegenerative diseases, neurological tumours, CNS trauma and cerebrovascular diseases [8].  These neurological diseases share nerve cellular mechanisms within pathogenesis, and are complicated processes from the limited knowledge that is currently available, thus cannot be treated or cured as of yet.  MiRNA-146a is important in the development of these diseases as it has been shown, at post transcriptional level, to act via the inhibition of target genes such as: IRAK1, IRAK2, IRF-5, PTC1, RIG-I, STAT-1, TRAF6, and Numb [9, 10]. 

MiRNA-146a and its polymorphisms are not distributed by random; its particular sequences are carefully arranged to occupy very specific cellular microenvironments.  Some of the miRNAs are expressed at higher levels in the exosomes than in the cells [7].  Two of the most important single-nucleotide polymorphisms (SNPs) in MiR-146a: rs2910164, and rs57095329, have been shown to influence the level of mature MiR-146a and are associated with the onset of several major neurological diseases, such as Alzheimer’s disease (AD), ischemic stroke (IS), epilepsy, and multiple sclerosis (MS) [8].  In animal models, it has been demonstrated that it is possible to improve and, in some cases, reverse neurological diseases and even tumours present on the brain and the central nervous system by restoring a normal level of MiRNAs and its polymorphisms [5].  For example, Giraldez et al. Discovered that zebrafish without MiRNA had problems with development of the brain, Chen et al. found that MiRNA-146a can protect the brain against cognitive decline in mice, Liu et al. Showed that treatment by restoring MiRNA-146a levels improves neurological and nerve function [11-13]. 

Polymorphisms of MiRNA-146a have possible clinical relevance and implication in pharmacogenetics [9]. As it is an upcoming, potential therapeutic target, its genetic polymorphisms would be critical in diagnosis and interindividual variation in drug response, as detecting underlying molecular responses and genetic environment can be detected earlier on, thus can prevent the onset of neurological diseases [14].  This epigenetic regulation of MiRNA-146 could justify why different patients respond differently to the same treatments, and as the brain and central nervous system are all so delicate and sensitive, further understanding how this gene works could be the answer to tailoring therapeutics and targets for treating neurological diseases [15]. 


Originally described by Alois Alzheimer in 1906 as “a peculiar severe disease process of the cerebral cortex”, Alzheimer’s disease (AD) is currently the most common cause of dementia in the elderly [16-18].  This neurodegenerative disorder is clinically defined as a progressive cognitive impairment including impaired cognition and judgement and in severe cases, psycho behavioural disturbances such as psychosis [19].  Disorders like AD are considered multifactorial, as they are currently recognised to emerge due to genetic programming and environmental influences but primary causes are still unknown.  Neurodegeneration in AD most often goes unknown until severe and is estimated to start 20-30 years before clinical diagnosis, and the time from diagnosis to death is typically ~8 years [19,20].  This underlines why it would be crucial to find prospective targets and genes that could be used for early diagnosis or the treatment for AD. 

AD is characterised by neuronal loss, the accumulation of senile plaques composed of β-amyloid proteins, neurofibrillary tangles (NFTs) and the activation of microglia and glia [21, 22].  These damaged and lost neurons, senile plaques and NFTs can ultimately pave way for the appearance of activated microglia [21].  These microglia, both in animal models and human brains, generate β-Amyloid, a pro-inflammatory agent, providing stimuli for neuroinflammation, inducing the activation of glia and many inflammatory components [22].  Though this just represents the very ‘tip of the iceberg’ of how AD can affect the brain, an understanding of this disease is critical in coming up with prevention and ways to combat AD before the damage to the nervous system becomes irreversible [23]. 

Inflammation clearly plays a critical role in the pathology of Alzheimer’s and is therefore recognised as a potential aspect to target, when it comes to treating AD.  As stated before, microglia are the major producers of inflammatory factors, clustering in the brain during the early stage of pathogenesis of AD [24].  Inflammation in the CNS can in some circumstances be beneficial however, most often it can worsen pathology and cause secondary damage [22, 25].  In a healthy adult CNS, microglia are dormant but remain a vigilant state, and only respond to infection or CNS damage in order to restore CNS homeostasis [25].   

