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Adamas Pharmaceuticals has entered into an agreement with HealthCare Royalty Partners (HCR) in an effort to get some quick cash so that it can continue development of its pipeline.
Under the terms of the agreement, Adamas will get $35 million upfront and then another $65 million when the Food and Drug Administration approves Parkinson's drug ADS-5102 and gives it orphan Drug exclusivity. The drug is currently under review and has a user fee action date of August 24.
Adamas will use the proceeds from the royalty deal to pay for general
expenses, as well as the commercialization of ADS-5102.
Dive Insight:
Adamas Pharmaceuticals currently has all its eggs in three baskets – its two marketed drugs Namenda XR (memantine extended-release capsules) and Namzaric (memantine/donepezil extended-release capsules) licensed from Forest Laboratories, part of Allergan, and ADS-5102 (amantadine extended-release capsules).
This much-needed cash isn't coming cheap; Adamas will pay 11% interest on the outstanding principal on a quarterly basis until it has paid back 200% of the principal. Interest and principal will be payable through a 12.5% royalty on the sales of ADS-5102, as well as up to $15 million annually of Adamas' royalties from Allergan from the sales of Namzaric until May 2020. The royalty rate on ADS-5102 would drop to 6.25% once the principal has been paid. On the flip side, the royalty rate increases to 22.5% in the event that Adamas doesn't keep up with payments.
In Adamas' Pharmaceuticals first quarter results, the company announced a net loss of $16.0 million, with an almost 40% increase in general and administrative expenses, including increased headcount for the hoped-for launch of ADS-5102.
"We are thrilled to partner with HCR in this transaction, providing us with the resources to advance our business and commercialize ADS-5102, which we believe will create significant and sustainable value for all Adamas stakeholders." said Gregory T. Went, chair and CEO of Adamas Pharmaceuticals.
Adamas' stock value swooped down and then up on the day its earnings results came up, closing stable, but has fallen 5% on the news of the HealthCare Royalty Partners deal.
Touted earlier this year as a potential acquisition target, if it gains Food and Drug Administration approval, ADS-5102 could be the first drug for Parkinson's patients with levodopa-induced dyskinesia.
Elto Pharma, a spinout from Amarantus BioPharma, is developing its Phase 2 drug eltoprazine, for a number of indications, including levodopa-induced dyskinesia in Parkinson's disease.
Adamas has one other drug in clinical development in its rather sparse pipeline, ADS-4101 (lacosamide), for the treatment of partial-onset seizures in epilepsy. This is a timed-release (chrono-synchronous) formulation of an existing drug, Vimpat, and has completed a Phase 1 trial.
Rep. Pete DeGraaf, a conservative Republican member of the House, said he would end his service in “several days,” leaving more than 18 months in an unexpired term. (2016 file photo/The Associated Press)
Mulvane Rep. Pete DeGraaf announced his decision Friday to resign from the Kansas Legislature due to complications of Parkinson’s disease.
DeGraaf, a conservative Republican member of the House, said he would end his service in “several days,” leaving more than 18 months in an unexpired term. A minister, he was elected a state representative in 2008.
“Today is the day that is filled with lots of emotions, ranging from a deep sense of gratitude and thanksgiving for the wonderful experience of serving with you in this House — the people’s House,” he said. “In spite of the current challenges that we now have, Kansas is a wonderful place to live, to work and to raise a family. There are many issues that still concern me, but I entrust those to you now.”
He said colleagues in the House had been a source of encouragement to him and his wife, Karen, as the incurable disease took a toll. He had complainedin 2015 to doctors about pain and being unusually tired, which resulted in the diagnosis.
“I don’t have jitters, like 30 percent of us don’t have jitters or shakes, and while I may look normal, and some of you may say I look great, that’s Pete on Parkinson’s medication. That’s Pete in public,” he said.
He’s used a makeshift bed in his Capitol office to conserve energy for work on committees dedicated to elections, higher education, veterans and information technology.
“I tell you these things not to make you feel sorry for me, but rather to help you understand that people with various kinds of disabilities may look normal, but we still need your patience, forbearance, mercy, forgiveness,” DeGraaf said.
