Meet our Summer Students: Tia Al Saidi and Adebola Adeniji!
Tia Al Saidi: Experiences as a Summer Research Student
As a recent graduate from the University of Winnipeg with an Honours degree in Psychology, I was fortunate to receive the ENRRICH Summer Studentship award to continue my passion for research. Over the summer of 2024, I worked in the Hearts and Minds Lab under the supervision of Dr. Leslie E. Roos, an Associate Professor of Psychology and Pediatrics and Child Health at the University of Manitoba. I was involved in multiple research projects that investigated programs designed to promote family wellbeing.
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Experiences as a Summer Research Student
As a recent graduate from the University of Winnipeg with an Honours degree in Psychology, I was fortunate to receive the ENRRICH Summer Studentship award to continue my passion for research. Over the summer of 2024, I worked in the Hearts and Minds Lab under the supervision of Dr. Leslie E. Roos, an Associate Professor of Psychology and Pediatrics and Child Health at the University of Manitoba. I was involved in multiple research projects that investigated programs designed to promote family wellbeing.
What was my summer project about?
The title of my summer research project is “The Impact of Elevated Attention Problems in Preschool Children of Mothers with Depression”. We looked at baseline data of mothers who took part in our Building Regulation in Dual Generations (BRIDGE) program. BRIDGE is a 16-week online program that combines Dialectical Behaviour Therapy (DBT) and parenting skills training to support mothers with depression who are parenting a 2.5 to 5-year-old child. With the assistance of Dr. Tasmia Hai, an Assistant Professor at McGill University, we looked at the prevalence of attention challenges in children of mothers who participated in the BRIDGE program to inform potential treatment support needs for at-risk families. We found that over 9.3% (19/205) of the preschool children were at-risk or met criteria for elevated attention challenges, and that mothers of these children reported more parenting stress, anxiety, sleep challenges, and anger compared to mothers of children who did not present attention challenges. In comparison, previous studies have found the prevalence rates of attention-deficit/hyperactivity disorder (ADHD) symptoms in preschool children to range from 4.6% to 15.6% (Nomura et al., 2013; Thomaidis et al., 2017; Willoughby et al., 2012). Our work highlights the need for more directive screening for attention challenges in young children of mothers with depression, because they may require additional support to promote child and family wellbeing.
What did I learn from this summer experience?
This experience helped me expand my research skills and knowledge in the field of psychology. Working in the lab as a summer student allowed me to collaborate with other students and academics, improved my scientific writing, presentation, and leadership skills. Another skill that I did not realize would be so important was organization. When you are involved in multiple research projects, it is easy to lose track of deadlines and details. To prevent this, I found it helpful to keep a running list of current tasks I am working on with their due dates and level of priority. It is also useful to add deadlines to a digital calendar that will notify you when an important date is approaching.
Future directions
Currently, I have taken on a new position in the Hearts and Minds Lab as a research coordinator. In this role, I am assisting with a new project, LightBEAM, which is a self-guided mental health app program that will be delivered to parents across Canada. For the future, my goal is to obtain a master’s and PhD in Clinical Psychology, where I would love to investigate how we can make online mental health programs more accessible and equitable for Canadian families.
References
Nomura, K., Okada, K., Noujima, Y., Kojima, S., Mori, Y., Amano, M., Ogura, M., Hatagaki, C., Shibata, Y., & Fukumoto, R. (2014). A clinical study of attention-deficit/hyperactivity disorder in preschool children--prevalence and differential diagnoses. Brain & development, 36(9), 778–785. https://doi.org/10.1016/j.braindev.2013.11.004
Thomaidis, L., Choleva, A., Janikian, M., Bertou, G., Tsitsika, A., Giannakopoulos, G., & Anagnostopoulos, D. C. (2017). Attention Deficit/Hyperactivity Disorder (ADHD) symptoms and cognitive skills of preschool children. Psychiatriki, 28(1), 28–36. https://doi.org/10.22365/jpsych.2017.281.28
Willoughby, M. T., Pek, J., Greenberg, M. T., & Family Life Project Investigators (2012). Parent-reported Attention Deficit/Hyperactivity symptomatology in preschool-aged children: factor structure, developmental change, and early risk factors. Journal of abnormal child psychology, 40(8), 1301–1312. https://doi.org/10.1007/s10802-012-9641-8
Adebola Adeniji: Neurodevelopmental Disorders through the Lens of Rett Syndrome
This summer I had the opportunity to be a research summer student in the Beattie Lab through ENRRICH’s studentship. My summer research was focused on Rett Syndrome, a poorly understood neurodevelopmental disorder. Before summer 2024 if someone had asked me what Rett Syndrome was, I would have had to look it up on the internet because I had never heard of it. As I started my summer research, I realized how little I knew about neurodevelopmental disorders in general.
