Toronto, ON – Canadian researchers pursuing answers to Alzheimer’s disease have just been awarded $4.5 million in funding, including a record $4 million from the Alzheimer Society of Canada’s Alzheimer Society Research Program (ASRP).

The money will be provided to 38 new research projects from across the country aimed at improving the prevention, diagnosis and treatment, as well as finding a cure for Alzheimer’s disease and other dementias.

“This is a significant boost for dementia research and further builds the capacity of Canadian researchers and research facilities,” says Mimi Lowi-Young, CEO at the Alzheimer Society of Canada.

“I never fail to be inspired by the exciting ideas that the researchers put forward and the possibilities for the outcomes of these studies to improve the quality of life,” says Dr. Lynn Beattie, chair of the Alzheimer Society’s Research Policy Committee. “Great promise is shown by these doctoral and post-doctoral candidates; they’re the foundation for building dementia research.”

This year’s record ASRP funding was made possible by a generous million-dollar donation from Paul Higgins Jr. and Michael Higgins, co-CEOs of Mother Parkers. The money was, raised through the Mother Parkers Remembers fundraising campaign to honour their father Paul Sr. who had Alzheimer’s disease.

Funding also includes $450,000 from the Pacific Alzheimer Research Foundation (Vancouver) in support of researchers based in British Columbia, and $75,000 from the Firefly Foundation (Toronto) to support postdoctoral trainees in Ontario.

The grants and awards are in four categories: Biomedical Doctoral and Post-doctoral Awards; Biomedical Grants; Quality of Life Doctoral and Post-doctoral Awards; and Quality of Life Grants. Recipents are as follows:

BIOMEDICAL AWARDS 2013

Biomedical Post-doctoral Awards

Chenjie Xia, Harvard University

Project: Affective processing in behavioural variant frontotemporal dementia

Diagnosing behavioural variant frontotemporal dementia (bvFTD) remains a challenge, despite it being as common as Alzheimer’s disease in patients younger than 65 and causing devastating functional deficits in those affected. This study investigates the emotion processing deficits in patients with bvFTD and how their social function is affected by these abnormalities. Through a battery of experimental tasks, questionnaires and MRI scans, we ask whether specific relationships can be found between patients’ ability to detect emotion cues, their physiologic changes in response to emotion cues (e.g. increased heart rate, blood pressure, sweating), and patterns of brain region changes on MRI. We will also look at how these changes relate to patients’ everyday life symptom severity. No previous study has looked at all these aspects of the disorder in conjunction. The results of this study could help diagnose bvFTD more accurately and better understand the basic mechanisms underlying their social function deficits.

Ido Strauss, University of Toronto

Project: The neuromodulatory effect of deep brain stimulation of the fornix on memory networks in Alzheimer’s disease

This study aims to explore the functional organization of memory related neural networks, and by doing so improve our understanding of how memories are encoded and how the process can be influenced by Deep Brain Stimulation (DBS) strategy in Alzheimer’s patients. Alzheimer’s disease is a progressive neurodegenerative disorder characterized by the gradual deterioration of affected individuals’ memory, intellect, and autonomy. A novel intervention consists of the implantation of Deep Brain Stimulation (DBS) electrodes of the fornix is currently taking place at the Toronto Western Hospital. The present study aims to evaluate the potential neuromodulatory effect of DBS stimulation of the fornix on memory performance in these patients and characterize the underlying neural changes. To accomplish this aim, patients will undergo a functional magnetic resonance imaging (fMRI) exam before and 12 months after the surgery. In each session the neural responses during an intentional formation of memories task will be tracked.

Liesel-Ann Meusel, University of Toronto

Project: Resting-State Network Connectivity in Older Adults with Impaired Fasting Glucose and Type 2 Diabetes Mellitus

Alzheimer disease and type 2 diabetes mellitus share a common pathology (namely, insulin resis-tance), and Alzheimer’s disease is thought to be a type of diabetes that affects the brain, specifically. While type 2 diabetes does not cause Alzheimer’s directly, it contributes to the progression of neurodegeneration; effects that are mediated by increasing brain insulin resistance. There is an abundance of research on the cognitive, structural, and functional brain changes in Alzheimer disease, but the early consequences of insulin resistance on functional brain networks are understudied. To address this, my project will use functional magnetic resonance imaging to study brain networks in individuals with type 2 diabetes, a condition that results in mild brain insulin resistance. This research will provide information about the early effects of insulin dysregulation on brain function and progression of Alzheimer pathology. This work may uncover potential targets for early intervention that could delay dementia onset.

