Neurology

How AI and neuromodulation could help with sleep disorders

siddiq22 — Tue, 11 Jul 2023 18:37:12 +0000

How AI and neuromodulation could help with sleep disorders

siddiq22 Tue, 07/11/2023 - 14:37

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Assistant Professor Xilin Liu and his collaborators are developing electronic devices that could help patients suffering from sleep disorders (photo courtesy Xilin Liu)

Selah Katona

Topic

Breaking Research

Artificial Intelligence

Faculty of Applied Science & Engineering

machine learning

Neurology

Research & Innovation

Sleep

Subheadline

'We still don’t fully comprehend what actually occurs in our brains during sleep'

A new partnership between the 91�Թ�'s Xilin Liu, assistant professor in the Edward S. Rogers Sr. department of electrical and computer engineering in the Faculty of Applied Science and Engineering, and Andrew G. Richardson, research assistant professor of neurosurgery at the University of Pennsylvania, will develop a new generation of electronic devices to investigate sleep modulation.

Their research will potentially develop new interventions that help deal with a wide range of sleep disorders.

On average, we spend a third of our life asleep. During sleep, the brain undergoes important processes that support memory consolidation, neural restoration and the clearance of toxins. Sleep disruptions can interfere with these processes. But while good "sleep hygiene" is increasingly recognized as crucial to both physical and mental health, sleep disorders remain widespread.

“40 per cent of Canadians have sleep disorders, with over 3 million suffering from insomnia,” says Liu, director of the X-Lab and affiliate scientist at the the KITE Research Institute.

“Sleep deficits negatively affect brain functions such as attention and memory, and immune function, metabolism and heart health. Chronic sleep-wake disruptions are connected to neurodegenerative disorders such as Huntington’s, Parkinson’s and Alzheimer’s disease, and cognitive decline with aging.”

This diagram describes the process of closed-loop sleep modulation via miniaturized electronics
(image courtesy of Xilin Liu)

Liu’s research focuses on developing integrated circuits and systems for advancing health care, digital communication and machine learning. In the new collaboration, he will be building fully integrated wireless systems-on-chips that can autonomously modulate sleep behavior in pre-clinical studies.

“Sleep is a complex procedure involving different stages and patterns,” he says. “To address this, we are integrating machine-learning algorithms into our devices. These new algorithms can recognize sleep patterns and identify sleep disorders that may not be distinguishable using traditional algorithms.”

Liu and his collaborators hope that these new approaches will enable them to gain a deeper understanding of how our brains function during sleep and how to modulate sleep circuits.

They also plan to incorporate various neural interfacing capabilities into the system, which will enable more accurate and precise interventions. The results of this research will contribute to the advancement of neuromodulation, a technology that involves placing devices inside a patient’s brain, spinal cord or peripheral nerves. These devices are designed to regulate neural activity and help reduce symptoms related to different disorders.

Liu is a faculty member of the CRANIA Neuromodulation Institute (CNMI) in the Faculty of Applied Science and Engineering, which brings together experts in engineering and neuroscience in a collaborative hub for neuromodulation research.

Liu’s project was recently awarded $2.2 million by the National Institutes of Health (NIH) through their Research Project Grant Program (R01), and is supported by industry partners such as the Canadian Microelectronics Corporation and Open Ephys.

The NIH R01 grant is a highly competitive award and Liu and Richardson’s proposal fell in the top 1 per cent of applications.

“This is a great sign that NIH recognizes the value and impact of this research and the caliber of the team,” Liu says. “We’re excited to receive this funding and over the next four years we hope to get to a stage where the technology can be used in clinical trials.”

Liu’s research team has a long-term goal of creating wearable devices for sleep modulation that people can use at home to enhance the quality of their sleep.

“While there are medications available to treat sleep disorders, the challenge lies in the fact that we still don’t fully comprehend what actually occurs in our brains during sleep,” Liu says.

“It’s possible that there are low-cost, high-efficacy treatments available for sleep disorders that we are currently unaware of.”

