This paper conducts a thorough investigation into both congenital and acquired anosmia, incorporating in-depth analysis, patient interviews, and smell tests to understand their distinct impacts and management strategies. Two case studies—one congenital, one acquired — provide personal insights into living with anosmia. The congenital case, a lifelong condition often due to suspected genetic factors, reveals adaptations in daily routines, safety strategies, and social interactions, highlighting the ingrained coping mechanisms developed from birth. The acquired case, exemplified by a long COVID patient, illustrates the abrupt sensory loss and its profound effects on quality of life, including altered food perception, emotional distress, and changes in social roles.
Diagnostic approaches and treatments are extensively discussed. For congenital anosmia, options focus on adaptation and include emerging treatments like olfactory training and gene therapy. Diagnostic imaging such as MRI and CT scans are crucial for uncovering structural anomalies. In contrast, treatments for acquired anosmia offer potential for recovery. Olfactory training, medications, and alternative therapies are evaluated for their efficacy in restoring smell. Also, the paper alludes to a societal problem—that some people in the world lack modern testing or scanning because of inequality.
Motivated by a close friend's experience with congenital anosmia and his inability to seek medical diagnosis due to financial constraints, I am conducting a study on anosmia. I aim to uncover the underlying causes of this condition and determine if any olfactory function remains. Additionally, I am interested in the potential of developing perfumes specifically designed for individuals with anosmia. Anosmia, derived from the Greek words “an” (without) and “osme” (smell), refers to the total loss or absence of the sense of smell.[1] This olfactory disorder can be congenital or acquired later in life.[2] On a molecular level, anosmia is linked to disruptions in the development and function of the olfactory system, which depends on numerous molecular signals and pathways.[3] Genetic factors, such as mutations in specific genes, can result in structural and functional abnormalities in the olfactory system, leading to anosmia.[4] Examining the genetic basis of anosmia offers insights into the complexities of olfactory system development and the broader clinical implications of the condition. The objective of this paper is twofold:
The primary objective of this paper is to delve into the neurobiological underpinnings and enduring ramifications of anosmia precipitated by genetic determinants. Individuals afflicted with congenital anosmia, stemming from genetic anomalies, navigate life devoid of olfactory capabilities, influencing their cognitive and emotional frameworks. Concurrently, this research seeks to elucidate the etiology and neural mechanisms behind the acquired anosmia observed in recent COVID-19 cases. The sudden onset of this symptom in the context of the pandemic offers a distinctive lens to examine the adaptability and resilience of the olfactory neural pathways, further underscoring the multifaceted nature of olfactory disruptions in society.
By comparing long-term genetic anosmia with acquired anosmia, this paper seeks to offer a thorough understanding of the neural mechanisms underlying these conditions and their wider effects on an individual's neurocognitive and emotional well-being.
In the United States, anosmia afflicts 3% of the adult population older than the age of 40.[5] The prevalence of impaired olfaction increases with age. In 2016, the National Health and Nutrition Examination Survey (NHANES) measured olfactory dysfunction, which involved 1818 participants. Data showed that olfactory dysfunction was 4% at ages 40 to 49 years of age, 10% at 50 to 59, 13% at 60 to 69, 25% at 70 to 79, and 39% for those over 80 years of age. Anosmia affected 14% to 22% of those over 60 years of age. [6][7]
However, there are several epidemiological factors that have to be taken into account.
The prevalence of anosmia varies across populations. Within the scope of anosmia's racial prevalence, a distinct disparity was observed. In the USA, Blacks exhibited a prevalence of 22.3%, nearly double the 10.4% found in whites.[8] Age and gender adjustments revealed that blacks were significantly more susceptible, with older black males being the most affected. Conversely, younger white females had the lowest incidence. Several factors, including education, cognitive health, and certain genetic markers, influenced anosmia prevalence.[9] However, even after accounting for these, the racial difference remained pronounced.