Razieh Eskandari, Simon Fraser University

Project: Improved Molecular Probes to Evaluate the Role of Glycosylation in Alzheimer Disease

The pathology of Alzheimer’s Disease (AD) is characterized by two different pathologies in the brain; plaques and intracellular aggregates known as neurofibrillary tangles. The formation of plaques result from accumulation of the insoluble amyloid β peptide. The tangles are made up of a protein called tau that normally ensures that the highway on which molecules are transported in cells of the brain remains stable. Recently, modification of tau with a sugar has been implicated in AD. Because this sugar modification is derived from glucose, its levels on tau decrease as glucose impairment occurs in the early stages of AD. Therefore, increasing levels of this sugar modification could be beneficial to slow the progression of AD. We aim to produce useful inhibitors that act efficiently to increase the levels of this sugar modification in models of AD. These inhibitors will ultimately advance this approach to prevents the death of the neurons.

Zhongxiao Wan, University of British Columbia

Project: Adiponectin as a novel mechanism linking obesity to increased risk of Alzheimer’s disease

Individuals with obesity have an increased risk for developing Alzheimer’s disease (AD) and related dementias, but it’s not clear how obesity increases the risk. We have identified a fat derived molecule called adiponectin as a potential factor linking obesity to increased risk of AD. Levels of circulating adiponectin are reduced in obesity and this results in negative effects in various peripheral tissues. However, very little is known about the effects of adiponectin in the brain. This project aims to uncover whether reduced adiponectin links obesity to increased AD risk. Using cell culture and rodent models, we will determine whether adiponectin can protect against the brain pathology that contributes to AD. Understanding the role of adiponectin in AD related pathology holds promise for identifying potential therapies that could target adiponectin for the prevention and/or treatment of AD and dementia in of the growing proportion of our society who are obese.

Anastasia Noel , Université Laval

Project: Repeated mild craniocerebral trauma: Impact on tau pathology and effects of an LXR agonist

Alzheimer’s disease (AD) is the primary cause of senile dementia. It is characterized by the presence of senile plaques, which are composed of amyloid peptides, and neurofibrillary tangles, which are composed of tau protein. Numerous studies suggest that craniocerebral trauma increases the risk of dementia and of AD in particular. Interestingly, senile plaques and neurofibrillary tangles are found in the brains of persons who have sustained craniocerebral trauma. This suggests that the characteristic proteins of AD are implicated in the neuropathogenesis of this type of trauma. Our objective is to study the effects of craniocerebral trauma on the development of abnormal forms of tau protein, in order to understand how this kind of trauma may promote the development of AD. This project may lead to the development of new therapeutic strategies to treat these pathologies and improve the treatment of patients who sustain craniocerebral injuries.

Biomedical Doctoral Awards

Wai Hang Cheng, University of British Columbia

Project: The interaction of mild repetitive traumatic brain injury and apolipoproteinE (apoE) genotype on the development and progression of Alzheimer’s Disease (AD)

Alzheimer’s disease (AD) is the most common form of dementia, affecting half of the population over 85 years old. There is currently no cure, yet its impact is increasingly significant as our population continues to age. Mild Repetitive Traumatic Brain Injury (mrTBI), which is common in contact sports like football and hockey, may increase AD risk. Importantly, apolipoprotein E4 (apoE4), a confirmed AD genetic risk factor, may be a common factor for poor recovery after mrTBI and increased AD risk. This study will investigate whether mrTBI accelerates AD in animal models with different apoE genotypes. Drugs that improve apoE function will be tested for their ability to prevent accelerated AD after mrTBI. This study may provide insights on how mrTBI may affect AD development, particularly for apoE4-carrying athletes in contact sports. It may also demonstrate the potential to ameliorate increased AD risk through regulating apoE levels after mrTBI.

Mahwesh Saleem, University of Toronto

Ceramides and Response to Exercise in a Cognitively At-risk Population

Alzheimer’s disease and heart disease are intimately linked. Those with heart disease show subtle early changes in memory performance and increased risk of Alzheimer’s disease. Early memory changes can sometimes be reversed by exercise; however, there is wide variability in response. The by-products of the breakdown of certain dietary fats, called ceramides, are involved in heart disease. We suggest that ceramides can also damage brain cells and limit cognitive response to exercise. We will follow 129 heart disease patients over a 6-month exercise intervention and measure blood ceramides and memory performance before and at 3 and 6 months during an exercise program. We will determine if those with higher ceramides show less improvement in memory performance despite exercise. A close relationship will suggest that blocking the effects of ceramides might prevent brain and memory changes, leading to new treatments that will preserve memory function later in life.