Wenk and colleagues have studied the effects of nitric oxide flurbiprofen in reducing inflammation in the brain in rats, and although not a MiRNA, the study suggests that anti-inflammatory therapies may be effective in slowing onset of AD, which is where MiRNA-146a steps in [21]. 

MiRNA-146a is known to be an anti-inflammatory regulator that uses a negative feedback response.  In conditions that are attended by cellular stress, such as Alzheimer’s, it is expected that MiRNAs have altered expression patterns and this is the case for MiRNA-146a [26].  It is known that MiRNA-146a is heavily upregulated in the brain of AD patients and in mice [27, 28].  In AD, MiRNA-146a levels are found to increase with disease severity and be local to brain regions most affected by neuroinflammation [29].  This is probably due to the anti-inflammatory nature of MiRNA-146a trying to decrease the inflammatory response from being too harsh and initiating more damage than good to the brain. 

Cui et al. found MiRNA-146a to be increased to an average of 2.6-fold over age-matched controls in the temporal lobe of AD brains, and with increased expression correlating to increased senile plaque density, it may be assumed that this upregulation of MiRNA-146a may contribute to the progression of Alzheimer’s [30-32].  In a study by Shaik et al. this increase in MiRNA-146a can be partially eliminated by inhibiting the gene through NFκB, a protein complex that is the cause of this upregulation of MiRNA-146a [33].  The significance of this study is that it shows that there’s potential to not completely eradicate the expression of MiRNA-146a, which would be crucial as this can further lead to neurodegeneration as shown in animal models [34].  This sparks prospects into the clinical utilisation of an inhibitor targeting MiRNA-146a to slow down the progression of AD.  As shown in a study by Mai et al., targeting and restoring normal levels of MiRNA-146a can alleviate the pathological process and the neurodegeneration of AD, thus further proving it possible to use MiRNA as a target in treating Alzheimer’s [35]. 

The ideal diagnostic technique and treatment for AD would be non-invasive and that can tackle the condition before onset of severe symptoms.  As of present day, there is also no cure for AD, only drugs that relieve some AD symptoms and the diagnosis techniques include cognitive testing, neuroimaging and biomarker detection, and others, most of which only detect AD at a moderate to severe progress [15, 36].  With the further exploration of MiRNA-146a, it may be possible to use as a target for the diagnosis and treatment of Alzheimer’s as it is most commonly reported to be found abundant in cerebrospinal fluid and has demonstrated the potential pharmacological value when overexpressed [36-39]. 


The research, literature, and execution of using MicroRNAs in the pharmaceutical industry and medicine is rapidly growing, ongoing and relatively promising.  Whilst the technological and biological discoveries are encouraging, there are still many risks and obstacles to overcome before scaling up the use of MiRNAs in the real world [6].  The CNS being one of the most delicate and difficult to reach aspects in the human body, in order to treat and prevent neurological disorders, it is crucial to have a reliable resource in order to achieve this.  MiRNAs being a natural agent, may have prospects in being able to assist clinically to the treatment of these diseases like Alzheimer’s but much more study is required.  The road for the use of MiRNAs might be a long and hard road for therapeutics but MiRNA-146a could potentially be an answer to unlocking many doors for medicine, more so neurology and research in this area. 


[1] Lee, R. C.; Feinbaum, R. L.; Ambros, V. (1993). “The C. Elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14”. Cell. 75 (5): 843–854. doi:10.1016/0092-8674(93)90529-Y 

[2] Bartel D. P. (2009). MicroRNAs: target recognition and regulatory functions. Cell, 136(2), 215–233. 

[3] McGeary, S. E., Lin, K. S., Shi, C. Y., Pham, T. M., Bisaria, N., Kelley, G. M., & Bartel, D. P. (2019). The biochemical basis of microRNA targeting efficacy. Science (New York, NY), 366(6472). 

[4] Rao, P., Benito, E., & Fischer, A. (2013). MicroRNAs as biomarkers for CNS disease. Frontiers in molecular neuroscience, 6, 39. 

[5] Wahid, F., Shehzad, A., Khan, T., & Kim, Y. Y. (2010). MicroRNAs: synthesis, mechanism, function, and recent clinical trials. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1803(11), 1231-1243. 

[6] He, L., & Hannon, G. J. (2004). MicroRNAs: small RNAs with a big role in gene regulation. Nature Reviews Genetics, 5(7), 522-531. 