Khalifa University holds exhibition to showcase solutions developed by students to help society
The projects that were developed were wide ranging covering a number of areas including health, clean energy
Abu Dhabi: Freshman engineering students at Khalifa University showcased their skills and talent at an exhibition hosted by the institution on Wednesday, with the students developing innovative projects intended to help society.
The exhibition saw the participation of 240 engineering students who were challenged to come up with ideas and solutions to community challenges. The projects that were developed were wide ranging covering a number of areas including health, clean energy and recycling.
One of the projects on display was the Smart Stethoscope, which saw the development of a device to help monitor breathing and heart rates to improve the diagnosis for pneumonia.
Smart stethoscope
“Our project is designed mainly for poor countries and hospitals that cannot afford the proper equipment to help diagnose patients. When you buy a stethoscope, you probably spend more than Dh200, and our goal is to provide a device that costs less,” said Kenan Al Aqeel, a Syrian student involved in designing the device.
“The device that we built has a sound detector sensor, and a covering with rubber material to get the vibration from the heart sounds. When the device gets the heart sound, it can start giving you the heart rate, thanks to a coding process we developed.
“So, for example, when we are monitoring the heart rate for one minute, it shows you the beats and after that you get the accurate heart rate, for instance, a measurement of 110 beats,” he added.
Al Aqeel said the device can be attached to the patient’s chest, and that their device should cost only Dh30, providing a big boost to poorer patients.
“The device provides a system that manages to monitor the breathing rate which can hopefully improve the diagnosis of pneumonia and save lives.
“The goal is to help poor people and provide a solution. In Africa, people sometimes use their bare hands to measure the heart beat, and this is not a very accurate way to measure the beats, it can lead to an insufficient analysis which doesn’t help with coming up with a suitable diagnosis,” he added.
Stopping tremor
Another innovative project on display was Tremor Free Me, a device intended to limit the tremors caused by Parkinson’s disease.
“The device took us around six weeks to make. It can predict the speed of the shakes caused by the tremors associated with Parkinson’s disease,” said Hassan Odeh from Jordan, and one of the team’s participating students.
“So if a person’s hands shake, the device detects this shake and sends a voltage to the motors and changes the frequency of the motors to match the person’s hand frequency. When the motor interacts with the shake of the hand, it causes a destructive interference which will cancel the shake of the hand.
“The device is very light, it can be worn as a bracelet or a strap, and as soon as they get a tremor, the device will be able to detect it and apply the opposite oscillations to cancel it,” he added.
Odeh said the device would be a benefit for people with Parkinson’s disease as it could limit their uncontrolled body movements.
“The range of a shake caused by Parkinson’s disease is between 3.5 to 7 hertz. The motor can vibrate in an opposite oscillation frequency which will cancel the shake of a person’s hand so they can write clearly without much shaking.
“The device may not fully reduce all of the shaking, but it can help minimise it to some degree,” Odeh added.
CHICAGO - The first drug using spherical nucleic acids to be systemically given to humans has been developed by Northwestern University scientists and approved by the Food and Drug Administration as an investigational new drug for an early-stage clinical trial in the deadly brain cancer glioblastoma multiforme.
A clinical trial has just been launched at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University and Northwestern Medicine.
The new drug is able to cross the challenging blood-brain barrier to reach tumors in animals, where it turns down a critical cancer-causing gene. Now, the Phase 0 clinical trial will investigate the drug’s ability to reach tumors in humans.
The glioblastoma drug represents a revolutionary new class of drugs. The novel spherical nucleic acid platform it is based on can be applied to other types of neurological diseases, such as Alzheimer’s and Parkinson’s, by similarly turning down the genes that lead to those diseases.
It’s highly unusual for a drug to be developed in preclinical research at a university, shepherded through FDA approval as an investigational new drug and studied in a clinical trial — all within the same university and without funding from a pharmaceutical company. In most cases, a drug is developed and licensed to a pharmaceutical company.