Leah Cuddy, University of Western Ontario

Project: Regulation of the high-affinity choline transporter activity and trafficking by its association with lipid rafts

Dysfunction of cholinergic neurons is responsible for the cognitive decline seen in several neurodegenerative disorders including Alzheimer’s disease. Choline is taken up into cholinergic nerve terminals by the high-affinity choline transporter (CHT) where it is used for acetylcholine production. Increasing evidence suggests a role for cholesterol in the pathogenesis AD. Cholesterol is enriched in lipid rafts; microdomains in the cell membrane that regulate protein activity. Lipid rafts may influence CHT activity by altering the ability of CHT to interact with the amyloid precursor protein (APP), which binds CHT and influences its activity in cholinergic neurons. APP is cleaved to generate toxic beta-amyloid peptides, which are a hallmark feature of Alzheimer’s disease pathology. My studies will provide the first mechanistic data on cholesterol-related changes to CHT function. This is required to understand the normal function of these widely distributed neurons and how they are altered in neurological disorders.

Daniel Felsky, University of Toronto

Project: Neuroimaging and Genetics to Detect Early Neural Risk for Alzheimer’s Disease

The proposed study aims to assess the genetic risk posed by a known Alzheimer disease (AD) risk gene using detailed neuroimaging and cerebrospinal fluid protein levels in healthy individuals before symptom onset. While basic disease-gene association studies have revealed important genetic risk pathways for Alzheimer disease, our approach analyzing specific brain structures in healthy individuals, before the onset of AD symptoms, across the lifespan and at multiple time points, has the potential to identify when, how, and where risk is conferred. Further, we will analyze cerebrospinal fluid levels of Alzheimer-related proteins in both healthy individuals and subjects with pre-AD symptoms and track how the same SORL1 mutations affect changes across time. If we are successful in identifying specific areas of the brain and crucial time points at which this genetic risk is exerted, we may be able to better inform future AD interventions targeting this risk pathway.

Anthony Dudilot, University of Montreal

Project: Implication of Regulator of Calcineurin1 (RCAN1) on the abnormal synaptic transmission and plasticity in Alzheimer disease

One of the early impairments believed to occur in Alzheimer disease is a weakening of connections between neurons, i.e. decrease in synaptic transmission. My goal is to study the implication of different proteins in this critical process. Due its key role in synaptic depression, the regulation of Calcineurin1 would be a potential mechanism to explain the erroneous synaptic transmission observed in the disease. To answer this question I will combine some of the most advanced technologies in neuroscience like electrophysiologic recordings from neurons expressing various proteins and confocal microscopy to analyze their localization in the cell. This fundamental research is innovative as it brings a different perspective on AD given that our hypothesis is not primarily driven by an Amyloid-beta or Tau-dependent mechanism but tries to integrate these mechanisms into a more global view of changes in synaptic transmission occurring during the development of AD.

Maya Dickler , Université Laval

Project: Effects of anesthesia on the pathological markers of Alzheimer’s disease

Alzheimer’s disease (AD) causes neuronal death and memory loss. Two types of protein clusters are present in the brains of patients who die from AD: senile plaques, composed of beta-amyloid peptides, and neurofibrillary tangles, composed of tau protein. General anesthesia may be a factor in the development of the disease since patients with AD are considered to be at particular risk of developing dementia. Our objective is to study the effects of different anesthetic drugs and surgery on the development of abnormal forms of tau protein. This project will thus provide a better understanding of the effect of anesthetic drugs and surgery on AD pathology. It also opens the door to more advanced clinical studies to evaluate the real impact of anesthetic and/or surgical interventions on patients.

BIOMEDICAL GRANTS 2013

Sébastien Hébert, Université Laval

Project: In vivo study of miR-132 dysfunction in sporadic Alzheimer’s disease

MicroRNAs (miRNAs) are short regulatory RNAs that have a huge impact on biological systems, with established roles in multiple human diseases. Our group recently identified a number of miRNAs that are downregulated in Alzheimer’s disease (AD). In this study, we will characterize the in vivo role of miR-132 in AD neuropathology. MiR-132 is among the most severely downregulated miRNAs in AD brain. Interestingly, accumulating evidence suggests that miR-132 plays a critical role in various neuronal functions and memory formation. In preliminary findings, we could demonstrate that miR-132 deficiency in mice caused increased Tau phosphorylation and BACE1 expression, reminiscent of AD symptoms in humans. We will now follow-up on these observations to understand the role of this miRNA in AD development. To this end, we will develop and study novel AD mouse models. This project will benefit from a unique combination of scientific expertise and state-of-the-art morphological, biochemical, and genetic analyses.

