Complex concerns come with determining when it’s time to hang up the keys: How can this topic be approached in a respectful way with loved ones? Can a plan be created for the future so that the person with dementia can continue to enjoy activities after they’ve decided to stop driving?

Dr. Mark Rapoport, geriatric psychiatrist, acting head of Geriatric Psychiatry at Sunnybrook, and one of the researchers behind a new Canadian online resource called the Driving and Dementia Roadmap shares insight into how individuals with dementia and those close to them can face this challenge together.

What is dementia?

Dr. Rapoport: Dementia occurs when a person experiences changes or a decline in memory, and the ability to think, problem solve, or make decisions, that are significant enough to affect their daily life and everyday activities. Although dementia is most common in older adults, it is not a ‘normal’ part of aging.

The Alzheimer Society of Canada says dementia impacts more than 600,000 people in Canada. It’s estimated that by 2030, one million Canadians will be living with dementia.

When is it time for a person with dementia to stop driving?

Dr. Rapoport: Some concerns around driving that are common with dementia can include forgetfulness or getting lost in familiar places. If a person is feeling unsure or anxious while driving or if there are any safety concerns expressed by family or friends about the individual’s driving abilities, it is important to seek information and the advice of a healthcare professional for next steps.

Some individuals with mild dementia may continue to drive safely and some may have to stop driving right away. It’s important to be aware that as the disease progresses, they will inevitably have to stop driving. It can be difficult to know exactly when driving has become or will become unsafe.

After receiving a dementia diagnosis, it is critical for the individual and their family to watch for changes in that person’s driving and consider whether they can continue to drive safely.

For people with moderate or severe dementia, driving is dangerous as the brain functions needed to react quickly and make rapid decisions for safe driving have deteriorated. By these stages, driving must stop.

What is the Driving and Dementia Roadmap?

Dr. Rapoport: The Driving and Dementia Roadmap or drivinganddementia.ca, is a free, online, and Canadian resource created to help older adults living with dementia, their family, friends, and healthcare teams, and provide them with information around the decision to stop driving.

The Driving and Dementia Roadmap was developed by researchers from Sunnybrook, Baycrest, and the Canadian Consortium of Neurodegeneration in Aging.

I have been working in the field of geriatric psychiatry for many years, and over time patients and families identified the need for easily accessible and credible information about driving and dementia and driving cessation. This is the first time that helpful materials have been curated into a one-stop-shop website that includes resources useful for all provinces and territories across the country.

The Driving and Dementia Roadmap website includes information, videos, worksheets, as well as strategies to help people living with dementia and their families navigate the challenging conversations, emotions, and planning that comes with the decision to stop driving.

Making a plan for the future

Driving cessation is a major life change for a person with dementia. There are often concerns about a loss of independence or identity.

It is important to include the individual with dementia in discussions about driving. This can help in creating a plan and making alternative transportation arrangements for when the person can no longer drive. The website provides strategies to ensure that the person with dementia continues to live a fulfilling life even after driving stops.

The Driving and Dementia Roadmap website doesn’t provide individuals with recommendations about their driving. It is for educational and informational purposes. Patients and families are strongly encouraged to reach out to a qualified healthcare provider with any concerns for their guidance, advice, and support as they navigate the driving and dementia journey.

Read the news release to learn more about the Driving and Dementia Roadmap.

For more information go to: drivinganddementia.ca

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In a recently published preclinical study, Dr. Isabelle Aubert, senior scientist at Sunnybrook Research Institute and postdoctoral researcher Dr. Kristiana Xhima successfully used focused ultrasound to non-invasively deliver a therapeutic in the brain, targeting brain cells affected by Alzheimer’s disease and improving cognition.

The study has been published in the journal BRAIN.

This is the first study to demonstrate that repeated focused ultrasound blood-brain barrier modulation in the basal forebrain is safe in the presence of Alzheimer’s pathology, and when combined with a growth factor-related therapeutic, can lead to therapeutic effects. Focused ultrasound harnesses the power of sound waves to transiently open the blood-brain barrier, a protective barrier that prevents toxins or potentially helpful therapeutics in the bloodstream from entering the brain.