The risk of developing anosmia tends to increase with age, and differs from country to country.
While it's commonly believed that women have superior olfactory abilities compared to men, a comprehensive meta-analysis of various studies suggests otherwise. Analyzing data from thousands of participants across different olfactory tests, the study found that although women might slightly outperform men in olfactory tasks, the effect sizes were notably small, ranging between g[16] = 0.08 and g = 0.30. Thus, the difference in olfactory abilities between genders is minimal and may not be significant in the context of anosmia.[17]
The olfactory system, important for our sense of smell, has several roles in our daily lives. Apart from helping us detect dangers like smoke or spoiled food, it is crucial for understanding flavors. It works with our taste system to influence what foods we like and what we eat.[18] The olfactory system is closely connected to the parts of our brain that handle emotions and memories.[19] Direct neural links connect the olfactory bulb to areas like the amygdala and hippocampus. Certain smells can trigger strong emotional reactions and vivid memories of past events.[20] Smell also plays a subtle but important role in social interactions, providing information about a person's health, emotions, and even genetic compatibility.[21]
To delve deeper into the mechanics of smell perception, as pictured in Figure 1, when an odorant molecule is airborne, it navigates through the nasal passages to the nasal cavity. Here, olfactory receptor neurons, extensions of the olfactory bulb situated atop the cribriform plate of the brain, come into play. Each nasal cavity is home to approximately 100 million receptor cells.[22] These cells boast between 500 to 1000 distinct odor-binding proteins on their surfaces.[23] Intriguingly, each olfactory receptor cell expresses a singular type of binding protein.[24] These afferent olfactory neurons, constituting cranial nerve I, are responsible for converting a chemical signal (airborne particles) into an electrical one, which is then relayed and ultimately interpreted by the brain. The olfactory bulb then processes this signal, which is further refined by various brain structures, including the piriform cortex, entorhinal cortex, amygdala, and hippocampus. Any obstruction or damage to the pathway through which the olfactory signal is relayed and processed can lead to anosmia, a loss of the sense of smell. Such impediments can arise from inflammatory conditions like simple infections that produce mucus plugs or nasal polyps.[25] Neurological factors encompass disruptions to the sensory nerves of the olfactory bulb or any segment of the pathway that transmits the olfactory signal to the brain.[26]
Figure: Human olfactory system; Illustration by Patrick J. Lynch, medical illustrator https://www.biocycle.net/odor-monitoring-and-detection-tools/
Congenital anosmia, denoting an absence of olfactory perception from birth, is an infrequent diagnosis. Notably, while 5% of the general population exhibits a complete loss of olfactory function, only 0.01% manifest this absence congenitally.[27] Congenital anosmia is in association with four conditions or diseases:
Congenital Anosmia can be caused by:
Kallmann Syndrome: Kallmann syndrome results from an isolated defect in the secretion or action of gonadotropin-releasing hormone (GnRH) and is associated with reproductive anomalies like infertility.[29] GnRH-producing neurons are situated in the hypothalamus but undergo a unique migration during embryonic life.[30] While several genes have been identified that affect this migration and the development of the GnRH neurons, the complete genetic framework of KS remains not completely understood.[31] The genes that can mutate to make someone be diagnosed with Kallman’s Syndrome are: ANOS1 (KAL1), TENM1, FGFR1, FGF8, PROK2, PROKR2, and SEMA3A.[32][33]
ANOS1, previously termed KAL1, is intimately linked with Kallmann syndrome. In fact, the earlier nomenclature, “KAL1,” draws its name directly from the syndrome.[34] The ANOS1 gene provides the instructions for producing a protein called anosmin-1. This protein plays a critical role during the embryonic development of the olfactory system and the hypothalamus, which are central to the sense of smell and the regulation of reproductive hormones, respectively.[35]
Mutations in the ANOS1 gene can lead to a deficiency or dysfunction of the anosmin-1 protein.[41] This protein plays a pivotal role in guiding the early movement of GnRH neurons (as illustrated in Figure 2). When the normal function of anosmin-1 is compromised, it can hinder the appropriate migration of the olfactory nerve axons and the gonadotropin-releasing hormone (GnRH) neurons during embryogenesis. This disturbed migration process results in the abnormal development or complete absence of the olfactory bulbs, leading to anosmia or hyposmia. Simultaneously, the affected migration of GnRH neurons can cause hypogonadotropic hypogonadism due to the reduced secretion or absence of GnRH, a pivotal hormone for triggering puberty and maintaining reproductive functions.[42]