“We want to get the drug to patients as quickly as possible,” said Jay Walsh, vice president for research at Northwestern. “We want to move the drug forward because there are patients with a disease with no current cure."
The drug, called NU-0129, will have to go through many more phases before it is approved for general use in a clinical environment.
“We know this drug works in mice. Now we need to know if it can cross the human blood-brain barrier and accumulate in the tumor of a human being,” said Alexander Stegh, an assistant professor of neurology at Northwestern University Feinberg School of Medicine.
Stegh developed the drug with Chad A. Mirkin, the George B. Rathmann Professor of Chemistry at the Weinberg College of Arts and Sciences and director of Northwestern’s International Institute for Nanotechnology (IIN).
“If the spherical nucleic acids cross the barrier and localize in the brain, the implications go beyond glioblastoma,” Mirkin said. “This would give us the ability to target diseases of the brain by targeting pathways that we know are associated with different diseases, including Huntington’s, Parkinson’s and Alzheimer’s diseases.”
The drug, which consists of short snippets of RNA densely arranged on the surface of spherical gold nanoparticles, changes the genetic makeup of the tumor cells and dampens their ability to divide. The drug targets the gene BCL2L12, which is involved in apoptosis, or programmed cell death. Mirkin and his group invented spherical nucleic acids, and Stegh identified the gene to target.
Glioblastoma patients are treated with chemotherapy, radiation and surgery, but there is no cure. The life expectancy for the estimated 30,000 people in the U.S. who are diagnosed with the aggressive brain cancer each year is 14 to 16 months.
“We desperately need an effective treatment for this deadly disease,” said Dr. Priya Kumthekar, an assistant professor of neurology and hematology-oncology at Feinberg and a Northwestern Medicine neuro-oncologist. Kumthekar is the lead investigator of the Northwestern trial, which will recruit six to eight glioblastoma patients.
The study will recruit individuals who have had regrowth of their tumors and are candidates for tumor removal. They will receive the drug intravenously prior to surgery. Following tumor removal, Kumthekar and her team will study the tumor’s drug content to determine how well the drug crossed the blood-brain barrier in patients.
“Based on animal studies, there is good penetration into the tumor,“ Kumthekar said. “We predict that will be the case here, too.”
“Northwestern is very focused on delivering better therapy to patients,” said Dr. Frank Giles, who serves as Northwestern University’s sponsor representative on the investigational new drug application and clinical study. “Applying new scientific knowledge is the best way to develop truly paradigm-changing novel therapies.”
Kumthekar, Stegh, Mirkin and Giles are members of the Lurie Cancer Center.
“This was a complex, meticulous process requiring intense collaboration across many facets and groups within the University and Northwestern Medicine,” noted Ann Adams, associate vice president for research at Northwestern and one of the quarterbacks who led the FDA application process with Giles and Caroline Ko, a research associate in the department of chemistry and chief scientific officer of the IIN.
Dr. Leon Platanias, director of the Lurie Cancer Center, said, “The technology of spherical nucleic acids used in this first-in-human study is very powerful and may result in new, more effective approaches for the treatment of brain tumors and possibly other tumors in the future.”
The birth of the drug: spherical nanoparticles meet genetics
Stegh and Mirkin have been collaborating since 2009 to tackle the difficult problem of developing better treatments for glioblastoma. They first came together through Northwestern’s Center of Cancer Nanotechnology Excellence, funded by the National Cancer Institute.
Mirkin had the perfect tool: spherical nucleic acids, new globular forms of DNA and RNA — rather than linear — which are nontoxic to humans. The nucleic acid sequence is designed to match the target gene.
Stegh had the gene: in 2007, he and colleagues identified the gene BCL2L12 as one that is overexpressed in glioblastoma tumors and related to glioblastoma’s resistance to conventional therapies.
How the therapeutic works
The therapeutic, because of its novel structure, is actively taken across the blood-brain barrier, allowing it to reach the brain tumor. Once inside cancer cells, the drug silences the disease-causing gene. The RNA’s programmed sequence acts as a dimmer switch, selectively impeding the cells from producing specific proteins related to the disease. The result is selective cancer cell death and reduced cell growth.
