Difference between revisions of "Team:McMaster/HP/Silver"

 
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   <h2><span style="color: #ebe8e8;">Dr. Paul Fraser</span></h2> <p style="line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;"><span style=" color: #ebe8e8; background-color: transparent; font-weight: 400; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;">— <i>July 13th, 2018; Tanz Centre, University of Toronto (Research stakeholder)</i></br></p>
 
   <h2><span style="color: #ebe8e8;">Dr. Paul Fraser</span></h2> <p style="line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;"><span style=" color: #ebe8e8; background-color: transparent; font-weight: 400; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;">— <i>July 13th, 2018; Tanz Centre, University of Toronto (Research stakeholder)</i></br></p>
   </br><p style="line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;"><span style=" color: #ebe8e8; background-color: transparent; font-weight: 400; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;">Our interview with Dr. Fraser allowed us to gain insight into how misfolding of amyloid-beta causes it to fold into fibrous structures known as neurofibrillary tangles. These tangles directly interfere with normal brain functioning and eventually lead to Alzheimer’s Disease. Contrary to our first hypothesis where the amyloid beta directly causes AD, the misfolded protein instead causes a chain of events to occur -- and only at the end of these events would a person develop AD. We relayed this knowledge to our Wet Lab team in order to better integrate expert insights into our own project development, seeing how different scientific theories lay the path to different scientific experiments and understandings.</br></br></br></br></br></br></span></p></br><p><hr /></p>
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   </br><p style="line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;"><span style=" color: #ebe8e8; background-color: transparent; font-weight: 400; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;">Dr. Fraser believes that current communication between researchers and the public is sufficient. He also described the difficulties that the research community has faced in finding a cause for Alzheimer's disease - if it is even possible to isolate a single cause. Dr. Fraser echoed what we have heard from other stakeholders; unfortunately, research into Alzheimer's disease was side-tracked by the amyloid-B hypothesis, which is now being questioned regarding its relation to the disease. More specifically, misfolding of amyloid-beta causes it to fold into fibrous structures known as neurofibrillary tangles. These tangles directly interfere with normal brain functioning and eventually lead to Alzheimer’s Disease. Contrary to our first hypothesis where the amyloid beta directly causes AD, the misfolded protein instead causes a chain of events to occur -- and only at the end of these events would a person develop AD. We relayed this knowledge to our Wet Lab team in order to better integrate expert insights into our own project development, seeing how different scientific theories lay the path to different scientific experiments and understandings.</br></br></br></br></br></br></span></p></br><p><hr /></p>
  
 
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Latest revision as of 04:00, 18 October 2018

The Interviews


In order to understand Alzheimer’s disease from multiple perspectives, the Human Practices team set out to interview experts from different backgrounds. We were able to learn about the physiological and biological aspects of Alzheimer’s disease by interviewing Dr. John Provias, Dr. Margaret Fahnestock, Dr. Ellen Ryan, and Dr. Paul Fraser. We also had the chance of interviewing people who understand Alzheimer’s disease in terms of its care and management, including clinical nurse Trish Corbett. Additionally, we spoke with Phyllis Fehr, who has Alzheimer’s disease and is an international advocate and partner in many Alzheimer’s initiatives – including the Ontario Dementia Advisory Group and the Dementia Alliance International. All together, these interviews provided us with a few main takeaways: the task of finding the cause of Alzheimer’s disease is an arduous one, and international research is uncoordinated; Alzheimer’s disease is poorly understood by the public and highly stigmatized; and appropriate care for individuals with Alzheimer’s disease is sorely lacking.



Dr. John Provias

July 6th, 2018; McMaster University (Research stakeholder)


Alzheimer’s Disease is not due to a single, simple biological cause, but rather is the outcome of a complex system of biological hallmarks. For many decades, the Amyloid Beta hypothesis, which focuses on the amyloid beta protein, has been the most dominant approach in studying AD. Dr. Provias shared four reasons why he thought we have still yet to find a treatment for AD. First, amyloid beta, which has traditionally received the most attention, may not be the most central player in AD pathogenesis. Second, most trials were implicated in patients who were in advanced stages of AD. Third, a combination of amyloid with other factors was not considered. Lastly, study designs may have been too simplistic to study a multifaceted condition like AD.
There is a huge need for AD treatment as a large proportion of the population is affected by this condition. Dr. Provias suggested it will be important to direct attention to earlier detection of the disease as that will make it easier to design a treatment.