This promising research comes at an urgent time. It is estimated that more than 600,000 Canadians are currently living with dementia. According to a recent report from the Alzheimer’s Society of Canada, rates of dementia, including Alzheimer’s disease, are projected to rise to nearly 1 million people in Canada by 2030. Below, Drs. Aubert and Xhima discuss how their breakthrough research is an important advancement on the road to developing effective therapeutic approaches for the disease.

Dr. Aubert and Dr. Xhima

What was the impetus behind your study?

Dr. Aubert: This preclinical study was a follow-up to our previous proof-of-concept study that used MRI-guided focused ultrasound to non-invasively deliver a type of growth factor-related therapeutic (D3) to brain cells called cholinergic neurons, which are important for learning and memory and most vulnerable in Alzheimer’s disease. D3 stimulates important signaling mechanisms in brain cells that are related to the tropomyosin receptor kinase A (TrkA) pathway. The TrkA pathway is critical for neuroprotection, plasticity and survival of cholinergic neurons; engaging it with D3 promotes the resilience of brain cells against Alzheimer’s pathology.

In our first proof-of-concept study, we had found that D3 combined with focused ultrasound efficiently stimulated key survival and neuroprotective pathways, and in the short-term, helped to restore brain cell communication (also known as neurotransmission). Yet for clinical translation and impact, it was critical for us to study whether focused ultrasound combined with D3 could rescue cognitive function – the rationale and goal of the current study.

What did your current study find?

Dr. Xhima: In this preclinical study, we demonstrated the therapeutic potential of D3 in a preclinical model of Alzheimer’s and showed its impact on learning, memory and cognitive flexibility. The D3 therapeutic agent, like many promising therapeutics, does not have the properties required to efficiently cross the blood-brain barrier (BBB) and reach its targets deep in the brain. To overcome this challenge, we coupled the intravenous administration of the therapeutic drug D3 with MR-guided focused ultrasound to non-invasively, locally and transiently increase BBB permeability in key brain regions for the effective delivery of D3 from the blood to the brain.

Following brain delivery of the therapeutic agent with focused ultrasound, performance in cognitive tasks was improved. The treatment of focused ultrasound with the therapeutic D3 led to enhanced neurotransmission in cholinergic neurons, which are highly vulnerable to injury in Alzheimer’s disease. We also observed beneficial effects on brain regeneration – new brain cells were formed in the hippocampus, an area of the brain that plays a major role in learning and memory, and amyloid plaques, common in Alzheimer’s, were reduced in targeted brain areas.

What could these results mean for patients and clinicians in the future?

Dr. Aubert: Although still early-stage, this work is an important and fundamental step in the development of potential treatments for the disease. The results also open the door for many other regenerative agents, that normally do not cross the BBB, to be tested and delivered using this drug-delivery platform. This is the first study to demonstrate that a growth-factor related agent delivered to the basal forebrain and associated cortical and hippocampal areas repeatedly using focused ultrasound BBB modulation is safe and can lead to therapeutic effects in the presence of Alzheimer’s pathology. These results provide a major step forward in terms of drug delivery that can be very promising for clinical translation.

Dr. Xhima: Another key feature of this preclinical research is that we tested focused ultrasound delivery of a TrkA-stimulating agent in the presence of established Alzheimer’s pathology. In contrast to many previous studies, here we showed that this therapeutic approach rescued cognition and improved Alzheimer’s related pathologies once they were already established, similar to how patients would present in the clinic. The beneficial effects of the treatment were also broad with respect to several key systems affected in Alzheimer’s disease. This makes us very hopeful about this therapeutic approach because it certainly represents an important step forward for potential clinical development.

What’s the next step in this work?

Dr. Xhima: The improvements in cognitive function we saw in the preclinical models studied lasted for several weeks, which raises the question: how often will treatment need to be repeated for therapeutic effects that can last over months and years?

Dr. Aubert: In addition to this, we’re interested in taking an exploratory approach to look at other molecular pathways in the brain that could also be affected by this treatment, since our results went beyond what was expected with target engagement on cholinergic neurons alone.

It’s important to note that this research is still at an early stage and has not yet moved to clinical trials. We are hopeful that this fundamental research will translate into the clinic in the near future, as we continue to explore therapeutic options to stop degeneration and promote regeneration in Alzheimer’s disease and dementia.