Key to the drug’s success is the nanostructure’s 3-D spherical shape and nucleic acid density. Normal (linear) nucleic acids cannot get into cells or cross the blood-brain barrier, but these spherical nucleic acids can. Strands of RNA attach to and surround a gold nanoparticle like a shell; the nucleic acids are densely packed and form a tiny sphere. The gold nanoparticle core is only 13 nanometers in diameter.
Pivotal animal study
In 2013, Mirkin and Stegh were the senior co-authors of an animal study published in Science Translational Medicine. Their research team was the first to demonstrate delivery of a drug by intravenous injection that turns off a critical cancer-causing gene in glioblastoma, reducing tumor progression and increasing survival rates significantly in mice with the deadly disease.
In mice with glioblastoma, approximately 1 percent of the injected dose accumulated in the intracranial brain tumor tissue. Interestingly, once in the brain, the spherical nucleic acids selectively accumulated in tumor tissue over normal brain tissue. This is likely due to the ability of nanoparticles to accumulate in tumor tissue because of leaky blood vessels created by the tumor.
The survival rate of the animals increased nearly 20 percent, and tumor size was reduced three to four fold, as compared to the control group.
Mirkin first developed the nanostructure platform used in this study at Northwestern in 1996. This new development targeting glioblastoma was the first realization that the nanostructures injected into an animal naturally find their target in the brain and can deliver an effective payload of therapeutics.
Mirkin also is a professor of medicine, chemical and biological engineering, biomedical engineering and materials science and engineering.
Editor’s note: Northwestern University and some of the researchers involved in the development of the drug have financial interests relative to the drug used in this research study. As a result of these interests, Northwestern University and/or some researchers could ultimately benefit financially from the outcomes of this research.
Sarah Clements does a walking exercise with help from Karen Simpson, therapy assistant, at the MaintainUs exercise group. Picture: DENISE BRADLEY
For some people with disabilities, keeping active can be a struggle.
Sue Clissold is put through some exercises by Wendy Hendrie, MS specialist physiotherapist. Picture: DENISE BRADLEY
Now a gym and exercise classes are available to help those who have neurological conditions to keep active.
MaintainUs is a weekly exercise group based at the Multiple Sclerosis Centre in Norwich.
It has a gym with specialist equipment and experienced staff that allows people with neurological conditions, such as multiple sclerosis (MS), to work out and maintain their standing ability.
The exercise machines are specially designed for people with disabilities to strengthen muscles affected by their condition.
Some of the group on exercise cycles, with expert help from Karen Simpson, right, therapy assistant, at the MaintainUs exercise group. Picture: DENISE BRADLEY
Sarah Clements, 36, from Banningham has Friedreich-ataxia which affects her balance and coordination.
Miss Clements said: “Being able to exercise in a safe environment is a really good thing, with people that are on hand to help you and everyone here is really friendly.”
Miss Clements uses a walker to get around but at the gym is able to use a Oswestry Standing Frame which allows her to stand, strengthening her legs and back.
“No one had ever mentioned an exercise class like this to me before and it has really helped me with walking and if people use a wheel chair, it’s a release to stand up.”
Sue Clissold, 64, is wheelchair bound and registered blind. She lives mostly alone and said she enjoyed the class for the social aspects. She said: “I can’t leave my house so when I come up here the people are all talking and chatting as they are exercising.
“It’s a sociable thing because I know I have a goal I’m aiming for, to get back standing. To be able to come here is an absolute godsend.”
Physiotherapy assistants Karen Simpson and Jacquie Wright are on hand to help gym goers alongside physiotherapists Wendy Hendrie and Rachel Hardy with a range of exercise and yoga classes.
Wendy Hendrie is an MS specialist with 35 years’ experience. She said: “Most of the general population aren’t doing enough activity, so it’s even harder for people with disabilities. We are opening our doors to people with Parkinson’s, who have had strokes, any spinal injury or any neurological condition.”
MaintainUs runs every Wednesday and Thursday at the MS Therapy Centre. For more information call 01603 485933.