[7] Paschon V, Takada SH, Ikebara JM, et al. Interplay Between Exosomes, microRNAs and Toll-Like Receptors in Brain Disorders. Mol Neurobiol. 2016;53(3):2016‐2028. doi:10.1007/s12035-015-9142-1 

[8] Fan, Weihao; Liang, Chunmei; Ou, Mingqian; Zou, Ting; Sun, Furong; Zhou, Haihong; et al. (2020): MicroRNA-146a Is a Wide-Reaching Neuroinflammatory Regulator and Potential Treatment Target in Neurological Diseases. Frontiers. Collection. 

[9] Li, L., Chen, X. P., & Li, Y. J. (2010). MicroRNA‐146a and human disease. Scandinavian journal of immunology, 71(4), 227-231. 

[10] Saba, R., Sorensen, D. L., & Booth, S. A. (2014). MicroRNA-146a: a dominant, negative regulator of the innate immune response. Frontiers in immunology, 5, 578. 

[11] Giraldez, A. J., Cinalli, R. M., Glasner, M. E., Enright, A. J., Thomson, J. M., Baskerville, S., Hammond, S. M., Bartel, D. P., & Schier, A. F. (2005). MicroRNAs regulate brain morphogenesis in zebrafish. Science (New York, N.Y.), 308(5723), 833–838. 

[12] Chen L, Dong R, Lu Y, et al. MicroRNA-146a protects against cognitive decline induced by surgical trauma by suppressing hippocampal neuroinflammation in mice. Brain Behav Immun. 2019;78:188‐201. doi:10.1016/j.bbi.2019.01.020 

[13] Liu XS, Fan B, Szalad A, et al. MicroRNA-146a Mimics Reduce the Peripheral Neuropathy in Type 2 Diabetic Mice. Diabetes. 2017;66(12):3111‐3121. doi:10.2337/db16-1182 

[14] Shin, J., Kayser, S. R., & Langaee, T. Y. (2009). Pharmacogenetics: from discovery to patient care. American Journal of Health-System Pharmacy, 66(7), 625-637. 

[15] Nuzziello, Nicoletta & Ciaccia, & Liguori, Maria. (2019). Precision Medicine in Neurodegenerative Diseases: Some Promising Tips Coming from the microRNAs’ World. Cells. 9. 75. 10.3390/cells9010075. 

[16] Alzheimer, A. (1907). Über eine eigenartige Erkrankung der Hirnrinde. Allg Zeitschr f Psychiatr. u Psych. Gerichtl Med, 64, 146-148 

[17] Alzheimer, A. (1911). Uber eigenartige Krankheitsfalle des spateren Alters. &s&r. C; rs. Nrurol. 

[18] Selkoe, D. J. (2001). Alzheimer’s disease: genes, proteins, and therapy. Physiological reviews, 81(2), 741-766. 

[19] Galimberti, D., Fenoglio, C., & Scarpini, E. (2008). Inflammation in neurodegenerative disorders: friend or foe?. Current aging science, 1(1), 30-41. 

[20] Williams MM, Xiong C, Morris JC, Galvin JE (2006) Survival and mortality differences between dementia with Lewy bodies vs Alzheimer disease. Neurology 67:1935–1941. 

[21] Wenk, G.L. (2003). Neuropathologic changes in Alzheimer’s disease. The Journal of clinical psychiatry, 64 Suppl 9, 7-10 . 

[22] Jellinger K. A. (2010). Basic mechanisms of neurodegeneration: a critical update. Journal of cellular and molecular medicine, 14(3), 457–487. 

[23] Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. T. (2011). Neuropathological alterations in Alzheimer disease. Cold Spring Harbor perspectives in medicine, 1(1), a006189. 

[24] Veerhuis, R., Van Breemen, M. J., Hoozemans, J. M., Morbin, M., Ouladhadj, J., Tagliavini, F., & Eikelenboom, P. (2003). Amyloid beta plaque-associated proteins C1q and SAP enhance the Abeta1-42 peptide-induced cytokine secretion by adult human microglia in vitro. Acta neuropathologica, 105(2), 135–144. 

[25] Gaudet, A. D., Fonken, L. K., Watkins, L. R., Nelson, R. J., & Popovich, P. G. (2018). MicroRNAs: Roles in Regulating Neuroinflammation. The Neuroscientist, 24(3), 221–245. 