The connection between the KAL1 (ANOS1) gene and Kallmann syndrome (KS) became apparent when researchers studied a 19-week-old male KS fetus with a full deletion of the KAL1 gene. This deletion resulted in the halted movement of the GnRH and olfactory axons' central projections at the cribriform plate, creating a complex network of neurons. Such findings indicate that KAL1 mutations can disrupt the proper movement of both olfactory and GnRH neurons, leading to a lack of smell sensation (anosmia) and Isolated Hypogonadotropic Hypogonadism (IHH).[43] While the exact function of anosmin-1 in the development of the olfactory bulb remains uncertain, it is known that anosmin-1 is present in the bulb's outer layers and interacts with cells that produce FGFR1.[44]
Figure: Schematic drawing depicting anosmin-1 (green star), FGFR1 (blue star), and GnRH (red circle) immunoreactivity in the olfactory system and rostral forebrain during human embryogenesis after 53–54 days (CS21). Red circles with blue stars at their centre represent GnRH cells that co-express FGFR1. Link
The FGFR1 gene codes for the protein fibroblast growth factor receptor 1, which belongs to a family of receptors pivotal in the transduction of cellular signals. These signals are responsible for regulating various biological processes, including cell growth, differentiation, and tissue repair.[45] The protein product of FGFR1 primarily acts as a receptor for specific molecules called fibroblast growth factors (FGFs). Upon binding to its ligand, FGFR1 activates intracellular signaling cascades, which further dictate cellular responses like proliferation or migration.[46] When mutations occur in this gene, it can impede the proper migration and development of neurons responsible for producing the gonadotropin-releasing hormone (GnRH).[47] Furthermore, it can disrupt the formation of the olfactory bulbs, which are critical for the sense of smell. Both these factors combined can manifest as the clinical features seen in KS.[48]
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Traumas, especially those targeting the cranial region, can inflict damage on the olfactory nerve or associated structures, leading to post-traumatic anosmia. The severity and permanence of the anosmia are contingent on the extent of neural damage. Olfactory dysfunction (OD) is a disorder associated with traumatic brain injury (TBI), which is prevalent in up to 20% of patients suffering from TBI. [61]
Diseases such as Alzheimer's and Parkinson's have been correlated with olfactory deficits, with anosmia often serving as an early clinical harbinger of these neurodegenerative processes.[62]
Exposures to toxic chemicals are believed to be responsible for approximately 1–5% of all olfactory dysfunctions. Given their anatomically exposed positions, both olfactory neurons and taste buds are directly exposed to environmental agents. This direct exposure renders them vulnerable to both acute and chronic toxic insults.[63]
Tumors, especially those in proximity to the olfactory structures, can impede olfactory function. For example, a 67-year-old woman reported a 2-year history of anosmia. Sinuscopic examination revealed no nasal or sinus abnormalities, and rhinomanometry confirmed normal nasal airway resistance. Despite no history of trauma, smoking, or decongestant overdose, an olfactory test indicated a complete loss of smell. A head CT scan revealed a sizable brain tumor at the anterior skull base, which was further characterized by T1-weighted MRI as a large extra-axial mass at the anterior skull base, impacting the cribriform plate.[64]
Certain pathogens, most notably the recent SARS-CoV-2, have been identified as causative agents of anosmia. The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has presented a unique and alarming symptom in a significant number of patients: anosmia, or the loss of the sense of smell. This symptom, observed in approximately 52.73% of COVID-19 patients, has raised questions about the underlying mechanisms.[65] This review delves into the potential pathways and cellular interactions that lead to anosmia in COVID-19 patients, focusing on the role of the olfactory epithelium, support cells, and the virus's interaction with the olfactory system.[66]
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Two individuals will be the focus of this study: one, 21, with congenital anosmia, and another, a 75-year-old woman, who experienced temporary anosmia due to COVID-19.