Cheryl Wellington, University of British Columbia

Project: Revisiting the vascular contribution to Alzheimer’s Disease

Alzheimer’s Disease (AD) is the most common cause of failing memory in the elderly. Because the brain uses 25% of the body’s total blood supply, keeping blood flowing properly through the brain is essential for neurons to remain healthy and functioning well throughout life. One way that amyloid-forming Aβ peptides leave the brain is by drainage along the brain’s blood vessels. In healthy people, Aβ drains efficiently. However, in AD, Aβ peptides get stuck within the brain’s blood vessels, which may impair blood flow and starve neurons. Our proposed studies will test whether genetic or drug-based methods that specifically enhance Aβ drainage from the brain’s blood vessels can prevent AD in mice. The significance of our work is that this approach may provide a novel therapeutic approach for AD that works from the inside of blood vessels and will be safe for all AD patients.

Margaret Fahnestock, McMaster University

Project: Role of Tau in BDNF Down-Regulation in Alzheimer’s Disease

Developing a cure for Alzheimer’s disease has been difficult, partly because it is not well understood how abnormal brain deposits (plaques and tangles) cause memory loss. Removing these brain deposits after they form has not been effective at restoring memory. In contrast, BDNF (brain-derived neurotrophic factor), a molecule required for survival and function of nerve cells and their connections, restores memory in Alzheimer’s disease animal models. This supports BDNF as a powerful therapeutic brain repair molecule. We have shown that components of abnormal brain deposits reduce BDNF in Alzheimer’s disease brain, causing memory loss. Our proposed research addresses how one such component, called Tau, contributes to reduced BDNF. Understanding how BDNF is lost in the Alzheimer’s disease brain will provide new ways to prevent it. It may also enhance development of new treatments to repair nerve cells and to monitor and restore memory loss associated with Alzheimer’s disease.

Benjamin Blencowe, University of Toronto

Project: Investigating the Function of Alternative Splicing Regulatory Networks Misregulated in Alzheimer’s Disease

This research aims to improve the lives of patients suffering from Alzheimer’s disease by identifying new methods for the detection and treatment of the disease. Previous studies suggest that mutations cause many diseases by disrupting the way proteins interact with each other. Additionally, changes in alternative splicing have been linked to Alzheimer’s disease. Alternative splicing is an important process that generates enormous functional and regulatory diversity in animals, and we have recently shown that it plays a widespread role in controlling protein interactions in cells. We will determine whether changes in alternative splicing associated with Alzheimer’s disease result in altered protein interactions and will investigate how these altered protein interactions contribute to disease pathology. Our proposed research thus represents a novel approach to facilitate the development of new methods to diagnose and treat Alzheimer’s disease.

William Jia, University of British Columbia

Project: Stress-related cytoplasmic TDP-43 aggregation and its role in neuronal apoptosis in a cell culture model of PGRN deficiency Alzheimer’s Disease

Neurodegeneration occurs in many neurological disorders such as and Alzheimer’s disease (AD). Two proteins named progranulin (PGRN) and TDP-43 have been found to be associated with Alzheimer’s disease (AD). We have established a cell culture model that recapitulates many aspects of human PGRN deficiency and leads to changes in TDP-43 as observed in AD patients. We have also developed peptides that can effectively prevent TDP-43 neuropathy and blocking the interaction between TDP-43 and caspase 3, a crucial protein for cell death. Surprisingly, the latter also protected neurons from dying caused by other neuronal insults. We will try to understand the role of TDP-43 in neurodegeneration. Particularly, we will study why blocking the interaction between caspase 3 and TDP-43 can protect neurons. This study will help us to understand more about the aging process of the brain as well as mechanisms of AD and other neurodegenerative diseases.

Ging-Yuek Hsiung, University of British Columbia

Project: Characterization of Dementia due to mixed Alzheimer and Subcortical Vascular Pathology

Over half a million people in Canada suffer from dementia today, costing the Canadian society over $15 billion dollars annually. Alzheimer disease and stroke are the first and second most common causes of dementia in the elderly. These two diseases often occur together in the brain, making it difficult to know which disease is contributing more to their cognitive decline. Recently, new tests on spinal fluid, magnetic resonance imaging, and positron emission tomography, have begun to allow us to identify and quantify Alzheimer and stroke pathology in the living brain. We will make use of these technologies to study how the two diseases interact with each other to cause memory and cognitive problems, and to understand how the two diseases cause changes in the brain. Our findings will greatly improve dementia patient care, and also improve testing of new drugs under development.