Hear Dr. Aubert and Dr. Xhima discuss their findings in further scientific detail on the BRAIN podcast, the official podcast of Brain and Brain Communications.

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Despite the statistics, innovative research is underway at Sunnybrook to help bring hope to the fight against Alzheimer’s and dementia.

“We may be entering a new era with possible effective treatments for this disorder which affects whole families and is increasingly prevalent with populations aging,” says Dr. Sandra Black, director of the Dr. Sandra Black Centre for Brain Resilience and Recovery. “Continued research is critical as we aim to develop and discover meaningful treatments and prevention strategies for Alzheimer’s and dementia.”

Here are just some of the innovative ways that Sunnybrook clinicians and researchers are on the leading edge of research in the detection, prevention, and treatment of Alzheimer’s and dementia.

Apathy and Agitation in Alzheimer’s

At Sunnybrook, clinical studies are underway on apathy and agitation in Alzheimer’s patients, where researchers are exploring ways to help decrease apathy in patients. This can help increase their interest in activities and their emotional responsiveness, which may help improve their quality of life, as well as their caregivers’.

Early on-set dementia

In a world-first study, a team of Sunnybrook scientists are trying to identify biomarkers, or biological clues in the brain, such as blood flow, that could demonstrate an early-onset frontotemporal dementia in people who have a genetic predisposition to the disease.

 

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Innovative technology

Researchers are also looking for innovative ways to deliver medicine or therapeutics directly to the areas of the brain involved in Alzheimer’s disease.

Preclinical research is exploring the delivery of gene therapy to treat Alzheimer’s and help improve memory and boost brain health.

One of those methods uses focused ultrasound technology, where ultrasound waves are precisely directed to a targeted area of the brain to help open the blood-brain barrier (BBB), which can allow potentially helpful medications to reach brain regions involved in Alzheimer’s and dementia, without having to use scalpels. Research teams have shown evidence that the BBB can be temporarily opened safely using focused ultrasound, an exciting first step in exploring a new way for therapeutics to be delivered to the brain.

Who will get Alzheimer’s disease?

Sunnybrook scientists are also using artificial intelligence and machine learning to try and detect early signs and symptoms of dementia to improve treatment and prevention of the disease.

Research is also underway to learn more about risk factors for dementia among diverse ethnic groups including individuals of South Asian and Chinese descent, as these groups are often under-represented in dementia studies.

The latest Sunnybrook research has also demonstrated that having poor vascular health may accelerate cognitive decline in patients with dementia and small vessel disease.

Preventing Alzheimer’s

Researchers are finding out how lifestyle can protect individuals from dementia.

While it is critical for cutting edge studies to continue in the search for new treatment and care for patients with Alzheimer’s and dementia, it can also be helpful for individuals to take action themselves to learn more about dementia and how activity can help boost brain health in more ways than one.

From prevention to diagnostics and potential treatment innovations, “We’re at the forefront of discovery for dementia and Alzheimer’s at Sunnybrook,” says Dr. Black. “There’s a lot to be optimistic about.”

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“The main theme of both studies is that people who have both Alzheimer’s disease and poor vascular health decline much more quickly than people who have only one of these conditions,” says Dr. Rabin, a scientist at SRI in the Hurvitz Brain Sciences Program.

There is growing evidence that vascular health and Alzheimer’s disease are closely intertwined, and that poor vascular health may promote the build-up of amyloid and tau in the brain, the two abnormal proteins associated with Alzheimer’s disease. “Preventing vascular disease may also help to prevent Alzheimer’s disease,” says Dr. Rabin.

The findings of the first study were published in Brain and the results of the second study were published in Neurology. Both are highly prestigious journals. Dr. Rabin, who was the only Canadian researcher involved in the studies, collaborated with U.S. colleagues to conduct the research.

Scientist Dr. Jennifer Rabin

What did you learn about the connection between CAA and Alzheimer’s disease?

The Brain study looked at a cerebrovascular condition known as cerebral amyloid angiopathy (CAA), which results from the build-up of amyloid in the blood vessel walls of the brain. When there is accumulating amyloid in the vessel walls it can cause vascular brain changes, such as small hemorrhages and blood flow problems. Although amyloid plays a central role in both CAA and Alzheimer’s disease, the two conditions are considered distinct.

The study is titled, “Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline.”