Based on Figure 3, taken from the Clinical assessment of patients with smell and taste disorders - PMC, a diagnostic algorithm will be developed by transforming the symptoms and factors listed in the figure into a series of questions. The patient with congenital anosmia will be assessed using this algorithm, and the responses will be integrated into a diagram to determine the specific type of anosmia they have and how they acquired it.
These questions provided here have already been asked to the patient based on the scheme in Figure 4. The reason they are more personalized is because the patient also answered since it’s an interview.
The University of Pennsylvania Smell Identification Test (UPSIT) is an integral tool in assessing olfactory function, particularly in anosmia research. It's recognized for its efficacy in diagnosing and determining the severity of smell disorders. The UPSIT involves a series of microencapsulated scratchable patches, each containing a different odorant. During the test, the patient scratches each patch to release the scent and then chooses the corresponding odor from a list of four options. This methodical approach ensures a comprehensive evaluation of the patient's ability to recognize and differentiate a wide array of common scents.
Figure of self-made questions scheme test. It is used to determine the type of anosmia the patient has.
Following the diagnostic algorithm, better described in Figure 4, the patient will be asked questions in a flow-chart order. In addition to this, in the scheme, a 40-element smell test was integrated from the UPSIT test, and will be performed in the experiment. This test will include Bubble Gum, Menthol, Mint, Banana, Leather, Coconut, Cinnamon, Gingerbread, Pineapple, Orange, Watermelon, Grass, Smoke, Soap, Natural Gas, Rose, Onion, Chocolate, Lilac, Peach, Root Beer, Pine, Lime, Clove, Liquorice, Gasoline, Strawberry, Peanut, Pizza, Cherry, Motor Oil, Fruit Punch, Cheddar Cheese, Cedar, Dill Pickle, Lemon, Wintergreen, Thinner, Grape, Turpentine. From all of these elements, 5 couldn’t be gathered, more specifically, Natural Gas, Liquorice, Motor Oil, Wintergreen, and Turpentine. So, a 35-element test will be performed. The manner this experiment will be performed is relatively simple. The elements will be gathered by the researcher, and then would be given to the patient to smell, but the patient will have no other senses except olfactory; meaning that the patient will be blindfolded, will not be allowed to touch, taste, or look at the elements. This test will help evaluate how anosmia impacts the patient's life, particularly in terms of flavor perception and dietary choices. A recording with the experiment can be provided at request.
The design of the UPSIT ensures that it comprehensively covers various scent categories, from fruits and spices to environmental and industrial odors. Such a broad range in the test aids in precisely assessing the extent of olfactory impairment across different odor types. The results of the UPSIT, especially in a modified form as in this study, are invaluable in quantifying the degree of smell loss and can be indicative of the underlying cause of anosmia. The outcomes from this test, in conjunction with other diagnostic measures, provide a thorough understanding of the patient’s olfactory dysfunction, guiding subsequent treatment and management approaches.
An interview will be conducted with a patient who experienced temporary anosmia due to COVID-19. The patient is a 75-year-old woman. The interview will explore the patient’s experience with long COVID and the impact of anosmia on neurocognitive and emotional well-being. Also, the same 35-elements UPSIT smell test will be performed on the patient with Acquired Anosmia, in the same manner. The questions are inspired by this report: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0256998 and they are listed down. They are more personalized because the questions have already been asked to the patient in an interview and they are a conversation with the patient.