Phyllis Fehr

July 12th, 2018; Alzheimer Society of Canada (Community stakeholder)


We had the amazing opportunity of speaking to and learning from Phyllis Fehr. Phyllis was able to tell us about her experiences with lewy-body dementia and early-onset Alzheimer’s disease. When she was referred to a neurologist, Phyllis was told to bring a family member to the follow-up appointment. She brought her husband to the second appointment and upon walking in the door, the neurologist spoke only to her husband. Throughout the entire appointment, including the diagnosis, Phyllis was ignored and made to feel as though she didn’t exist. At that point, Phyllis argues that she was “prescribed disengagement”. This was a phrase that came up often in our discussion with her, and she uses it to demonstrate that when someone is diagnosed with Alzheimer’s disease, they are told that they cannot do the same things that they used to do, and that they should essentially give up. By telling patient this, Phyllis believes that it causes them to withdraw from activities and society, which only fuels the progression of the disease. This was understandably frustrating for Phyllis, who feels as though people with Alzheimer’s should be encouraged to remain active in their community and to keep doing things that they enjoy. She argues that we need to stop labelling these individuals as disabled and start seeing them for the individuals that they are, who still have things to offer.




Dr. Paul Fraser

July 13th, 2018; Tanz Centre, University of Toronto (Research stakeholder)


Dr. Fraser believes that current communication between researchers and the public is sufficient. He also described the difficulties that the research community has faced in finding a cause for Alzheimer's disease - if it is even possible to isolate a single cause. Dr. Fraser echoed what we have heard from other stakeholders; unfortunately, research into Alzheimer's disease was side-tracked by the amyloid-B hypothesis, which is now being questioned regarding its relation to the disease. More specifically, misfolding of amyloid-beta causes it to fold into fibrous structures known as neurofibrillary tangles. These tangles directly interfere with normal brain functioning and eventually lead to Alzheimer’s Disease. Contrary to our first hypothesis where the amyloid beta directly causes AD, the misfolded protein instead causes a chain of events to occur -- and only at the end of these events would a person develop AD. We relayed this knowledge to our Wet Lab team in order to better integrate expert insights into our own project development, seeing how different scientific theories lay the path to different scientific experiments and understandings.








Trish Corbett

July 20th, 2018; Joseph Brant Hospital, HELP program (Community stakeholder)


Trish Corbett is a clinical nurse specialist who leads the Hospital Elder Life Program, a hospital volunteer program which provides physically and mentally stimulating checkups for patients over 70 years old.
She emphasized how no two patients with dementia are alike, and that the harmful stereotype that associates AD with a deprivation of personhood is false. Trish shared with us how families often do not understand dementia well, and how important it is for a family member to access community resources in order to better take care of themselves and their loved one. Above all else, she encouraged those without dementia to advocate strongly for patients so that their voices are not diminished.







Dr. Margaret Fahnestock

July 24th, 2018; McMaster University (Research stakeholder)


Dr. Fahnestock studies neurotrophins- proteins that induce survival, development, and functions of neurons- in pathogenic systems such as AD simulated mice models. Two important neurotrophins she studies are Brain Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF). She explained to us how the scientific community had been preoccupied with explaining AD through looking at the amyloid beta protein, and how limited gains from this endeavor have made many corporations withdraw from research of AD. For this reason, there have been significant reductions in available funding for basic biological research studying AD in Canada.
Dr. Fahnestock believes that there should be more communication from researchers to the general public, although the lack of platforms to communicate and translate technical vocabulary into simpler terms remain as obstacles. She expects the field will begin to get more interesting as the scientific community finally is becoming more perceptive to different models of studying AD than just through amyloid beta.




Dr. Ellen Ryan

July 26th, 2018; McMaster University (Community stakeholder)


Members from our team also enjoyed speaking with Dr. Ellen Ryan, a psychologist of aging at McMaster University. Dr. Ryan is extremely knowledgeable about the way that society treats individuals with Alzheimer’s disease and, in turn, how these individuals view themselves. Dr. Ryan began by talking about some misconceptions surrounding Alzheimer’s disease - one of them being that individuals with the disease are unable to do everything that they used to be able to do. She explained that, even when a person with Alzheimer’s cannot do something - for example, continue a conversation with someone that took place a day before - that does not mean that they are never able to do those things. They may not be able to do it one day, but the next they might.
Additionally Dr. Ryan discussed how the nature of conversation surrounding Alzheimer’s is always negative. Nobody, she says, ever really focuses on things that might be gained from Alzheimer’s. She gave us an account of someone she knew who, after developing Alzheimer’s disease was able to create beautiful paintings. Dr. Ryan encourages everyone to not focus solely on the things that someone with Alzheimer’s cannot do, but to also focus on the things that they can do. She also encourages us to see the person underneath the disease because that person is still there.



The Future of mGEM Human Practices

This year, the topic of the iGEM project was on understanding alzheimer's, a debilitating neurodegenerative disease and socially relevant to the broader McMaster, Hamilton, and Canadian communities. Building upon conversations with researchers and community stakeholders, has led McMaster iGEM to pursue research projects in an area of public health relevance for the Hamilton and Canadian community. Through this strategic alignment, we hope to pursue issues relevant to our local community and engage with stakeholders to advocate and raise awareness for these important issues, beyond just the lab. We see this relationship of conducting basic scientific research on a core public health issue as a strength of our team, and we look forward to continuing and building upon our relationship with the Hamilton community.