Dr. Rabin and colleagues from multiple U.S. centres asked the question: What influence does CAA have on the build-up of tau (the more detrimental hallmark pathology of Alzheimer’s disease) and cognitive decline, either alone or in combination with amyloid burden?

They analysed data from 1,722 autopsied subjects recruited from one of three long-running medical studies. Data included annual clinical and cognitive evaluations, along with neuropathology. The researchers tested associations between CAA, tau burden and cognitive decline, both independently and together with amyloid burden.

They found that the combination of CAA and higher amyloid levels were associated with the greatest tau burden and the fastest rates of cognitive decline.

“Not everyone with CAA has Alzheimer’s disease and not everyone with Alzheimer’s disease has CAA. But they do co-occur at a high rate,” says Dr. Rabin. “We found that if you have both of these conditions, you were much more likely to have tau burden and faster cognitive decline.”

How do classic vascular risk factors affect the brain?

The study in Neurology looked at whether classic vascular risk factors, such as obesity, high blood pressure, smoking and diabetes, leads to faster brain tissue loss and faster cognitive decline when they co-occur with amyloid.

The study is titled “Association of β-Amyloid and Vascular Risk on Longitudinal Patterns of Brain Atrophy.”

Dr. Rabin and colleagues from Massachusetts General Hospital analysed clinical and neuroimaging data from 196 subjects in the Harvard Aging Brain Study, a long-standing, community-based study.

They found that people who had multiple vascular risk factors and high levels of amyloid had greater rates of brain tissue loss and cognitive decline over time. “The take away,” says Dr. Rabin, “is that managing vascular risk factors may slow the progression of Alzheimer’s disease dementia.” This includes controlling blood pressure, lowering cholesterol, maintaining a healthy weight, and refraining from smoking. A good rule of thumb is that what’s good for the heart is good for the brain.

What do these results mean for patients and care providers?

These two studies provide greater support for the idea that vascular health and Alzheimer’s disease interact in ways that increase the likelihood of a dementia diagnosis. “These findings have implications for developing treatments for Alzheimer’s disease,” says Dr. Rabin, “because they suggest that vascular health should be taken into account. Treatments that target poor vascular health and Alzheimer’s pathology are likely to be the most effective.”

How you can get involved

If you are interested in getting involved in Dr. Rabin’s research studies, please send an email to cbhlab@sunnybrook.ca.

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By developing advanced machine learning and artificial intelligence (AI) models and applying them to some of the largest data sets in the world, Dr. Goubran’s team is learning to detect, with greater precision than ever before, cognitive decline years before symptoms arise. Also at the heart of this work is discovering what minute structural and functional changes and network breakdown within the brain can be used as biomarkers, or early/accurate indicators, of neurodegenerative disorders.

“A key missing piece in neurodegeneration research are the algorithms that learn from large amounts of individual data from magnetic resonance imaging (MRI), PET scanning, genomic analysis, and demographics, combined with results from cognitive testing, that can be applied in the clinic,” says Dr. Goubran, a scientist in the physical sciences platform at SRI. “This work is of critical importance because it can provide urgently needed guidance on prevention and personalized treatment decisions.”

[mks_pullquote align=”left” width=”300″ size=”20″ bg_color=”#ffffff” txt_color=”#000000″]“This work is of critical importance because it can provide urgently needed guidance on prevention and personalized treatment decisions.”

Dr. Maged Goubran
Scientist
Sunnybrook Research Institute

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Alzheimer’s disease is one of Canada’s greatest healthcare challenges, currently having a devastating emotional and physical burden (directly or indirectly) on more than 1.1 million people. This number is expected to rise dramatically in the next 20 years. The disease has an estimated health care cost of $10.4 billion annually.

A big focus of Alzheimer’s research and care has been on preventing symptoms earlier in the progression of disease. This tactic relies on identifying healthy adults at high risk of future cognitive decline; these people may have small changes in their brains starting a few decades before the first symptoms appear. While much research has been done in this area, Dr. Goubran and his team are improving on previous approaches in several ways: by building more powerful computational models than in the past, by using larger, more robust population data sets, by focusing on individual rather than group-level predictions (to address the large patient variability) and by pinpointing Alzheimer’s progression in asymptomatic rather than only symptomatic individuals.