Researchers identify a potential new therapeutic target in Parkinson’s disease

siddiq22 — Mon, 24 Apr 2023 13:50:47 +0000

Researchers identify a potential new therapeutic target in Parkinson’s disease

siddiq22 Mon, 04/24/2023 - 09:50

Cutline

A new study by researchers from UHN and 91�Թ� examined how to prevent the accumulation in the brain of a protein that contributes to Parkinson's disease (photo by Christian Wiediger via Unsplash)

Topic

Breaking Research

Temerty Faculty of Medicine

Tanz Centre for Research in Neurodegenerative Diseases

Donnelly Centre for Cellular & Biomolecular Research

Medical Research

Neurology

Parkinson's

University Health Network

A team of researchers from the Krembil Brain Institute (KBI) and the 91�Թ� have identified a protein-protein interaction that contributes to Parkinson’s disease.

In a study published in Nature Communications, KBI scientists Lorraine Kalia and Suneil Kalia and 91�Թ� researcher Philip M. Kim examined a protein called alpha-synuclein (a-syn) that accumulates in the brain in patients with Parkinson's and leads to cell death.

Much research is currently focused on clearing a-syn with antibodies or using small molecules to prevent a-syn from aggregating. In their study, the researchers took an alternate approach by looking for protein-protein interactions that may be promoting the accumulation of a-syn in Parkinson’s disease.

Protein-protein interactions govern most inner workings of the cell, including breaking down disease-causing proteins. Inhibiting certain interactions has emerged as a promising approach to treat diseases such as stroke and cancer.

“Identifying a particular interaction that contributes to a disease, and then finding ways to disrupt it, can be a painstaking and incredibly slow process,” says Lorraine Kalia, who is also a staff neurologist at University Health Network, a scientist at 91�Թ�’s Tanz Centre for Research in Neurodegenerative Diseases and an assistant professor in the division of neurology and in the department of laboratory medicine and pathobiology in the Temerty Faculty of Medicine.

“We all started out a bit skeptical that we would have something useful at the end, and so the fact that we do have something that warrants further work is much more than we anticipated.”

Kim, who is a professor in 91�Թ�’s Donnelly Centre for Cellular and Biomolecular Research and in the department of molecular genetics in the Temerty Faculty of Medicine, notes the team took an approach they hoped would expedite the discovery of potential therapies.

“We developed a platform to screen molecules called peptide motifs – short strings of amino acids that can disrupt protein-protein interactions – for their ability to protect cells from a-syn,” Kim says. “Once we identified candidate peptides, we determined which protein-protein interactions they target.”

Through this approach, the team identified a peptide that reduced a-syn levels in cells by disrupting the interaction between a-syn and a protein subunit of the cellular machinery called “endosomal sorting complex required for transport III” (ESCRT-III).

“ESCRT-III is a component of a pathway that cells use to break down proteins, called the endolysosomal pathway. We discovered that a-syn interacts with a protein within ESCRT-III – CHMP2B – to inhibit this pathway, thereby preventing its own destruction,” Lorraine Kalia says.

“We were impressed that the platform worked. But I think what was more interesting is that by doing this kind of screening, we were able to find an interaction that was really not previously characterized, and we also found a pathway that’s not yet been targeted for therapeutics.”

Once the group identified this interaction, they confirmed that they could use their peptide to disrupt it – preventing a-syn from evading the cell’s natural clearance pathways, notes Suneil Kalia, who holds the R.R. Tasker Chair in Stereotactic and Functional Neurosurgery at UHN and is an associate professor in the division of neurosurgery in the Temerty Faculty of Medicine.

“We tested the peptide in multiple experimental models of Parkinson’s disease, and we consistently found that it restored endolysosomal function, promoted a-syn clearance and prevented cell death,” he says.

These findings indicate that the a-syn-CHMP2B interaction is a potential therapeutic target for the disease, as well as other conditions that involve a buildup of a-syn, such as dementia with Lewy bodies (another disease associated with abnormal deposits of a-syn in the brain).

The next steps for this research are to clarify exactly how a-syn and CHMP2B interact to disrupt endolysosomal activity. Ongoing studies are also determining the best approach for delivering potential therapeutics to the brain.

“This research is still in its early stages – more work is definitely needed to translate this peptide into a viable therapeutic,” cautions Lorraine Kalia. “Nonetheless, our findings are very exciting because they suggest a new avenue for developing treatments for Parkinson’s disease and other neurodegenerative conditions.”

This study also highlights the value of multidisciplinary collaborations in health research.