Kari Hoffman, York University

Project: Memory and neural circuit function following direct stimulation treatment for Alzheimer’s disease

The explosive growth in the prevalence of Alzheimer’s disease underscores the need to improve therapies and outcomes. Deep-brain stimulation (DBS) of the fornix – one of two main pathways to the hippocampus – reversed the drop in neural connectivity typically seen in the hippocampus of Alzheimer’s patients and improved memory in some. What remains unclear is how to obtain the greatest benefits, and for the greatest proportion of Alzheimer’s patients. For this, we need a better understanding of the neural–circuit changes that occur following a given stimulation protocol, to improve the type of memory that is a hallmark of impairment in Alzheimer’s patients. We propose to test in preclinical models the effects of various DBS-f stimulation protocols on declarative/relational memory and hippocampal function. The outcomes will inform the optimal treatment parameters for the patient population, leading to the best treatment strategies to alleviate the debilitating memory impairments in Alzheimer’s disease.

Maria Rahja, McGill University

Project: Neu
ral correlates of context memory in middle aged adults with vs. without a family history of late onset Alzheimer’s Disease

Our episodic memory declines with age and can be an early sign of Alzheimer’s disease (AD). The brain changes linked to this memory loss is present in preclinical stages of AD and may precede the disease onset by several years. In fact, early deficits in memory are already apparent by midlife. I propose using novel brain imaging methods to measure brain activity and brain volume in healthy middle aged adults with, and without, risk factors for AD, and compare these results to young adults not at risk for AD. Results from my research will inform us: 1) what initial brain changes are linked to the onset of memory deficits in midlife, and 3) which of these changes are associated with increased AD risk. This information will provide us with possible neural targets for the design and tracking of future programs aimed and preventing memory decline and AD in our society.

Edith Hamel, McGill University

Project: Hypertension as an exacerbating contributor to cerebrovascular and memory deficits in Alzheimer’s disease

Hypertension is a major risk factor for Alzheimer’s disease (AD), and both represent the most prevalent diseases of the aging population. Surprisingly, however, there is virtually no information on how they interact and how hypertension can initiate or precipitate the onset of AD. We suggest that hypertension will worsen the impact of the AD promoting molecule amyloid beta (Aß) by impairing its clearance from brain, which will aggravate the already compromised capacity of the brain to maintain proper perfusion and homeostasis in key areas involved in learning and memory. Using transgenic AD mice, we will ask i) whether the pathology develops earlier or more aggressively in AD mice with concurrent hypertension, ii) if the aggravating effect of hypertension on AD pathology is related to increased cerebrovascular oxidative stress, and iii) if antihypertensive and antioxidant treatments will be equally effective in preventing or reversing the detrimental effects of hypertension on AD.

Stephane Lefrancois, Université de Montreal

Project: Characterization of a novel therapeutic target for the treatment of Alzheimer’s disease

Alzheimer’s disease is a progressive, neurological disorder that is predicted to affect 1 in 85 people by 2050. Current treatments offer symptomatic relief, but do not delay or halt the progression of the disease. The cause of Alzheimer’s disease is thought to be due to the accumulation of plaques in the brain composed of the amyloid-beta peptide generated by cleavage of the amyloid precursor protein (APP) by the beta-secretase 1 (BACE1). Blocking the function of or decreasing the amount of BACE1 could help reduce the amount of amyloid-beta peptide produced and provide a therapeutic strategy to treat Alzheimer’s disease. So far, specific inhibitors of BACE1 activity have not been clinically successful. Our previous work has identified a mechanism to decrease the levels of BACE1 in cells. Our findings could lead to development of novel therapeutic approaches to Alzheimer’s disease by understanding in greater details the basic biology of BACE.

Susan George, University of Toronto

Project: Reduced BDNF signaling in cortical parvalbumin-positive inhibitory interneurons underlies cognitive impairment in Alzheimer’s disease: Therapeutic role for dopamine D5 receptors

Alzheimer’s disease (AD) is a progressive brain disease that severely impacts cognitive and mental functions e.g. memory, learning, reasoning, and is characterized by the presence of plaques and tangles in brain neurons. There is no cure for AD and no effective therapy exists to relieve these cognitive impairments. We will focus on how a reduction in AD brains of brain-derived neurotrophic factor (BDNF), may cause these defects by inducing a cascade of events within the neurons. We will also examine a novel therapeutic role for activation of the dopamine D5 receptor in AD as we showed that this could increase BDNF and improve cognitive function in animals and thus may potentially reverse the process. The D5 receptor belongs to a family of receptor proteins in the body that 40-50% of currently available drugs work through, making it a very effective molecule to which a drug can be designed.

