Smells Like Parkinson’s Disease




Parkinson’s disease has always been primarily seen as a movement disorder resulting in symptoms of shaking, tremors, rigidity, and trouble walking. Interestingly, however, at least 90% of patients with Parkinson’s experience either loss or decreases in the sense of smell. Studies have shown that problems with olfaction actually generally precede the onset of other motor symptoms. Most people are not personally aware of changes in their olfactory acuity, but the increasing range and prevalence of smell tests offer a quick, easy, cheap, and non-invasive diagnostic test, as well as a measure of disease progression. In addition, the shift of focus for researchers from Parkinson’s as a motor disorder to a more global neurodegenerative disorder allows consideration of new paradigms about the causes and disease progression.

The cellular basis of olfactory dysfunction in Parkinson’s remains an enigma. Post-mortem studies have confirmed shrinkage of the olfactory bulb, but this fails to shed light onto the root causes as it only demonstrates the end effect. Experimental models of Parkinson’s have demonstrated various results such as protein aggregation in the olfactory bulb, changes in levels of neurotransmitters, microglial activation, and loss of cells in the olfactory bulb. However, as all of these effects are inter-related, none of these clarify the actual initial cause of damage.
Many of the hypotheses as to why olfactory dysfunction occurs and precedes other symptoms remain grounded in the long-held paradigm of Parkinson’s as a motor disease caused by the loss of dopaminergic neurons in the substantia nigra. For example, in some experimental models an increase in dopamine was found in the olfactory bulb. The researchers suggested this occurs as a compensatory mechanism in response to the loss of dopamine in the substantia nigra. As it has also been shown that sense of smell is particularly vulnerable to changes in dopamine, excess dopamine in the olfactory bulb would, thus, lead to olfactory dysfunction.

However, a number of other theories have been proposed suggesting that perhaps the olfactory bulb is the first brain structure to exhibit signs of damage because Parkinson’s could be caused by respiratory viruses or inhaled toxins that enter the brain through the nose. The cause of Parkinson’s has not been conclusively determined. And while a genetic component has been uncovered, the causes are clearly much more complex with various environmental factors involved. A number of studies have been performed demonstrating Parkinson’s-like symptoms following exposure to viruses, heavy metals, and pesticides in experimental models. Epidemiological studies have also linked pesticides exposure to an increased risk of Parkinson’s. It is certainly an interesting hypothesis that inhaled toxins could cross the blood brain barrier, and that the damage in Parkinson’s could begin first in the olfactory bulb and then spread from there to the substantia nigra. In addition, as the olfactory bulb is heavily involved in adult neurogenesis, any damage to this structure could severely limit the brain’s ability to repair itself by replenishing damaged neurons with new ones. Perhaps, then, Parkinson’s disease does not depend on a single source of damage, but rather multiple insults occurring. For example, genetically induced damage to the dopaminergic neurons in the substantia nigra combined with inhaled toxins damaging the olfactory bulb could, together, cause Parkinson’s, while one or the other would be insufficient.

References

Prediger, R., Aguiar, A., Matheus, F., Walz, R., Antoury, L., Raisman-Vozari, R., & Doty, R. (2011). Intranasal Administration of Neurotoxicants in Animals: Support for the Olfactory Vector Hypothesis of Parkinson’s Disease Neurotoxicity Research, 21 (1), 90-116 DOI: 10.1007/s12640-011-9281-8

Doty, R. (2011). Olfaction in Parkinson’s disease and related disorders Neurobiology of Disease DOI: 10.1016/j.nbd.2011.10.026

Ubeda-Bañon, I., Saiz-Sanchez, D., Rosa-Prieto, C., & Martinez-Marcos, A. (2011). ?-Synuclein in the olfactory system of a mouse model of Parkinson’s disease: correlation with olfactory projections Brain Structure and Function DOI: 10.1007/s00429-011-0347-4

  • Edith L Clark

    Approximately 4 years before my diagnosis of Parkinson’s I had a virus that took my total sense of taste and smell. When these senses started to return my smells for everything was altered. I was a working BSN nurse at the time. And when I drove to and from work I had to drive my cotton fields where the plants were defoliated for picking the cotton and they used plane dropped defoliation and pesticides. I worked for the Immigration Service in USPHS and drove 21 miles through the countryside to work 5 days a week.
    My sense of taste and smell have come close to normal as the years have come closer to normal however some things still smell and taste funny and nothing taste or smell as they did before the virus.