Tracking progression of disease

Dr. Goubran is building on earlier research that establishes shrinkage of the hippocampus as a possible early sign of dementia. The hippocampus is the brain’s centre for memory and navigation; it is often one of the first areas to be impacted by Alzheimer’s disease.

The team is developing AI algorithms to map changes in not just the volume but also the shape of the hippocampi (and its subdivisions), as well as other important structures and vascular lesions of the brain during aging. The models are informed by hundreds of brain MRIs from multiple studies including the Sunnybrook Dementia Study led by Dr. Sandra Black, senior scientist and director of the Sandra Black Centre for Brain Resilience and Recovery at SRI. The researchers will use these imaging biomarkers and a normative population of thousands of Canadians to track and predict patient progression.

Others around the world will benefit from these AI techniques, as the team will validate and share them as open-source tools. “We plan to make our algorithms publicly available and easy to use for the research community,” says Dr. Goubran. For patients and clinicians, this could mean improved diagnosis, customized treatments, and better ways to monitor disease-modifying therapies currently being studied.

Mapping network changes

Another area of his research involves studying how well different brain regions are connecting with one another. Altered connectivity could signal problems down the road. “In neurodegenerative diseases like Alzheimer’s, a network disorder, there are a lot of changes in function and structure of brain networks, so we’re doing also a lot of work on that front, trying to develop novel signatures of network dysfunction,” says Dr. Goubran.

This research direction has two foci. One is preclinical work in the laboratory to develop newer signatures (read-outs) of network dysfunction in Alzheimer’s models. The other is developing new computational techniques to analyse functional and diffusion MRI scans in order to better understand and map network changes in-vivo and develop biomarkers. Dr. Goubran was recently awarded a New Investigator Grant from the Alzheimer Society of Canada to help support this work. He collaborates closely on these projects with Dr. Bojana Stefanovic, Dr. JoAnne McLaurin, Dr. Jennifer Rabin, and Dr. Black, as well as groups at McGill and Harvard universities.

The hope is that when altered connectivity between brain regions is detected, a combination drug treatment that targets abnormal buildup of two proteins involved in Alzheimer’s disease – amyloid and Tau – will slow deterioration of key cognitive networks or, if caught early enough in the pre-symptomatic stage, may be able to restore normal connectivity and cognition.

“We’re hoping our work will lead to larger scale efforts to develop combined therapies that will eventually get to the clinic and really push the development of personalized medicine for neurodegenerative diseases,” says Dr. Goubran.

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Dementia is an umbrella term used to describe a decline in thinking abilities that is severe enough to interfere with one’s day-to-day activities. While some degree of forgetfulness is completely normal as we age, the memory loss experienced in the context of dementia is much more severe.

AD is the most common cause of dementia, and is defined by the abnormal build-up of two proteins in the brain: amyloid plaques and tau tangles. The build of these proteins leads to the death of brain cells, which causes the brain to shrink and impacts memory and thinking abilities.

There are many risk factors for dementia. Some, like older age and genetics, can’t be changed. But recent research has shown that up to 40 per cent of dementia cases are linked to risk factors that people can control.

Vascular Risk Factors

Vascular Risk Factors (VRF) are conditions that affect the health of blood vessels that supply oxygen and nutrients to the brain. These include high blood pressure, high cholesterol, obesity, diabetes and smoking. Each of these conditions on their own can increase the risk of dementia, and when they present together, the risk is even higher.

The good news is that we know how to treat VRF. If you have been prescribed medication for high blood pressure, high cholesterol or diabetes, take it as directed and keep up with routine doctor visits. Eat a healthy diet and exercise regularly, as these lifestyle changes can reduce the risk of these conditions. There are also effective strategies to manage obesity and smoking, so don’t hesitate to reach out to your health care team. A good rule of thumb is that what’s good for the heart is good for the brain!

Cognitive Reserve

Cognitive reserve refers to your brain’s ability to cope and keep working, even in the face of damage from diseases like AD. Research has suggested that engaging in mentally stimulating activities throughout own’s life can help build up a high cognitive reserve, offering some protection from AD and other dementias.

Because of these findings, researchers now recommend keeping your mind active throughout your whole life, especially after you retire.

It’s not clear which activities may be most beneficial for the brain, so choose any challenging activity you enjoy. Some examples include playing chess, learning a new instrument or language, doing a puzzle or even socializing with family and friends.