“We simply could not have conducted this study in a silo. The endolysosomal pathway is underexplored, so it was not an obvious place to look for potential disease-related protein-protein interactions. Dr. Kim’s screening platform was critical for pointing us in the right direction,” Suneil Kalia points out.

“It is really extraordinary to see this platform – which we initially used to find potential therapeutics for cancer – yielding advances in brain research. The pathways that cells use to stay healthy are fundamentally very similar across tissues, so the insights that we gain about one organ system or disease could have important implications in other contexts,” Kim says.

“It’s really brand-new science and targets that haven’t been a focus for drug development for Parkinson’s," Lorraine Kalia adds. "We hope this changes the landscape for treatment of this disease, which is so in need of new therapies.”

The research was supported by the Canadian Institutes of Health Research, the Michael J. Fox Foundation for Parkinson’s Research, Parkinson’s UK, the Canada Foundation for Innovation, the Ontario Research Fund, the Krembil Research Institute and the UHN Foundation.

This story was originally published on the website of the Krembil Brain Institute, University Health Network.

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Neurodegenerative Diseases

Biomolecular Research

'A creative perspective': Neurologist Suvendrini Lena on her path to playwriting

Christopher.Sorensen — Mon, 13 Mar 2023 21:12:38 +0000

'A creative perspective': Neurologist Suvendrini Lena on her path to playwriting

Christopher.Sorensen Mon, 03/13/2023 - 17:12

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Suvendrini Lena, an assistant professor in 91�Թ�'s Temerty Faculty of Medicine, bridges the gap between medicine and theatre in her work as a playwright (photo courtesy of Suvendrini Lena)

Tabassum Siddiqui

Topic

City & Culture

Temerty Faculty of Medicine

Women's College Hospital

Suvendrini Lena has a foot in two worlds: she’s a staff neurologist at Women’s College Hospital and an assistant professor of neurology and psychiatry in the 91�Թ�’s Temerty Faculty of Medicine – and a successful playwright.

After earning a B.A. in history and political science as an undergraduate student at Trinity College, Lena went on to a graduate degree in neurology at 91�Թ� – all while exploring her longstanding interest in theatre and writing.

But the path to writing her first play was a bit of a surprise – certainly to her neurology professors. Instead of presenting a final research project, she wrote a piece of theatre – The Enchanted Loom – that explored the experience of a patient with epilepsy. It was later produced by Toronto’s Cahoots Theatre and published as a book.

Since then, Lena has continued to work in both medicine and theatre – her latest play, Rubble, is currently on stage at Theatre Passe Muraille until March 18. A dramatic imagining of the works of Palestinian poets Mahmoud Darwish and Lena Khalaf Tuffaha, the play was inspired by Lena’s work in Gaza in 2002 while still a medical student. Years later, Tuffaha’s poetry reminded her of the struggles – and the rubble – she witnessed while there.

Including fellow 91�Թ� alumni Roula Said and Lara Arabian among the cast of five, Rubble unfolds in Gaza as a mother and her family receive a life-changing call: they have 58 seconds to leave their home before an explosion. Drawing on the poems of Darwish and Tuffaha, Lena examines the meaning of poetry amidst a state of siege.

Lena spoke to 91�Թ� News about how her university experience informed her path to bridging the gap between medicine and the arts.

You’re a neurologist by training but now also a playwright – how did you find your way from medicine to theatre?

I always wanted to be a writer. In the neurology program at 91�Թ�, you have to do a big research project in your last year of the program, but I realized my heart wasn’t really in research. I’m definitely interested in understanding things well and the arts are another way to do that – you get to interrogate something, but from a creative perspective. I ended up writing a play about a Sri Lankan patient with a complex case of epilepsy and all the difficult choices facing him and his family as a result of his illness. So that became the centre of my first play.

What was your professors’ reaction when you asked to submit a play as your final project instead of a research paper?

There’s an art to pitching – it’s about taking an idea that has legs and having people understand and feel invested. So, I think I did that convincingly and I had open-minded supervisors – I was very lucky that way. I had great support and supervision, and we presented a reading from that play at the research presentation at the end of the year. The audience gave it a standing ovation. I think there was something compelling for them because they could see themselves depicted in a very human way. Doctors are so often portrayed in a one-dimensional way in TV and film, so I try not to do that myself.

What inspired you to write Rubble?