  • Great piece Emily! Are you working with Thomas Meyer’s group at all? We have been collaborating on ALS work together but I’ve also worked in PD in the past and have a few projects ongoing. Come find me @paullikeme on Twitter!

    Cheers

    Paul

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  • Tina.counsellormelbourne

    this is great input. Even if there is still a lot to know about Parkinson’s, slowly progress is being done. Hopefully in the near future we will be able to know what we should know about Parkinson’s up to the point that certain tests will be able to help us identify that a patient is at high risk for PD before it actually happens.

  • Matt

    Thanks for this very interesting post about Parkinson’s Disease. My friend’s grandmother has the disease. I hope someday, some would discover the cure for the disease. I know that there’s a lot of skillful doctors around the world especially in America. I know a very good doctor there which is a respected cardiologist. If you want to know more about him and learn about health especially the heart, you can checkout his sites. His name is Dr. Hugh Calkins by the way. Here is a link to one of his interesting sites.

    http://www.hopkinsmedicine.org/doctors/results/directory/profile/0001055/hugh-calkins

  • G Harrison

    This is the first time I have visited this web site – it’s great and I would like to add my comments about what’s happening to me re the smell and parkinsons. My father lost his sense of smell prior to being diagnosed with Parkinsons in the 70’s and now it’s my turn. I had a nasty virus and ended up with Pneumonia 6 years ago and had abnormal sense of smell – some things smelt very strong and others not at all. I did not look into parkinsons until recently as the doctors have all missed the symptoms but the other very interesting thing is, before I looked at parkinsons, I thought it was Fibromyalgia and took a high dose of Anti Virals used for treating the Herpes virus (Acylovir) Which a doctor in the US recommended as a treatment. And to my amazement the Sympoms went after a few weeks and I was symptom free for 6 months, so I stopped taking the Anti Virals. Sadly it didnt last and when I tried it again it did not work this time. But please think about this as a possible way of helping with the research etc as it was like a mirricle at the time and there must be a reason for it. I would be pleased to answer in more depth anything you would like to know. Good luck and keep up the hard work.

    Gary Harrison UK

  • Marilyn Johnson

    Thanks for this very interesting information. I am a 69-year-old woman who has always enjoyed excellent health, except that I totally lost my sense of smell several years ago. Just figured it was because I have a deviated septum, and the olfactory center was blocked or something, as I always have a stuffy nose. My brother also has lost his sense of smell. Two months ago I became ill with what was diagnosed as a virus. My original symptoms were *Exhaustion such as I had never, ever experienced. *Severe chills, with shaking that took at least 15 minutes to calm by piling on blankets, but no fever – in fact a lowered body temperature (95 degrees at the Instacare). * Headache. *Nausea/loss of appetite (I lost 5 or 6 pounds in about 6 weeks).* Slower gait which surprised me when I noticed it – I thought “Why am I walking so slowly?” *Constipation (I gained a hemorrhoid)* Blurred vision. *very dry mouth that led me to drink copious amounts of water.
    Very gradually over the past 2 months, the exhaustion, chills, headache, loss of appetite, slower gait and blurred vision have improved greatly, and I almost feel normal in those regards. But some other symptoms have appeared: Weak, achy, rubbery legs – a feeling of internal twitchiness and shaking, both in my right leg and right hand; several instances of imbalance when standing or turning; sudden urge to urinate and consequent bladder leakage; continued constipation, but not as severe. I am not aware of any abnormal exposure to toxins or chemicals during my life.
    Could these symptoms be due to the virus I had? Or should I see a doctor and be tested for Parkinson’s?

  • Congratulations Emily, certainly an interesting article!
    I wonder if beyong Parkinson’s, such olfactive deficiencies could easily diagnosed, precisely measured and then used for monitoring and possibly as companion diagnostics, it will enable drug development.
    It is likely such concepts could be applied to additional neurology related disorders.

    Happy holidays
    Chalom

  • Anonymous

    Over the past 12 months I have had 5 dental implants, one being my front tooth. I am showing signs of Parkinson’s and wonder if they could be related as my sense of smell has certainly deteriorated as has my balance since the receiving the implants,

Emily Haines, MSc, PhD (c)

Emily Haines, MSc, PhD candidate, is an expert on the cellular aspects of neuroimmunology and neurodegeneration. She holds a MSc in neuroscience from University College London. She is currently PhD candidate at Charite Medical University in Berlin and has worked as a biotechnology financial analyst researching and writing investment reports on companies developing and commercialising new therapies.
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