Tiina Kauppinen, University of Manitoba

Project: The role of PARP-1 as a modulator for microglial functions in Alzheimer’s disease

Activation of brain immune cells is well established in Alzheimer’s disease, but their role on disease progression is not completely understood. Cell culture studies have shown that certain functions of immune cells can kill brain cells, while others are protective. Understanding the role of microglia could identify a treatment for Alzheimer’s disease and related dementia. In this study I will use novel system that allows me to specifically manipulate brain immune cell activation in Alzheimer’s disease mouse models. I will prevent immune cell activation and evaluate effects on different cell types present in brain, and overall disease progression. I will similarly evaluate effect of continuous brain immune cell activation in Alzheimer’s disease mice model. I will also evaluate whether brain immune cells have similar role in female and male mice.

Biomedical Young Investigator Grants

Lisa Munter, McGill University

Project: Lipid/APP metabolism as a new target for therapeutic exploration in Alzheimer’s disease

The research project investigates the contribution of cholesterol and vascular risk factors to Alzheimer’s disease. Recent genetic studies observed one key regulatory protein of cholesterol metabolism to be protective against Alzheimer’s disease. When this protein, named CETP, is impaired and cannot work properly, the plasma lipid levels are overall beneficial and the prevalence of Alzheimer’s disease decreases. Interestingly, drugs which impair CETP currently are being evaluated as a treatment for atherosclerosis in large clinical trials. We want to investigate how (i) impaired CETP proteins affect the molecular pathways leading to Alzheimer’s disease and (ii) if the novel drugs, i.e. Anacetrapib and Evacetrapib, will prevent the pathogenic processes of Alzheimer’s disease. If so, our findings may suggest the use of these well-tolerated drugs not only in the treatment of atherosclerosis but also of Alzheimer’s disease. Thereby, we hope to contribute to finding effective treatment strategies against Alzheimer’s disease.

QUALITY OF LIFE AWARDS 2013

Quality of Life Post-doctoral Awards

Pooja Viswanathan, University of Toronto

Project: A Wizard-of-Oz Study to Inform the Design of An Intelligent Wheelchair for Long-Term Care Residents with Dementia

This research involves the evaluation of an intelligent powered wheelchair for older adults with dementia in long-term care facilities. Cognitively-impaired older adults are often excluded from powered wheelchair use because of safety concerns, even when they cannot walk or self-propel in manual wheelchairs. This leads to reduced mobility and increased caregiver burden. My objective is to determine how intelligent wheelchairs can increase mobility and independence for older adults with dementia. I will conduct an exploratory study with the target users who will use an intelligent wheelchair to navigate in realistic scenarios. Few intelligent wheelchair studies have been carried out with the target population, and they only provide collision avoidance support and/or are tested in controlled environments. My rese
arch will provide key insights on user needs and inform the design of a safe and effective method for independent navigation, thus potentially improving quality-of-life for users with Alzheimer’s disease and other dementias.

Renée Biss, Baycrest Centre for Geriatric Care

Project: Co-opting implicit strategies to boost memory for face-name associations in individuals with amnestic mild cognitive impairment

Improving memory important for social interactions can benefit quality of life for individuals at risk of dementia, such as those with mild cognitive impairment (MCI). One of the most effective ways to keep aging well and slow the progression of dementia is to stay engaged in social and leisure activities. Unfortunately, many individuals with MCI withdraw from social activities because of difficulty remembering the names of new friends and acquaintances. This proposal will test a new method to help individuals with MCI remember connections between names and faces, by tapping into preserved implicit memory (memory without conscious awareness) to compensate for declines in conscious, effortful memory. More specifically, presenting reminders of face-name associations in an unrelated task may boost memory by providing an opportunity to unconsciously rehearse the connections. Results will be integrated into a memory intervention program that helps individuals with MCI to maintain social engagement and cognitive health.

Carlos Roncero, McGill University

Project: Anomia in Alzheimer’s Disease: What causes an inability to name objects and how could the situation be improved?

Why do people with Alzheimer’s Disease often forget the names of things, and what can be done to improve naming? We will examine if people with Alzheimer’s Disease have problems naming objects because they have lost their memory for objects or have difficulty expressing what they do have stored in memory. In truth, both possibilities could exist in people with Alzheimer’s Disease; and be caused by the area of the brain most impacted by the disease. Therefore, we expect to separate people with Alzheimer’s disease who have lost knowledge from memory from those individuals who have difficulty expressing what they still have stored in memory, and check if these different groups of people also have different areas of brain damage. We also believe that stimulating certain areas of the brain can help people with Alzheimer’s Disease express better the information they have stored in memory.