Summary: Study reveals 46.5% of people who were diagnosed with MCI later tested as ‘normal’ during a follow-up assessment.
Source: University of New South Wales.
MCI is associated with a higher risk of dementia and for some people is an intermediate stage between normal cognitive ageing and dementia. NeuroscienceNews.com image is adapted from the UNSW news release.
Closer examination of Mild Cognitive Impairment (MCI) is critical in identifying individuals at high risk of developing dementia, new research finds.
Researchers looking at the trajectory of Mild Cognitive Impairment (MCI) say examining specific subtypes is critical in identifying individuals at high risk of developing dementia.
MCI is defined as having noticed cognitive decline which is confirmed by objective tests in people who are functioning well.
MCI is associated with a higher risk of dementia and for some people is an intermediate stage between normal cognitive ageing and dementia.
But there are many reasons why a person’s cognition might have declined such as depression, infection or reaction to medications.
So, it is not surprising that many individuals with MCI “revert” to normal cognition. What is less well known is that people who revert to normal from MCI have an increased risk of re-transitioning to MCI or progressing to dementia.
Dr Liesbeth Aerts of the Dementia Collaborative Research Centre at UNSW says the relevance of reversion for progression risk depends on the MCI subtype.
In a paper published in the journal Neurology, four biennial assessments of 705 elderly people in the UNSW Centre for Healthy Brain Ageing Sydney Memory and Ageing Study showed reversion from MCI was common.
Almost half of the people who had MCI at the start of the study (46.5%) tested as “normal” at least once during follow-up assessment.
But risk of progression to dementia was only lower for those who reverted from amnestic MCI, a subtype of MCI in which memory is affected.
Dr Aerts, the paper’s lead author, says it highlights the importance of subtype specificity.
“We need to be mapping these cognitive problems much better, because just saying ‘MCI’ is not enough to really know about dementia risk,” she says.
Longitudinal follow-up is crucial to determining which individuals with MCI are at high risk of developing dementia.
“In our study people’s performance on cognitive tests fluctuated or zig-zagged over time,” Dr Aerts says.
“Our results highlight that we need better assessment over time. Snapshot assessments should be considered in a larger perspective.
“Before, no one was thinking of reversion, we were only trying to capture people on decline.”
A bigger picture issue is the limitations of the cognitive tests, and the important role that biomarkers (biological indicators of dementia, for example changes in brain chemicals and imaging) will play in the future.
Changes in the brain occur long before the first symptoms become apparent, so being able to measure those will be crucial to identify people in the earliest stages of dementia.
“Researchers are shifting the frame to studying to what happens long before the onset of dementia in the hope of stopping the degenerative process in the brain in its tracks before dementia takes hold.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Gabrielle Dunlevy – University of New South Wales Image Source: NeuroscienceNews.com image is adapted from the UNSW news release.
Original Research:Abstract for “Effects of MCI subtype and reversion on progression to dementia in a community sample” by Liesbeth Aerts, Megan Heffernan, Nicole A. Kochan, John D. Crawford, Brian Draper, Julian N. Trollor, Perminder S. Sachdev, and Henry Brodaty in Psychological Science. Published online May 10 2017 doi:10.1212/WNL.0000000000004015
Abstract
Effects of MCI subtype and reversion on progression to dementia in a community sample
Objective: We sought to understand the trajectory of mild cognitive impairment (MCI) better by examining longitudinally different MCI subtypes and progression to dementia and reversion to normal cognition in a community sample.
Methods: We evaluated the stability of MCI subtypes and risk of dementia over 4 biennial assessments as part of an ongoing prospective cohort study, the Sydney Memory and Ageing Study.