Physical Activity

Several studies have shown that regular exercise can significantly reduce the risk of developing dementia. In our own research, we found that people who engaged in regular physical activity – even in older adults with Alzheimer’s changes in their brain – had less decline in their memory over time compared to those who were sedentary.

It doesn’t really matter what type of physical activity you engage in, as long as it elevates your heart rate. We know that people are more likely to exercise if they participate in activities they enjoy. Choosing social activities, like walking and dancing, can have the added benefit of exercising the body and the mind. Current guidelines suggest doing at least 150 minutes of moderate intensity activity per week, but remember that some movement is always going to be more beneficial than nothing.

Sleep

All of us know that a bad night’s sleep can impair our ability to think the following day. Research has also shown that getting too few hours of sleep may also increase the risk of  developing AD and dementia. It appears that sleep acts like a dishwasher, helping clear out harmful toxins – including amyloid –  from the brain.

To optimize quality sleep, try to go to bed at the same time each night and get up at the same time each morning. Make sure your bedroom is quiet, dark and at a comfortable temperature. Avoid using electronic devices two to three hours before going to sleep. Also, engaging in physically activity during the day can reduce the time it takes to fall asleep at night.

For people who gravitate towards naps, keep in mind that in some cases they can be a sign of a larger health issue or insufficient stimulation during waking hours. Generally, naps can be restorative, as long as they are limited and don’t interrupt your normal and healthy wake/sleep cycle.

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Dr. Rikke Kofoed and Dr. Isabelle Aubert

In a new study, postdoctoral researcher Dr. Rikke Kofoed and senior scientist Dr. Isabelle Aubert and their team at Sunnybrook Research Institute determined the feasibility and safety of two noninvasive methods for delivering gene therapy to the brain in a preclinical model of Alzheimer’s disease.

The study has been published in Molecular Therapy – Methods & Clinical Development.

Alzheimer’s disease is the most common form of dementia, which impacts more than 430,000 Canadians aged 65 years and older. Hallmarks of the neurodegenerative disease include “plaques” and “tangles” composed of toxic protein that develop in the brain and eventually prevent the production of nutrients and the transmission of signals that are necessary for the health of brain cells. Over time, this causes deficits in cell-to-cell communication and functions, leading to memory loss, confusion and difficulty reasoning. There is currently no effective treatment for the disease.

Researchers at Sunnybrook are interested in gene therapy as a potential treatment for Alzheimer’s disease and other disorders of the brain. Gene therapy can replace a gene that is missing or defective. Specific genes can also be added to allow brain cells to stay healthy, produce therapeutics, or generate new cells to curb the disease.

Although gene therapy shows promise in Alzheimer’s disease, the blood-brain barrier poses a challenge for delivering it to the brain. In this study, the research team evaluated two innovative methods to non-invasively deliver gene therapy across the blood-brain barrier: a) focused ultrasound combined with intravenous microbubbles, which increase the permeability of the blood-brain barrier at targeted sites, and b) modified gene carriers, which are capable of crossing the blood-brain barrier and delivering genes to brain cells.

Dr. Kofoed and Dr. Aubert share thoughts on their research.

Dr. Rikke Kofoed in the lab

What did your study find?

Dr. Kofoed: In this preclinical study, we found that depending on which delivery method is used (focused ultrasound or modified gene carriers), a unique distribution of genes is seen in the brain. These findings tell us that in the future, gene therapy can likely be tailored to achieve personalized deliveries of genes depending on disease stage and the type of therapeutic gene.

We also determined that these non-invasive delivery methods have a good safety profile and that the immune response triggered is similar to what is seen after gene delivery using brain surgery. Our findings suggest that the immune response to non-invasive gene delivery can be controlled, as it is currently done in the clinic for other gene therapy approaches.

What could these results mean for patients in the future?

Dr. Aubert: In the past, the delivery of therapeutic genes required invasive surgeries for patients with Alzheimer’s disease. ​Non-invasive and personalized gene delivery to the brain has the potential to increase beneficial clinical effects for the treatment of Alzheimer’s disease. Our preclinical study confirms that focused ultrasound and modified gene carriers are feasible strategies for gene delivery to the brain, and that their immunological effects can be controlled.