Quality of Life Doctoral Awards

Nicole Carson, York University

Project: Promoting Autobiographical Memory in amnestic Mild Cognitive Impairment with the Self-Reference Effect

The Self-Reference Effect, enhanced memory for self-related information, is an established cognitive phenomenon that has never been investigated in amnestic Mild Cognitive Impairment, a condition that is a risk factor for Alzheimer’s Disease. Mild Cognitive Impairment is characterized by a greater decline in memory than expected for age while other cognitive abilities remain intact. The Self-Reference Effect may specifically benefit the decline in Autobiographical Memory, memory for past personal episodes, exhibited in amnestic Mild Cognitive Impairment. Individuals with amnestic Mild Cognitive Impairment will be compared with healthy controls on three paradigms that measure whether the Self-Reference Effect extends to those with amnestic Mild Cognitive Impairment and improves memory for narrative and autobiographical information. The maintenance of past personal memories in amnestic Mild Cognitive Impairment, due to learned Self-Referential strategies, may slow the functional decline exhibited as individuals progress from this condition to Alzheimer’s Disease.

Chun Liang Hsu, University of British Columbia

Project: Does a history of falls indicative of increased dementia risk?

Impaired mobility may serve as a useful clinical indicator for increased risk for progressive cognitive impairment. Worldwide, one new case of dementia is detected every four seconds. Older adults with mild cognitive impairment (MCI) – a transition stage between normal aging and dementia – are at significant risk for developing dementia. Older adults with MCI also tend to have impaired mobility, consequently leading to falls. My M.Sc. work showed that falls negatively impact neural networks. It is unknown whether older adults with history of falls are at greater risk for progressive cognitive decline. The objective of this project is to investigate whether older fallers with MCI are at higher risk for progressive cognitive decline than non-fallers. Fallers and non-fallers with MCI will be recruited and asked to undergo fMRI scanning and cognitive testing. The goal is to provide an efficient method for clinicians to identify those with MCI at high risk for conversion to dementia.

Quality of Life Grants 2013

Sherry Dupuis, University of Waterloo

Project: Enhancing Person-Centred and Relational Care through Research-Based Drama

Recent culture change initatives in dementia care in Canada have called for the adoption of person-centred and relational care models in long-term care settings, yet translating these care models into practice has proven difficult. Traditional approaches to translating the principles of person-centred and relational care models have not had sustained impact. Recent research suggests that the arts may be a more effective means of shifting images, understandings and actions in healthcare. This project aims to explore how an innovative educational tool, a new research-based drama on dementia care, might enhance understandings of person-centred and relational care and the adoption of these care principles into practice for staff working in long-term care homes. Results from this study will expand our understanding of the ways in which research-based drama works as a knowledge translation strategy and ultimately enable more humanistic and relational care practices in dementia care.

Roger Butler, Memorial University of Newfoundland and Labrador

Project: Telegerontology: A novel approach to optimize health and safety and to “age in place” among people with dementia in Newfoundland and Labrador

Over 500,000 Canadians (7500 in NL) suffer from dementia which will balloon to 1.1 million in the next generation according to the “Rising Tide” document by the Alzheimer Society of Canada, 2010. The objective of this project is to enhance the caregiver/patient dyad and thereby improve care ‘in place’ for people with dementia by using computer technologies linking the specialist care to rural remote areas. 4 primary care practices in rural areas will be randomized such that their patients will receive either telegerontology( computer based home support) or control intervention(usual care) for 6 months with follow-up at 6 and 12 months. This research is original and has not been done before. Primary outcomes include caregiver stress ,home safety, and reduction in agitated, aggressive behaviours with secondary outcomes being delay to institutization and improved caregiver satisfaction. By providing specialized care in place we hope people suffering from dementia will stay home longer.

Vanessa Taler, University of Ottawa

Project: Cognitive function and neuropsychological assessment in bilingual MCI and AD

Over half the world’s population is bilingual, as are an increasing number of Canadians. While bilingualism is known to affect cognitive function, clinicians still lack tools and measures to accurately assess French-English bilinguals in Canada. This research will develop suitable tools
and norms for this population, focusing on tasks that are most affected by bilingualism (picture naming, verbal fluency, and tasks examining executive function). We will assess 360 monolinguals and bilinguals: healthy younger and older adults, and people with mild cognitive impairment (MCI) and Alzheimer’s disease (AD). The research has clinical importance, as we will produce a picture naming task specifically developed for these populations, as well as norms for verbal fluency and executive function performance that are critically needed by clinicians. It is also of theoretical importance, as it will shed light on the alterations in language and cognitive performance that are observed in bilinguals with MCI and AD.