Results:While prevalence of MCI and different MCI subtypes remains relatively stable across all assessments, reversion from MCI and transitions between different MCI subtypes were common. Up to 46.5% of participants classified with MCI at baseline reverted at some point during follow-up. The majority (83.8%) of participants with incident dementia were diagnosed with MCI 2 years prior to their dementia diagnosis. Both reverters and participants with stable MCI were at an increased risk of progression to dementia compared to those without MCI at baseline (HR 6.4, p = 0.02, and HR 24.7, p < 0.001, respectively); however, the risk of dementia in participants with MCI who did not revert was higher than in reverters (HR 2.5, p = 0.01). This effect was specific to amnestic subtypes (MCI reverters vs nonreverters: amnestic MCI HR 3.3, p = 0.006; nonamnestic MCI: HR 1.3, p = 0.67).Conclusion: Our findings indicate that the relevance of reversion for progression risk depends on the MCI subtype. Subtype specificity and longitudinal characterization are required for the reliable identification of individuals at high risk of developing dementia.
“Effects of MCI subtype and reversion on progression to dementia in a community sample” by Liesbeth Aerts, Megan Heffernan, Nicole A. Kochan, John D. Crawford, Brian Draper, Julian N. Trollor, Perminder S. Sachdev, and Henry Brodaty in Psychological Science. Published online May 10 2017 doi:10.1212/WNL.0000000000004015
A hallmark of Parkinson’s is loss of dopaminergic neurons — which produce the neurotransmitter dopamine — in a brain region called the substantia nigra. Neurons are nerve cells.
Dopaminergic neurons’ deaths affect the normal functioning of another region, the basal ganglia, which governs voluntary movements. This makes the basal ganglia a good target for Parkinson’s therapies. But treatments developed so far don’t last long.
“A major limitation of Parkinson’s disease treatments is that they provide transient relief of symptoms,” Aryn Gittis, the study’s senior author, said in a news release. “Symptoms can return rapidly if a drug dose is missed or if deep brain stimulation is discontinued.
“There is no existing therapeutic strategy for long-lasting relief of movement disorders associated with Parkinson’s,” she added.
To investigate the basal ganglia’s role in Parkinson’s, researchers studied two groups of neurons in a structure called the external globus pallidus (GPe) that is in the same region. GPe neurons suppress motor pathways in the basal ganglia, but researchers didn’t know how they behave in Parkinson’s.
The team genetically altered mice to produce GPe neurons activated by light, a technique called optogenetics. This approach allowed them to follow two subtypes of GPe neurons, called PV-GPe neurons and Lhx6-GPe neurons.
Mice with Parkinson’s had abnormal basal ganglia activity and movement problems. Stimulating the activity of PV-GPe neurons stopped the basal ganglia neuron problems and restored the mice’s movement for four hours, significantly longer than other treatments.
“These results establish the utility of cell-specific interventions in the GPe to target functionally distinct pathways, with the potential to induce long-lasting recovery of movement despite the continued absence of dopamine,” researchers wrote.
Therapies based on the team’s findings could be more effective than current treatments, such as deep brain stimulation, Gittis concluded.
A recent study has found that Parkinson’s disease could be triggered by a protein in the stomach that travels to the brain through the vagal nerve. Researchers found that those who had the vagal nerve removed had a 40 percent lower chance of developing the disease.
Vagotomies are often performed on those who have chronic duodenal ulcers or a gastric outlet obstruction. The Swedish study compared the medical histories of 9,400 people who’d had a vagotomy to 377,000 who hadn’t had the procedure over a 40-year period.
According to the Daily Mail, 101 people who had a vagotomy went on to develop Parkinson’s disease (or 1.07 percent) compared to 4,829 people (or 1.28 percent) who still had their vagal nerve intact. Those who had undergone a truncal vagotomy were even less likely to have developed Parkinson’s disease (0.78 percent).
Other evidence that Parkinson’s disease may start in the digestive system is the fact that many Parkinson’s disease patients report GI problems like constipation years before the onset of any Parkinson’s symptoms.
Go to: https://parkinsonsnewstoday.com/2015/06/24/study-suggests-parkinsons-disease-may-start-gut/
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Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
In this video from Talks at Google, the Michael J. Fox Foundation (MJFF) and Verily Life Sciences host a discussion about Michael’s life with Parkinson’s disease.
Head of clinical neurology for Verily Life Sciences, Dr. Bill Marks, talks to the famous actor about his work with the Michael J. Fox Foundation and the importance of accountability when it comes to awarding grants.