What’s next in this research?

Dr. Kofoed: In this study, we used an easily visible “reporter” gene to explore the potency of gene delivery. The next stage of our research will look to deliver a therapeutic gene to target Alzheimer-related pathology in a preclinical model. These studies will help us determine the therapeutic potential of our delivery strategy.

Dr. Aubert: Gene therapy has tremendous potential for the treatments of brain disorders. The current study and the next stage of our research are required steps to evaluate the safety and efficacy of gene therapy approaches. With colleagues and collaborators at Sunnybrook and other institutions, these approaches could one day be brought to patients to halt degeneration and promote brain health for conditions such as Alzheimer’s disease.

Key drivers of Sunnybrook’s research are funding agencies and philanthropic investment. This study was funded with support from the Alzheimer Society Research Program, the Carlsberg Internationalisation Fellowship, the Canada Research Chairs Program, Canadian Institutes for Health Research (CIHR), the Weston Brain Institute, the National Institute of Biomedical Imaging and Bioengineering of the National Institutes of Health and Temerty Chair in Focused Ultrasound Research. Additional funding was received from the FDC Foundation, the WB Family Foundation and Gerald and Carla Connor.

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Answer: In the final stages of dementia, usually around the time when patients are no longer able to communicate or walk, and become bed-bound, a number will also develop swallowing problems, and some will refuse to eat. The swallowing problems can lead to fluids and food entering the lungs instead of the digestive system which can cause “aspiration pneumonia”. This is an agonizing time for caregivers and families who not only recognize eating and drinking as essential for survival, but also as one of the few remaining pleasures that contribute to quality of life for the patient in the end stages of the disease. Support from the medical team, and a realistic review of all available options is essential at this stage.

Exploring the options

Nutritionists and dietitians can provide a variety of recommendations, depending on the severity of the swallowing difficulties. At times this will involve changing the consistency of the diet to make it easier to swallow, and/or thickening the fluids to ensure they end up in the stomach, rather than the lungs. Proper positioning of the patient during the meals will also be suggested. At this point, caregivers and family often begin to think ahead, and wonder whether a feeding tube will be necessary. Feeding tubes, also referred to as “percutaneous endoscopic gastrostomy” (PEG) tubes are inserted through the skin, into the stomach by a brief surgical procedure, allowing artificial liquid nutritional fluids to be given, thus avoiding the need to eat by mouth. While this might sound like an ideal proposition to families, there are no current medical or nutritional scientific societies who recommend this for these situations. Why is that?

A difficult decision

It is generally acknowledged that for patients with end-stage dementia, feeding tubes do not actually improve nutritional status, and they do not improve survival. In fact, there are numerous complications associated with feeding tubes including pain, agitation, and diarrhea. Feeding tubes may not even prevent the aspiration pneumonia they are used for! Some patients will be so uncomfortable with the tubes, that they attempt to pull them out, which can lead to acute medical emergencies. Most importantly, there is no evidence that feeding tubes improve quality of life for the patient.

When treatment teams recommend against the use of a feeding tube, families sometimes argue that they just cannot let their relative “starve to death”. The decision to use a feeding tube needs to be made with the caregiver and family, taking into account the patient’s culture, religion and previously expressed wishes. The team will likely review the information summarized above, and inform caregivers that in general, tube feeding is not recommended as the risks outweigh the benefits.

The best alternative to feeding tubes is “assisted oral feeding”, in which a caregiver helps the patient eat small amounts of food and fluids slowly and carefully. The benefit of this procedure is the close contact between patient and caregiver (the “human touch”), and the more natural form of nutrition. These likely go a longer way to improving quality of life for patients, than any form of nutrition provided through a feeding tube.

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Answer: The studies on the effect of alcohol consumption and the risk of dementia are complicated, confusing, and conflicted. What is known for sure is that prolonged and excessive alcohol use can lead to dementia and other neurological complications. What is much less clear is whether light or moderate drinking might actually prevent dementia.