George Heckman, University of Waterloo

Project: Ensuring High Quality Care for Canadians with Alzheimer’s Disease and Related Disorders: Developing Quality Assurance and Standardized Care Processes for Primary Care Memory Clinics

The assessment and management of people with dementia can be improved with primary care-based and specialist-supported Memory Clinics. The primary aim of this study is to develop Quality Assurance (QA) procedures for such Memory Clinics. The QA procedures will be used first to optimize the physical examination. Memory Clinic clinicians and supporting specialists will be surveyed with questionnaires and interviews to agree on QA processes, define which components of the physical examination are necessary in a Memory Clinic, develop a training program, and evaluate the effectiveness of the QA processes in optimizing physical examination in Memory Clinics. Findings from this study will lead to formal QA mechanisms to ensure the ongoing provision of high quality primary care for patients with dementia, and more effective use of health system resources. Results will further develop this model of care and the QA process which can be applied to other chronic diseases.

Anne Bourbonnais , Université de Montreal

Project: Pilot evaluation of an intervention approach based on the meaning of screaming in persons with Alzheimer’s disease

Screaming in long-term care facility (CHSLD) residents who have Alzheimer’s disease may indicate a diminished state of well-being. Until now, no study has been able to identify effective interventions to deal with screaming. An intervention approach based on the meaning of screaming has been developed. However, the efficacy of this promising approach has yet to be documented. The goal of this project is to evaluate the approach with elderly CHSLD residents with Alzheimer’s disease who are given to screaming, as well as with their families and caregivers. An action-research approach will be used with 18 to 24 elderly patients and their respective family caregivers and primary care providers. Interviews and measures will be used to document the process and the effects of the intervention on screaming frequency and well-being. The ultimate goal of the project is to improve the well-being of the entire CHSLD population.

Isabelle Rouleau, Université du Québec à Montréal

Project: Alzheimer’s disease in long-term care facilities

Memory is the first cognitive ability to be affected in AD. It is surprising to find that few studies have examined prospective memory (PM) problems (difficulty remembering to perform an intended action at the appropriate time, such as taking one’s medication, presenting for an appointment, etc.), since such problems are very common and have a marked impact on functional independence. Since they manifest early, PM problems may constitute a marker for dementia. This project has two objectives. The first will consist of using an ecological PM task to improve the characterization of PM problems observed in persons who present amnesic mild cognitive impairment. The second objective is to apply a cognitive remediation program designed to promote PM functioning, increase functional independence, and enhance quality of life.

QUALITY OF LIFE YOUNG INVESTIGATOR GRANTS

Simona Maria Brambati, Universite de Montreal

Project: Differentiating language symptoms and anatomical features in Alzheimer’s disease and semantic variant of primary progressive aphasia

Patients with Alzheimer’s disease not only exhibit memory problems but may also manifest difficulty in finding the right word for objects or pictures at early stages of the disease. However, these symptoms often represent the early manifestation of another dementia syndrome, a semantic variant of Primary Progressive Aphasia (PPA-SV). The general goal of this research proposal is to better understand and differentiate between the nature of these language deficits and the anatomical features of these patients. To achieve this goal, a set of experimental language measures and sophisticated imaging approaches will be combined. This represents a fundamental challenge in the field of Alzheimer’s disease and related dementia research. In fact, understanding the nature of the language deficits in diseases of dementia may be beneficial for (1) developing specific language rehabilitation programs and (2) recommending communication strategies for caregivers and family members to improve social interactions.

Dominique Giroux , Université Laval

Project: Evaluation of the capacity of elderly persons with cognitive deficits to care for themselves and administer their property: validation of a computer-based decision model to guide health professionals and social services

The Canadian population is aging and this phenomenon is having an impact on the work of health professionals and social services, who are increasingly called on to assess the capacity of elderly persons with cognitive deficits to care for themselves and administer their property. The objective of this project is to test a new computer-based tool designed to guide and support these assessments. It is a complex process that can have major consequences for the individual because declaring an elderly person legally unfit involves important legal procedures. Yet, no adequate or comprehensive tool is currently available to ensure that the assessment process employed by health professionals is rigorous and systematic. This study will make it possible to test a computer-based tool and evaluate its capacity to support health professionals in their assessments and decision-making.