I’m a lover of poetry – especially these two particular poets; their lyrical poems exist on many levels. You have to hear it out loud to be able to appreciate the meaning – the poems also give you a window into the humanity of people who might feel distant from you, but you can see that’s not the case. I felt like it was a doorway to explore and give voice to the Palestinian experience – in the last 60 years, they have been displaced and under occupation, and there’s been very little clarity about that historical experience; very few places for them to really tell their story. So, the play is trying to create that space as well.

Lara Arabian in Rubble (photo courtesy of Theatre Passe Muraille/Aluna Theatre)

When you think back to your 91�Թ� studies, were there any mentors or faculty who made an impact on your educational and career path?

In my neurology program, Marika Hohol [Unity Health] and Richard Wennberg [University Health Network] were people I learned a lot from and who supported me. And during my undergrad years, I took courses in English and modern drama, including with an amazing professor, Alexander Leggatt – that’s really where my love of theatre was nurtured. He opened up the world of drama to many, many people. He was interested in ethics, philosophy and poetry – and really made it all accessible to us.

Left to right: Roula Said, Lara Arabian and Sam Khalilieh in Rubble (photo courtesy of Theatre Passe Muraille/Aluna Theatre)

How did your time at 91�Թ� help shape the work you do today?

I first studied history and political science, but got heavily into theatre when I directed plays with the Trinity College Dramatic Society. Afterwards, I swore I would never direct anything again – everything was so complicated! But I got to understand that when you study a text as a director, it’s a completely different experience than reading it in class, right? You step into building a theatrical world – which is what playwriting and theatre-making is all about.

How does your work as a doctor intersect with your work as a playwright?

In medicine, we deal with a lot of very difficult things all the time – and there's a bit of trauma in there. If you empathize with your patients, then you can’t help but witness suffering. These are very moving things and you’ve got to stay open and alive to all that. I need an outlet – writing provides me with that outlet and theatre is special because you can explore human issues and relationships in a unique way. All kinds of writing can touch on that, but when something is written for the theatre and embodied by an actor, it gives an added dimension of reality.

What’s your approach to teaching?

I mostly do small-group teaching in the medical school curriculum and a seminar on medicine and the humanities. This semester, we’re doing a staging where we explore medical experiences and how physicians examine their own subjectivity. We also try to engage with issues of contemporary relevance, including issues of voice and representation in medicine and society.

91�Թ� researchers find key differences in symptoms between early- and late-onset Alzheimer's

geoff.vendeville — Thu, 20 May 2021 14:04:15 +0000

91�Թ� researchers find key differences in symptoms between early- and late-onset Alzheimer's

geoff.vendeville Thu, 05/20/2021 - 10:04

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Carmela Tartaglia and Melisa Gumus of the Temerty Faculty of Medicine are among the co-authors of a study that found key differences in symptoms between people with early- and late-onset Alzheimer's (photos courtesy of UHN and Melisa Gumus)

Andrea Haman

Topic

Breaking Research

Insulin 100

Temerty Faculty of Medicine

Tanz Centre for Research in Neurodegenerative Diseases

Graduate Stories

Neurology

University Health Network

While Alzheimer’s disease most often appears in late life, as many as one in 10 people who develop it begin to experience the disease before age 65. This young-onset version is often undetected and misdiagnosed, with debilitating results.

In a recent study, 91�Թ� researchers have found key differences in symptoms between people who develop Alzheimer’s earlier versus later. The researchers showed that two mental illness symptoms – depression and anxiety – are much more common in people with young-onset Alzheimer’s than in those with late-onset Alzheimer’s.

The findings underscore the need to consider Alzheimer’s in midlife when these symptoms occur with cognitive or thinking problems, and may improve diagnosis and the quality of life for affected individuals.

“If you get cognitive impairment at age 55, people are not thinking about Alzheimer’s disease,” says Carmela Tartaglia, an associate professor in the Tanz Centre for Research in Neurodegenerative Diseases in the Temerty Faculty of Medicine and the senior author of the study published earlier this year in the journal GeroScience. “The fact that people get Alzheimer’s disease before age 65 is less well known, so many people have considerable delay in diagnosis, often up to five years.”