[26] Nelson, P. T., Wang, W. X., & Rajeev, B. W. (2008). MicroRNAs (miRNAs) in neurodegenerative diseases. Brain pathology, 18(1), 130-138. 

[27] Li, Y. Y., Cui, J., Hill, J. M., Bhattacharjee, S., Zhao, Y., & Lukiw, W. J. (2011). Increased expression of miRNA-146a in Alzheimer’s disease transgenic mouse models. Neuroscience letters, 487(1), 94-98. 

[28] Gupta, P., Bhattacharjee, S., Sharma, A. R., Sharma, G., Lee, S. S., & Chakraborty, C. (2017). miRNAs in Alzheimer disease–a therapeutic perspective. Current Alzheimer Research, 14(11), 1198-1206. 

[29] Lukiw, W. J., Dua, P., Pogue, A. I., Eicken, C., & Hill, J. M. (2011). Upregulation of micro RNA-146a (miRNA-146a), a marker for inflammatory neurodegeneration, in sporadic Creutzfeldt–Jakob disease (sCJD) and Gerstmann–Straussler–Scheinker (GSS) syndrome. Journal of Toxicology and Environmental Health, Part A, 74(22-24), 1460-1468. 

[30] Cui, J. G., Li, Y. Y., Zhao, Y., Bhattacharjee, S., & Lukiw, W. J. (2010). Differential regulation of interleukin-1 receptor-associated kinase-1 (IRAK-1) and IRAK-2 by microRNA-146a and NF-κB in stressed human astroglial cells and in Alzheimer disease. Journal of Biological Chemistry, 285(50), 38951-38960. 

[31] Ayers, Duncan & Scerri, Charles. (2018). Non-coding RNA influences in dementia. Non-coding RNA Research. 3. 10.1016/j.ncrna.2018.09.002. 

[32] Madadi, S., Schwarzenbach, H., Saidijam, M. et al. Potential microRNA-related targets in clearance pathways of amyloid-β: novel therapeutic approach for the treatment of Alzheimer’s disease. Cell Biosci9, 91 (2019). 

[33] Miya Shaik, M., Tamargo, I. A., Abubakar, M. B., Kamal, M. A., Greig, N. H., & Gan, S. H. (2018). The role of microRNAs in Alzheimer’s disease and their therapeutic potentials. Genes, 9(4), 174. 

[34] Hébert, S. S., & De Strooper, B. (2009). Alterations of the microRNA network cause neurodegenerative disease. Trends in neurosciences, 32(4), 199–206. 

[35] Mai, H., Fan, W., Wang, Y., Cai, Y., Li, X., Chen, F., Chen, X., Yang, J., Tang, P., Chen, H., Zou, T., Hong, T., Wan, C., Zhao, B., & Cui, L. (2019). Intranasal Administration of miR-146a Agomir Rescued the Pathological Process and Cognitive Impairment in an AD Mouse Model. Molecular therapy. Nucleic acids, 18, 681–695. 

[36] Swarbrick, S., Wragg, N.M., Ghosh, S., & Stolzing, A. (2019). Systematic Review of miRNA as Biomarkers in Alzheimer’s Disease. Molecular Neurobiology, 56, 6156 – 6167. 

[37] 37 Burgos, K. L., Javaherian, A., Bomprezzi, R., Ghaffari, L., Rhodes, S., Courtright, A., … & Van Keuren-Jensen, K. (2013). Identification of extracellular miRNA in human cerebrospinal fluid by next-generation sequencing. Rna, 19(5), 712-722. 

[38] Kiko, T., Nakagawa, K., Tsuduki, T., Furukawa, K., Arai, H., & Miyazawa, T. (2014). MicroRNAs in plasma and cerebrospinal fluid as potential markers for Alzheimer’s disease. Journal of Alzheimer’s Disease, 39(2), 253-259. 

[39] Cui, J. G., Li, Y. Y., Zhao, Y., Bhattacharjee, S., & Lukiw, W. J. (2010). Differential regulation of interleukin-1 receptor-associated kinase-1 (IRAK-1) and IRAK-2 by microRNA-146a and NF-κB in stressed human astroglial cells and in Alzheimer disease. Journal of Biological Chemistry, 285(50), 38951-38960. 