The data collected from the algorithm-based diagnosis, UPSIT smell test, and interview will be analyzed to compare the neurobiological foundations and lifelong consequences of congenital anosmia with the acquired anosmia experienced by COVID-19 patients.
All participants will provide informed consent, and the study will adhere to ethical guidelines to ensure the privacy and well-being of the participants. (Appendix)
In the context of this study, it's pertinent to note that the subject, diagnosed with congenital anosmia, had never undergone magnetic resonance imaging (MRI) or computed tomography (CT) scanning. This is primarily attributable to the limited accessibility and affordability of these advanced imaging services in the subject's healthcare environment. Consequently, the potential presence of any underlying structural anomalies or abnormalities in the brain remains unascertained. Given this limitation, the experimental phase of the research will omit the “Olfactory testing of individual or combined nostrils and imaging of nasal cavities, olfactory bulbs, and brain with CT/MRI”.
This methodology will allow for a thorough understanding of the neural mechanisms underlying different types of anosmia and their wider effects on an individual's life, behaviors, emotions, and interactions.
The responses of the 21-year-old patient with congenital anosmia are as follows:
The fact that the patient showers twice a day and uses a lot of perfume suggests an approach to overcompensate for inability to self-monitor odors. This behavior highlights the impact of anosmia on daily life, particularly in social contexts. The fear of having an unpleasant smell and the inability to detect it themselves can lead to anxiety in social interactions, driving them to take extra measures to ensure the subject does not have an offensive odor. Thus, the patient's response illustrates how anosmia affects not just the subject’s sense of smell but also the subject’s social interactions and personal habits.
The patient's response indicates that the subject’s taste buds function normally, allowing them to experience basic tastes. What they might miss is the flavor complexity that arises from the combination of taste and olfactory cues.
There is no mention of any illness, injury, or other event that could have led to the loss of smell, which supports the classification of the anosmia as congenital rather than acquired. This absence of a causative event aligns with the earlier responses and reinforces the understanding that the patient has always been without the sense of smell. Such a realization during a routine family activity highlights how anosmia can often go unnoticed until specific situations bring the condition to light. It also underscores the importance of familial observation and engagement in the identification of sensory deficits in children.
From a research perspective, this underscores a gap in the full clinical picture of the patient's anosmia. The reliance on self-reported symptoms and history, without the support of imaging, may limit the depth of understanding of the condition's etiology and its potential neurological basis. It also highlights a broader issue within the healthcare system related to the accessibility of diagnostic resources for individuals from lower socioeconomic backgrounds.
(After the test)
The ability to identify the flavor of bubble gum after chewing it, despite the inability to smell any of the provided scents, are consistent with the functional taste perception the patient previously reported. This ability to taste, despite the absence of smell, differentiates the subject’s condition from disorders where both taste and smell are affected.
Please refer to the report for complete details of the test conducted.
The responses of the 75-year-old patient with Acquired Anosmia are as follows:
Questions, answers, and specific analysis for patient with acquired anosmia as a result from COVID-19.
For a 75-year-old, the impact of such sensory loss can be profound, affecting nutritional intake, enjoyment of food, and overall quality of life, while also posing safety concerns. The specific mention of altered smell rather than complete anosmia could be a hopeful sign for eventual, partial, or complete recovery of the sense of smell, which can sometimes occur after such viral infections.
Moreover, the inability to enjoy familiar comforts, such as the smell of one's own home or personal scent from perfumes, can be disheartening and disorienting.
The patient's laughter when mentioning the inability to smell the subject’s favorite linen laundry softener hints at a resilient attitude towards the subject’s condition. Despite the challenges posed by the loss of smell, this response may indicate an effort to maintain a positive outlook, which can be an important aspect of coping with the sudden change in the subject’s quality of life.