This delay can have dire consequences. “Many patients have gone through several doctors, psychiatrists or other specialists, and medications,” says Tartaglia, who also cares for patients in the Memory Clinic in University Health Network. “They've been told that they’re having a midlife crisis, are depressed or anxious, or are going through menopause. They may experience significant anxiety about losing their memory. Some people have even lost their jobs.”

The delay in diagnosis is not surprising, given that mental illness symptoms are common in people with Alzheimer’s – more than 80 per cent of people develop at least one mental illness symptom, such as depression, anxiety or apathy, as the disease progresses.

In the study, the researchers – including 91�Թ� master’s student Melisa Gumus, the study’s first author – determined the prevalence and severity of mental illness symptoms over a four-year period in 126 people diagnosed with young-onset Alzheimer’s and 505 people with late-onset Alzheimer’s. When examining questionnaires about mental illness symptoms completed by caregivers, the researchers included people who were taking medications to treat mental illness symptoms as having mental illness symptoms, even if the person no longer exhibited symptoms. This novel approach provides the clearest picture of prevalence.

The study showed that depression and anxiety are much more common in young-onset patients, both at the start of and throughout the four years. For example, at the start of the study, 64 per cent of people with young-onset Alzheimer’s had depression and 33 per cent had anxiety, while 41 per cent with late-onset Alzheimer’s had depression and 17 per cent had anxiety. There was no significant difference between the two groups in the prevalence of other mental illness symptoms or in the severity of any symptoms.

While the study didn't explore why depression and anxiety are more common in young-onset patients, in addition to possible differences in disease processes, there are psychosocial differences such as heavy responsibilities for raising children, earning income or caring for elderly parents that may play a role.

“Our hope is that the findings help patients get diagnosed earlier,” says Tartaglia. “If, for example, a patient is 55 years old and has a new onset of depression or anxiety that is not situational, consider this as the beginning of neurodegenerative disease.” While there is no cure to stop the progression of Alzheimer’s, an accurate diagnosis allows people to take steps early. People at the early stages of the disease may be eligible to participate in clinical trials to slow the progression of Alzheimer’s or reduce specific symptoms. As well, people may be able to modify their work, apply for disability benefits or make other changes to improve their quality of life.

Fragmented sleep may affect brain’s immune cells, impair cognition: 91�Թ� study

Christopher.Sorensen — Thu, 12 Dec 2019 21:49:55 +0000

Fragmented sleep may affect brain’s immune cells, impair cognition: 91�Թ� study

Christopher.Sorensen Thu, 12/12/2019 - 16:49

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The study by 91�Թ� researchers showed the cells of adults with fragmented sleep showed signs of accelerated aging and other abnormalities, and could be associated with worse cognition in older adults (photo by EMS-Forster-Productions via Getty Images)

Topic

Research & Innovation

Sunnybrook Hospital

Fragmented sleep in older people with and without Alzheimer’s disease may have an effect on the brain’s immune cells and impact people’s cognitive abilities, according to a new study by 91�Թ� researchers.

The study by Dr. Andrew Lim, an associate professor in neurology at 91�Թ�’s Faculty of Medicine, and Kirusanthy Kaneshwaran, a third-year 91�Թ� medical student, was published this week in Science Advances. It shows that in adults with fragmented sleep – where people were waking up repeatedly instead of sleeping soundly – there was an effect on microglia, and the cells showed signs of accelerated aging and other abnormalities.

The researchers were then able to identify that the changes in the microglia, described by Lim as the “brain’s innate immune cells,” could be associated with worse cognition in older adults, both with and without Alzheimer’s disease.

“There are two important takeaways from this paper,” says Lim. “One is that poor sleep is associated with brain immune dysregulation or dysfunction. The second part is that dysfunction appears to be further associated with impaired cognition.”

The research in the paper supports the hypothesis “that poor sleep may lead to brain immune dysregulation,” adds Lim, who is also a scientist at the Hurvitz Brain Sciences Research Program at Sunnybrook Research Institute.

It also supports the idea that poor sleep may be a possible cause of cognitive decline and dementia.

“Greater expression of genes characteristic of aged microglia was associated with worse cognition and partially accounted for the association between sleep fragmentation and worse cognition,” write the researchers.

“These findings raise the possibility that microglial aging and activation may be a consequence of sleep fragmentation and may link sleep fragmentation to poor cognition in older adults.”