Health and Disease

Medical Implications and Remedy for Alzheimer’s

We all know the grave effects of Alzheimer’s disease on a person. The serious and fatal forgetfulness, along with the dissociation from the outside world and family, makes the disease the “6th leading cause of death in the United States.” Although these patients are often living at senior homes with caregivers, a place to live and someone to take care of you is not enough to combat the severity of the disease. A more innovative and common solution is in many people’s households: cinnamon. Although the research regarding the effects of cinnamon on patients with Alzheimer’s is not yet fully developed, there have been insights into what cinnamon can truly do. 

For some background information, patients with Alzheimer’s have certain proteins known as tau proteins that have mutated to form into clumps and tangles, which has been noted to be the cause of AD (Sauer). In cinnamon, there are two main compounds, cinnamaldehyde and epicatechin, which can potentially help stop the aggregation of tau proteins. 

According to a research paper conducted by the University of California Irvine, “ cinnamon extract has been reported to have positive effects in fruit fly and mouse models for Alzheimer’s disease” (Pham et al.). The experiment was conducted with 16 to 400 mM of cinnamaldehyde maintained at 25°C and 55% humidity and first generation offspring in a type of fruit flies called Drosophila melanogaster. Not only was overall memory tested, but in addition a RING assay (Rapid Iterative Negative Geotaxis assay) was “conducted to evaluate the impact of cinnamaldehyde on fly directionality and climbing ability” (Pham et al.).

The results were as followed:

The 16nM dose of cinnamaldehyde had “no significant effect on the lifespan of AD flies overexpressing Aβ42” (Pham et al.). For reference, Aβ42 is an amyloid beta peptide that is involved with Alzheimer’s disease. The 400 mM dosage “had toxic effects on the lifespans of both male and female AD flies expressing Aβ42” (Pham et al.). The sweet spot was cinnamaldehyde at 80 mM which “increased the lifespan of Alzheimer’s disease fly models that overexpress the Tau protein by 11% in males (P < 0.0001) and by 20.7% in females (P < 0.0001)” (Pham et al.). With the control tau flies, there was no reported improvement. These results prove that certain concentrations of compounds found in cinnamon have the potential to increase the lifespan of those with Alziemer’s. Although this experiment was conducted on fruit flies, this data can be further used to incorporate correct concentrations of cinnamaldehyde for humans. 

With the RING assay, “cinnamaldehyde significantly improved the climbing ability of male AD flies overexpressing Tau protein” (Tau et al.) In addition, “the compound also improved short-term memory of male AD flies overexpressing the Tau protein” (Tau et al.). 

 It is also worth noting that diabetes and Alzheimer’s have a strong connection (Sauer). Almost “70% of people with type II diabetes ultimately [develop] Alzheimer’s” (Sauer).  In one study conducted by researchers, the blood sugar levels of diabetic patients decreased by 24% with daily cinnamon intake of ½ to 2 teaspoons for 40 days. This research shows how cinnamon has the possibility to  help with Alzheimer’s, as it can also help with diabetes since these two are closely related. Through these research examples, it is without a doubt certain that cinnamon is beneficial for patients with AD. However, some scientists do speculate that “the complex neurodegenerative Alzheimer’s disease is still far from being clear” (Pham et al.). Although it is known that abnormal levels of amyloid beta causes the buildup of plaque between neurons and tangled Tau proteins causing AD, more research needs to be conducted to further prospect this novel method of solving the problems of Alzheimer’s. 

Starting young, one can easily incorporate cinnamon in his/her daily diet. Here are some ways according to Alissa Sauer of “put cinnamon in your morning coffee or tea; take cinnamon in a capsule (two 500 mg capsules are recommended); put cinnamon on your toast, cereal, or oatmeal; add cinnamon to baked or raw fruit”. If these methods are incorporated into the daily routine of people with Alziemer’s, the effects of AD can be lessened. 


Pham, Hanh, et al. “Cinnamaldehyde Improves Lifespan and Healthspan in

     Drosophila melanogaster Models for Alzheimer’s Disease.” Hindawi, Accessed 27 June 2020. 

Sauer, Alissa. “Why Cinnamon May Hold Secrets to Alzheimer’s Prevention.”, 2 July 2014,

     cinnamon-prevents-alzheimers/. Accessed 27 June 2020.