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The patient with congenital anosmia has never experienced the sense of smell. This lifelong absence means the subject has developed and adapted to a world without olfactory cues from the beginning. Their adaptations, like regular checks for personal odor and reliance on others for feedback, are ingrained and normalized parts of the subject’s life. The subject has never known the sensations they are missing, which shapes the subject’s relationship with food, social interactions, and safety precautions in a unique way. The congenital nature of the subject’s condition has led to a life built around the absence of smell, with strategies and support systems in place to compensate for this deficit.
In contrast, the patient with acquired anosmia due to long COVID has experienced a drastic change in the subject’s sensory world. Previously accustomed to the nuances of smell, the sudden loss has led to a significant alteration in the subject’s quality of life. This patient's anosmia has led to a decrease in appetite, weight loss, and reliance on others for taste confirmation, indicating a disruption to the subject’s previously established routines and pleasures. The impact is more pronounced because it represents a loss of an integral part of the subject’s sensory experience, affecting the subject’s enjoyment of food, social roles, and emotional well-being. The subject’s longing for the return of smell and the joy at detecting even a few scents during the UPSIT smell test reflect a deep sense of loss and hope for recovery.
This contrast highlights how the timing and nature of the onset of anosmia (congenital versus acquired) can lead to significantly different experiences and coping mechanisms. The congenital anosmia patient has a lifetime of adaptation without ever knowing the sense, while the acquired anosmia patient experiences a profound sense of loss and adjustment to a new way of sensing the world. This difference is crucial for understanding the psychological and emotional ramifications of anosmia and the support needed for individuals facing either form of this condition. ____ Please refer the report for further details ____
My name is Matei Mihai Serban, and I chose to write about Anosmia because of a dear friend of mine's struggle with it their entire life. My paper conducted a thorough investigation into both congenital and acquired anosmia, incorporating in-depth analysis, patient interviews, and smell tests to understand their distinct impacts and management strategies. Also, I wrote an in-depth review of everything Anosmia consists of. Elio's neuroscience research program was a key turning point for me. It gave me hands-on experience in neuroscience research, showing me that I have a real passion for this field. The program was challenging, but it taught me valuable skills in scientific research and critical thinking. It also confirmed my desire to keep doing research in the future and contribute to the science community. Overall, the program was a great learning experience that helped shape my career goals.
[1] “Anosmia Definition & Meaning.” Merriam-Webster, Merriam-Webster, www.merriam-webster.com/dictionary/anosmia.
[2] Cleveland Clinic medical. “Anosmia.” Cleveland Clinic, my.clevelandclinic.org/health/diseases/21859-anosmia-loss-of-sense-of-smell.
[3] Karimian, Ali, et al. “Molecular Mechanisms Involved in Anosmia Induced by SARS-COV-2, with a Focus on the Transmembrane Serine Protease TMPRSS2.” Archives of Virology, U.S. National Library of Medicine, Oct. 2022, www.ncbi.nlm.nih.gov/pmc/articles/PMC9358639/.
[4] Alkelai, Anna, et al. “Next-Generation Sequencing of Patients with Congenital Anosmia.” European Journal of Human Genetics : EJHG, U.S. National Library of Medicine, Dec. 2017, www.ncbi.nlm.nih.gov/pmc/articles/PMC5865213/.
[5] Anosmia - StatPearls - NCBI Bookshelf www.ncbi.nlm.nih.gov/books/NBK482152/.
[6] Anosmia - StatPearls - NCBI Bookshelf www.ncbi.nlm.nih.gov/books/NBK482152/.
[7] VB;, Hoffman HJ;Rawal S;Li CM;Duffy. “New Chemosensory Component in the U.S. National Health and Nutrition Examination Survey (NHANES): First-Year Results for Measured Olfactory Dysfunction.” Reviews in Endocrine & Metabolic Disorders, U.S. National Library of Medicine, pubmed.ncbi.nlm.nih.gov/27287364/.