To answer the question about the possible effects of alcohol consumption on preventing Alzheimer’s disease, it’s important to understand how these studies were done. The studies looking at alcohol use are generally observational in nature. They pick a given population without dementia, ask them about their alcohol intake, and then follow them over time to see who develops dementia. As you might imagine, it can be challenging for researchers to characterize the amount of alcohol consumed, because subjects often underestimate (purposely or subconsciously) the amount they drink. Different subjects will vary in terms of the pattern of drinking (e.g. daily vs weekly binging) and the type of alcohol they drink (e.g. spirits vs wine vs beer). All of these could affect the relationship between alcohol and dementia risk.

Most importantly however, while these observational studies might suggest there is a link between modest alcohol consumption and a decreased risk of dementia, establishing a direct causal (cause and effect) link between the two is impossible. The reason for this is that alcohol consumption might be associated with other, perhaps more important factors that reduce the risk of dementia. For example, modest drinking is also likely associated with greater social contacts, and social stimulation itself likely protects against dementia.

There have been numerous studies over the past few decades investigating this association described above. When the results of these studies are combined, it appears that light-to-moderate alcohol consumption is associated with about a 25 per cent reduction in the risk of Alzheimer’s disease and other dementias compared to people who are non-drinkers. The risk of dementia then increases in those who are heavy drinkers. However, as an example of how conflicting the results of these studies can be, there are two studies, both published in 2015, and both using data from Norway, that come to different conclusions. In the first study of over 25,000 Norwegians followed for up to 17 years, the risk of dementia was significantly higher in abstainers. In the second study of over 40,000 Norwegians followed for up to 27 years, abstaining from alcohol was not found to increase the risk of dementia, though drinking frequently (defined as more than five times in the previous 14 days) was associated with an increased risk of developing Alzheimer’s disease or other dementias.

In terms of the type of alcohol that might be most likely to provide some protective benefit, red wine has received the most attention. Red wine contains a compound called resveratrol, that has been associated with numerous (though largely unsubstantiated) benefits including protecting against heart disease and even increasing longevity. A recent study of resveratrol for patients with Alzheimer’s disease however, failed to demonstrate any clear evidence of benefit and was actually associated with greater brain shrinkage.

While my primary clinical and research practice is devoted to Alzheimer’s disease and memory disorders, my training as a Psychiatrist has certainly coloured my opinions about alcohol use. For prevention purposes, I would clearly prefer that my patients avoid alcohol use, and engage in a “brain healthy lifestyle” which includes exercise, mentally stimulating activities and a Mediterranean type diet. When I’m asked specifically about alcohol intake, I generally recommend avoiding regular use, and certainly no more than one drink per day. Once I have diagnosed dementia, I stress the absolute need for abstinence given the harmful effects alcohol can have on the brain, memory and behaviour once dementia is present.

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Answer: Most definitely. Optimizing hearing and vision for the person with dementia is a valuable and important contribution to care. It makes obvious sense that if a person cannot see, or struggles to hear, they are less likely to attend to information or understand it, and as a result they are less likely to remember. There is good research to suggest that hearing and vision problems are common sources of “excess disability” – a term meant to describe worse cognitive and functional impairment as a result of causes beyond the degree of dementia pathology per se.

Ensuring vision and audiology assessments have been completed is a simple and relatively painless process for most patients and caregivers. Wearing appropriate eye glasses is also a fairly simple intervention with good compliance. Arranging for cataract surgery, may be more challenging, but given the increasing simplicity and excellent tolerability of the surgery, mild to moderate dementia should definitely not be seen as a barrier to improving vision through this procedure. Dealing with hearing loss can be more problematic. Not all types of hearing loss can be improved by hearing aids, and hearing aids can be very difficult to use, or can be poorly tolerated for some people with dementia. While I always recommend consultation with an audiologist, for some patients however, use of a “pocket talker” can be a simple and inexpensive alternative that might be better tolerated than traditional hearing aids.

Regardless of the difficulty involved in optimizing hearing and vision, these interventions are well worth the effort. For example, a recent study in elderly people suggested that wearing hearing aids improved performance on cognitive testing compared to people who didn’t wear hearing aids, even though the group who wore hearing aids had worse hearing. Sensory impairment has also been associated with emotional symptoms like depression in people with dementia. Perhaps even more surprising, psychotic symptoms such as visual hallucinations (seeing things that aren’t there) and auditory hallucinations (hearing imaginary voices) have been associated with vision and hearing problems in people with dementia. Most importantly, there are reports that some of these symptoms can be improved when hearing and vision are improved.

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