The paper points to other potential factors that lead to cognitive impairment.

“Our findings are compatible with three scenarios: microglial aging and activation may lead to sleep fragmentation, sleep fragmentation may lead to microglial aging and activation, or both may be caused by other brain changes, such as dementia-related brain pathologies,” the researchers write.

The research was based on 685 adults who were more than 65 years old, including more than 260 who had Alzheimer’s disease.

The adults had been participants in the Religious Orders Study and Rush Memory and Aging Project.

The study was undertaken by Dr. Andrew Lim, an associate professor in neurology in 91�Թ�’s Faculty of Medicine, and Kirusanthy Kaneshwaran, a third-year 91�Թ� medical student (photo by Gabrielle Giroday)

For the study, researchers measured the participants’ sleep patterns using wearable devices. They also measured participants’ cognitive function on an annual basis.

Researchers quantified the number and state of the brain’s innate immune cells for each participant by examining the gene expression patterns of the cells and by looking at the cells’ shape under the microscope.

“I have a relative with Alzheimer’s disease and I have always been fascinated about memory and what is the underlying mechanism of memory,” says Kaneshwaran, the first author of the study.

“Sleep is something that a lot of people have problems with. Losing your memory is something very deep – it’s like losing yourself as a person. I feel like it’s very important that if we can prevent that in any way, we do.”

The findings emphasize the importance of getting a good night’s rest, according to Lim.

“Poor sleep is not something that should be ignored. It should be something that is taken seriously, and pursued,” he says.

“If you are sleeping poorly, you should bring it up with your doctor. If you need to, you can then can bring it up with a sleep specialist and do the appropriate testing, and try to solve the problem. Improving sleep might potentially be a way of improving brain immune function, which may potentially improve cognition.”

Lim adds that there are promising research implications from the study.

For example, further research may target brain immune dysregulation as a way of preventing unfavourable impacts on brain health for people with unavoidable sleep disruption, including shift workers or airline workers.

The researchers received support from the Canadian Institutes of Health Research, among others.

Melanie Woodin to become new dean of 91�Թ�’s Faculty of Arts & Science

Christopher.Sorensen — Wed, 27 Feb 2019 15:05:13 +0000

Melanie Woodin to become new dean of 91�Թ�’s Faculty of Arts & Science

Christopher.Sorensen Wed, 02/27/2019 - 10:05

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Melanie Woodin, who will serve a five-year-term beginning July 1, says her new role is an opportunity to celebrate and build upon the interdisciplinary nature of the faculty (photo by Lisa Sakulensky)

Romi Levine

Topic

Our Community

Cell and Systems Biology

Faculty & Staff

Faculty of Arts & Science

Neurology

Professor Melanie Woodin, a neuroscientist in the department of cell and systems biology, will become the 91�Թ�’s next dean of the Faculty of Arts & Science.

Woodin, who is currently the faculty’s vice-dean of interdivisional partnerships, will serve a five-year term beginning on July 1.

“I'm incredibly humbled and honoured to have this role,” says Woodin.

“We have outstanding faculty members who are working at the forefront of their research disciplines and have an incredible dedication to undergraduate and graduate students. My primary role is to ensure I'm supporting those faculty members so they can be supporting the students to have the best educational experience they can.”

Cheryl Regehr, 91�Թ�’s vice-president and provost, calls Woodin an “exceptional leader.”

“Her experience and commitment to strengthening and building relationships within and beyond the Faculty of Arts & Science will help to advance the faculty’s academic goals and enrich the experiences of our students,” she says.

Woodin replaces David Cameron, who has led the faculty since 2013. Cameron, a professor of political science, has held a number of leadership roles within the university, including chair of the department of political science and vice-president of institutional relations. Outside of academia, Cameron has worked with countries around the world to rebuild and reform their governance structures amid conflict.

Woodin says her new role is an opportunity to celebrate and build upon the interdisciplinary nature of the faculty.

“We have colleagues with expertise in a broad range of disciplines, so we want to make sure we’re leveraging the full range of educational and research opportunities this breadth provides.”

This means continuing to provide undergraduate and graduate students access to experts in a variety of fields across the humanities, social sciences and sciences, she says.

“If we continue to produce students who can approach a problem from a variety of different perspectives, this leads to a creativity in thinking – which is of course critical for problem-solving and for innovation.”