The discussion covers many aspects of living with Parkinson’s, from the importance of staying optimistic to the advancement of Parkinson’s disease research.
Michael talks about his own journey with Parkinson’s and some of the treatments he’s tried over the years. He also shares some of the frustrations and lessons that have come from living with the condition.
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Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
When it comes to our sense of smell, we have been led to believe that animals win out over humans: No way can we compete with dogs and rodents, some of the best sniffers in the animal kingdom.But guess what? It's a big myth. One that has survived for the last 150 years with no scientific proof, according to Rutgers University-New Brunswick neuroscientist John McGann, associate professor in the Department of Psychology, School of Arts and Sciences, in a paper published on May 12 inScience.
McGann, who has been studying the olfactory system, or sense of smell, for the past 14 years, spent part of the last year reviewing existing research, examining data and delving into the historical writings that helped create the long-held misconception that human sense of smell was inferior because of the size of the olfactory bulb.
"For so long people failed to stop and question this claim, even people who study the sense of smell for a living," says McGann, who studies how the brain understands sensory stimuli using information gleaned from prior experience.
"The fact is the sense of smell is just as good in humans as in other mammals, like rodents and dogs." Humans can discriminate maybe one trillion different odors, he says, which is far more, than the claim by "folk wisdom and poorly sourced introductory psychology textbooks," that insist humans could only detect about 10,000 different odors.
McGann points to Paul Broca, a 19th century brain surgeon and anthropologist as the culprit for the falsehood that humans have an impoverished olfactory system—an assertion that, McGann says, even influenced Sigmund Freud to insist that this deficiency made humans susceptible to mental illness.
"It has been a long cultural belief that in order to be a reasonable or rational person you could not be dominated by a sense of smell," says McGann. "Smell was linked to earthly animalistic tendencies." The truth about smell, McGann says, is that the human olfactory bulb, which sends signals to other areas of a very powerful human brain to help identify scents, is quite large and similar in the number of neurons to other mammals.
The olfactory receptor neurons in the nose work by making physical contact with the molecules composing the odor, and they send this information back to that region of the brain.We can detect and discriminate an extraordinary range of odors; we are more sensitive than rodents and dogs for some odors; we are capable of tracking odor trails; and our behavioral and affective states are influenced by our sense of smell," McGann writes in Science.
In Broco's 1879 writings, he claimed that the smaller volume of the olfactory area compared to the rest of the brain meant that humans had free will and didn't have to rely on smell to survive and stay alive like dogs and other mammals.
In reality, McGann says, there is no support for the notion that a larger olfactory bulb increases sense of smell based solely on size and insists that the human sense of smell is just as good and that of animals.
"Dogs may be better than humans at discriminating the urines on a fire hydrant and humans may be better than dogs at discriminating the odors of fine wine, but few such comparisons have actual experimental support," McGann writes in Science.
The idea that humans don't have the same sense of smell abilities as animals flourished over the years based on some genetic studies which discovered that rats and mice have genes for about 1000 different kinds of receptors that are activated by odors, compared to humans, who only have about 400.
"I think it has been too easy to get caught up in numbers," says McGann. "We've created a confirmation bias by working off a held belief that humans have a poor sense of smell because of these lower numbers of receptors, which in reality is still an awful lot."
The problem with this continuing myth, McGann says, is that smell is much more important than we think. It strongly influences human behavior, elicits memories and emotions, and shapes perceptions.
Our sense of smell plays a major, sometimes unconscious, role in how we perceive and interact with others, select a mate, and helps us decide what we like to eat. And when it comes to handling traumatic experiences, smell can be a trigger in activating PTSD.
While smell can begin to deteriorate as part of the aging process, McGann says, physicians should be more concerned when a patient begins to lose the ability to detect odors and not just retreat back to the misconception that humans' sense of smell is inferior.
"Some research suggests that losing the sense of smell may be the start of memory problems and diseases like Alzheimer's and Parkinson's," says McGann. "One hope is that the medical world will begin to understand the importance of smell and that losing it is a big deal."