[8] Dong, Jing, et al. “The Prevalence of Anosmia and Associated Factors among U.S. Black and White Older Adults.” The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, U.S. National Library of Medicine, 1 Aug. 2017, www.ncbi.nlm.nih.gov/pmc/articles/PMC5861899/.
[9] Dong, Jing, et al. “The Prevalence of Anosmia and Associated Factors among U.S. Black and White Older Adults.” The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, U.S. National Library of Medicine, 1 Aug. 2017, www.ncbi.nlm.nih.gov/pmc/articles/PMC5861899/.
[10] Murphy C, Schubert CR, Cruickshanks KJ, Klein BE, Klein R, Nondahl DM. Prevalence of olfactory impairment in older adults. JAMA. 2002;288:2307–2312.
[11] Schubert CR, Cruickshanks KJ, Fischer ME, et al. Olfactory impairment in an adult population: The Beaver Dam Offspring Study. Chem Senses. 2012;37:325–334. doi:10.1093/chemse/bjr102.
[12] Karpa MJ, Gopinath B, Rochtchina E, et al. Prevalence and neurodegenerative or other associations with olfactory impairment in an older community. J Aging Health. 2010;22:154–168. doi:10.1177/0898264309353066
[13] Pinto JM, Schumm LP, Wroblewski KE, Kern DW, McClintock MK. Racial disparities in olfactory loss among older adults in the United States. J Gerontol A Biol Sci Med Sci. 2014;69:323–329. doi:10.1093/gerona/glt063
[14] Landis BN, Konnerth CG, Hummel T. A study on the frequency of olfactory dysfunction. Laryngoscope. 2004;114:1764–1769. doi:10.1097/00005537-200410000-00017.
[15] Mullol J, Alobid I, Marino-Sanchez F, et al. Furthering the understanding of olfaction, prevalence of loss of smell and risk factors: A population-based survey (OLFACAT study). BMJ open. 2012;2(6).
____ Please refer the report for complete list of references ____
The research project entitled “Deep Dive in Anosmia; Case Studies of Congenital & Acquired Anosmia” supports the practice of protection of human participants in research. The following will provide you with information about the experiment that will help you in deciding whether or not you wish to participate. If you agree to participate, please be aware that you are free to withdraw at any point throughout the duration of the experiment without any penalty.
In this study I will ask you to smell 40 different scents (Bubble Gum, Menthol, Mint, Banana, Leather, Coconut, Cinnamon, Ginger bread, Pine Apple, Orange, Watermelon, Grass, Smoke, Soap, Natural Gas, Rose, Onion, Chocolate, Lilac, Peach, Root Beer, Pine, Lime, Clove, Liquorice, Gasoline, Strawberry, Peanut, Pizza, Cherry, Motor Oil, Fruit Punch, Cheddar Cheese, Cedar, Dill Pickle, Lemon, Wintergreen, Thinner, Grape, Turpentine) and try to identify them. Also, you will be asked questions about your Anosmia with the “Algorithm of evaluation of the patient who has olfactory loss” method.* If you have any discomfort with discussing Anosmia, or if any scents give you displeasure, please inform the experimenter, and the study will end now. All information you provide will remain confidential and will not be associated with your name. If, for any reason during this study, you do not feel comfortable, you may leave the laboratory and receive credit for the time you participated, and your information will be discarded. Your participation in this study will require approximately 40 minutes. When this study is complete, you will be provided with the results of the experiment if you request them, and you will be free to ask any questions. If you have any further questions concerning this study, please feel free to contact me by phone or email: Serban Matei Mihai at matei**@gmail.com (+Phone number). Please indicate with your signature in the space below that you understand your rights and agree to participate in the experiment.
Your participation is solicited, yet strictly voluntary. All information will be kept confidential, and your name will not be associated with any research findings.
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Signature of Participant NAME, Investigator
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The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of Elio Academy.