In her own lab, Woodin says such an approach has been beneficial when it comes to research on neurodegeneration, including the ethical implications of neurotechnologies.

“When you form strong collaborations, you don't need to be an expert in every field because you're going to use the expertise of your colleagues to combine the power of multiple techniques.”

Woodin first came to 91�Թ� as an undergraduate student at Victoria University, studying biology. The program was then part of the departments of zoology and botany, which later became cell and systems biology, and ecology and evolutionary biology.

While earning her master’s degree at 91�Թ�, Woodin studied the relationship between respiration and circadian systems by researching whether a duck’s ability to hold its breath while diving for food is affected by the time of day.

Woodin’s research ignited an interest in how the brain facilitates the interaction of the body’s systems – a topic she continued to explore at the University of Calgary, where she completed her PhD, and at the University of California, Berkeley, where she did post-doctoral work.

Today, Woodin continues her research in neuroscience, focusing on how neurons communicate in the brain through the release of chemical neurotransmitters and electrical activity. Changes in the strength of that communication, called plasticity, help people learn and remember. Woodin’s lab looks at what happens when plasticity fails in neurological disorders and diseases, primarily Huntington’s disease and amyotrophic lateral sclerosis, or ALS.

Her research is supported by the Natural Sciences and Engineering Research Council of Canada, the Canadian Institutes of Health Research, the Simons Foundation Autism Research Initiative and the Amyotrophic Lateral Sclerosis Society of Canada.

Woodin is also a recipient of the New Ideas Award, a Medicine by Design initiative that aims to accelerate advances in regenerative medicine, for her work using gene therapy to delay the onset of symptoms in neurodegenerative disease.

Woodin’s administrative work in the Faculty of Arts & Science has led to closer and more effective collaboration between the faculty and other divisions across the university. That includes making enhancements to the commerce program, shared with the Rotman School of Management, and first-year mathematics courses in partnership with the Faculty of Applied Science & Engineering.

Woodin says she has enjoyed getting to know people from across the university as vice-dean, sparking her curiosity about a range of subjects.

“I'm making a long list of programs I’m going to have to take many years down the road when I retire,” she says, adding that she has particular interest in cinema studies, criminology and sociolegal studies, and industrial relations and human resources.

Is that 'midlife crisis' really Alzheimer's disease?

noreen.rasbach — Wed, 12 Sep 2018 18:51:43 +0000

Is that 'midlife crisis' really Alzheimer's disease?

noreen.rasbach Wed, 09/12/2018 - 14:51

Cutline

Early-onset Alzheimer’s disease presents unique challenges, when a patient is still working or parenting children. The film Still Alice, starring Julianne Moore, tackled the issue (photo of Gregg DeGuire/Wire Image)

Topic

Research & Innovation

The Conversation

Imagine you tell your 55-year-old mom you’re going to get married and she’s too disorganized to help you with the wedding preparations. Or you put your kids on the bus to elementary school and the 57-year-old driver forgets the route.

These are real scenarios, drawn from my clinical work with patients who have young-onset Alzheimer’s disease.

This is the other face of dementia – no white hair or wrinkles. And it is relatively common. Approximately five per cent of Alzheimer’s patients are younger than 65.

While the underlying pathology of both young-onset and late-onset Alzheimer’s is the same – the abnormal accumulation of proteins called amyloid and tau in the brain – there are significant differences in how the two diseases are experienced.

Patients who are under 65, for example, often have difficulties with language, visual processing and organizing and planning. They have less of the classic memory complaints.

There is also accumulating evidence that young-onset Alzheimer’s progresses faster.

Dementia confused with depression

The path to a diagnosis of Alzheimer’s or other dementia is often long, meandering and riddled with misdiagnosis.

A correct diagnosis is essential for every patient but especially important for younger people. They are often still working and at risk of losing their jobs. They may have young children. When they tell people that something isn’t quite right, they are told they are depressed or must be going through a midlife crisis.

Anne Hunt looks to her husband, Bruce, to be reminded if she already added sugar or not to her dough in their home in Chicago in July 13. Diagnosed with Alzheimer’s in 2016, Anne, who once ran a Chicago cooking school, now has to separate the ingredients into two different sections of the kitchen to prevent errors (photo by Annie Rice/AP)

Many times, younger patients will notice changes in their cognition at very early stages. They may notice increased difficulty in organization or planning. They may forget how to do complex tasks or forget appointments. Cognitive impairment is more obvious when completing highly demanding tasks at work or co-ordinating family logistics.

When a young person goes to see their doctor and reports such changes in cognition, the “d” word brought up is usually depression and not dementia.

Until the correct diagnosis is made, there can be many misinterpretations of their changes in thinking – resulting in conflicts with family, friends and colleagues.

Divorce before diagnosis

Initially, a change in personality can be misinterpreted by the partner as indifference, as a midlife crisis or as something else.

There can be a changing of roles within a couple and it is not uncommon for separation or divorce to occur before a diagnosis is even made.

If young children are involved, it can be difficult for them to understand the change in their parent’s personality.

Getting services for young-onset Alzheiner’s can be especially challenging. There are very few programs that cater to people with dementia under the age of 65.

Support for caregivers and family members of these patients is also lacking. There is a dire need for specialized programs and long-term care facilities that can accommodate those under 65.

‘Use it or lose it’

Although we have no cure for any patients with Alzheimer’s, there are clinical trials that are targeting the abnormal proteins that build up during the disease.

There is symptomatic medication – such as acetylcholinesterase inhibitors – that can help memory.

We also promote a healthy lifestyle that includes aerobic exercise because evidence shows this can slow neurodegeneration. We want people to remain cognitively active and go on learning to help their brain reserve.

Although patients with young-onset Alzheiner’s are impaired in some activities, there are many other activities that they can participate in. “Use it or lose it” is the motto we should live by when it comes to the brain and preserving its function.

Young-onset Alzheimer’s is not the only dementia that typically affects the young. Frontotemporal dementia also strikes young people. And although there are differences in presentation in these two illnesses, many of the challenges facing patients are the same.

Ongoing research is required to better understand this disease. While we search for a cure, we need to appreciate the special needs of this population. We need to target research and services to better serve patients and their families.

Carmela Tartaglia is a clinician-scientist at University Health Network and associate professor at the 91�Թ�.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

91�Թ� joins international ALS project

ullahnor — Thu, 19 Jan 2017 16:05:02 +0000

91�Թ� joins international ALS project

ullahnor Thu, 01/19/2017 - 11:05

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The project will map the DNA profiles of 15,000 people with ALS and create a global database of genetic information on the disease (photo by MV Maverick via Flickr)

Dan Haves

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Dan Haves

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Ekaterina Rogaeva, a professor of neurology at the 91�Թ�'s Faculty of Medicine, is joining an international team of researchers trying to determine why some people develop ALS.

Known as Project MinE, the team helped discover the gene linked to ALS. It includes researchers in 17 nations, and now thanks to support from the ALS Society of Canada (ALS Canada), Canadian researchers have joined the team.

“About half of ALS heritability remains to be explained,” says Rogaeva (pictured left), who is also a researcher at the Tanz Centre for Research in Neurodegenerative Diseases.

In an effort to accelerate the search for a cure, Project MinE plans to map the DNA profiles of 15,000 people with ALS along with a control group of 7,500 people and create a global database of genetic information on the disease. With this new data, the hope is that researchers around the world can better target ALS by understanding the genetic mutations that lead to disease.

“Only together can we obtain sufficient power to analyze DNA samples from several thousand cases and controls so the ongoing whole genome sequencing of each MinE sample is critical,” say Rogaeva.

ALS, or amyotrophic lateral sclerosis, is a neurodegenerative disease that gradually paralyzes the body. Most people who are diagnosed with ALS die within two to five years of diagnosis as there is currently no effective treatment or cure. One thousand Canadians are diagnosed with ALS each year.

Project MinE will receive both the financial support of the ALS Canada and the scientific support of some of Canada’s leading ALS researchers. This is the first cross-Canada collaboration on ALS research and is one of the six projects funded by the ALS Ice Bucket Challenge.

ALS Canada and its research team hope to contribute up to 1,000 DNA profiles to the MinE Project. They are currently seeking federal funding, which would also allow the stored DNA profiles of Canadians with ALS to be added to the database.

“Having such a large sample set could improve understanding of the disease in order to provide the best medical advice to ALS carriers,” Rogaeva notes.