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Neurodevelopmental Disorders through the Lens of Rett Syndrome
This summer I had the opportunity to be a research summer student in the Beattie Lab through ENRRICH’s studentship. My summer research was focused on Rett Syndrome, a poorly understood neurodevelopmental disorder. Before summer 2024 if someone had asked me what Rett Syndrome was, I would have had to look it up on the internet because I had never heard of it. As I started my summer research, I realized how little I knew about neurodevelopmental disorders in general. The truth is, to most people just like me, Rett Syndrome is a foreign concept. There is a disconnect between those impacted by Rett Syndrome and those who are not. I would explain it as a lack of interest in things that do not affect us. This lack of interest is usually unconscious—you don’t see what you are not looking for. The knowledge gap between those affected and those unaffected by Rett Syndrome was something that interested me as I continued my summer research. And while I am not an expert in all things Rett Syndrome, I know more than I did prior to my summer studentship and for that, I am grateful because I can help bring awareness to neurodevelopmental disorders in particular Rett Syndrome. So where do I begin?
Meeting Rett Syndrome
Rett Syndrome is a neurological disorder linked to the X-chromosome, primarily affecting females. Previously, it was believed that males with Rett Syndrome rarely survived until birth. However, it is now recognized that some males can be affected, though this is far less common, and the syndrome appears different in males. Males with Rett Syndrome also have a higher mortality rate, largely because they have only one copy of the X-chromosome, whereas females have two, allowing one to compensate for mutations in important genes. Rett Syndrome mainly impacts brain development with symptoms worsening over time. There is a wide range of neurological and developmental impairments associated with Rett Syndrome such as growth delays, regression in motor development, difficulties with social interaction, and epilepsy. In most patients (>95%), the alteration of the MeCP2 (Methyl-CpG binding protein 2) gene has been discovered to be the root cause of Rett Syndrome. MeCP2 is a fundamental gene necessary for major body functions, such as protein production. It is also a conserved gene which means it has not changed much with evolution, highlighting how important it is.
Fan1: A potential therapeutic target
In patients with Rett Syndrome, a loss of MeCP2 can damage their DNA. When DNA is damaged, the cell usually repairs it using a similar piece of DNA as a template, a process called homology-directed repair (HDR). You can think of it like when you are fixing a broken bookshelf. To repair it, you could try to find an identical bookshelf (a template) and use its parts or design as a reference to fix yours to be exactly the way it was. This method ensures precise repair but only works if you have access to that second identical bookshelf, which isn't always available. In DNA repair, HDR requires a similar DNA template (like a sister chromatid) to make sure the repair is accurate, but this template is only available at certain times in the cell cycle.
Another method to repair DNA is called non-homologous end joining (NHEJ) which is an approach that does not require a template to repair DNA. Now imagine fixing the same broken bookshelf, but instead of finding an identical one to copy, you just glue the broken pieces together. It’s a faster method, and you don't need anything else to complete the repair. It might not be as perfect, but it gets the job done quickly with the materials you have. In DNA repair, NHEJ doesn’t need a template; it just joins the broken ends of DNA together. While it might be less precise, it's a quicker and more readily available fix.
Fan1 is a gene that produces an enzyme capable of breaking down unusual DNA structures caused by alterations. Research using mouse models has shown that losing Fan1 function can actually improve Rett Syndrome symptoms caused by the complete loss of the MeCP2 gene. One hypothesis of how it is able to do this is by switching from the HDR method of DNA repair to the NHEJ repair mechanism. This may cause less stress for certain cells in the brain, resulting in a reduced level of damage, and potentially better patient outcomes. However, the exact mechanism of how a loss of Fan1 can improve the health of MeCP2 mice still needs to be resolved.
My Role
As a summer research student, my role was to analyze the differences in the shape and size of the brain of aged mice with different Rett phenotypes (characteristics). The cortex is the region of the brain that is the most affected by Rett Syndrome. The purpose of my research was to identify the differences in phenotypes so we could further observe these changes at a cellular level to track their development over time and potentially pinpoint when the characteristics started to develop. We do this because we want to understand how these phenotypes affect brain development over time. We also want to target a potential treatment window. My analysis looked at three different phenotypes, namely wildtype (both copies of Fan1 present) as the control to see what the mice look like untouched, Fan1 homozygous (both copies deleted) as the first experimental model, and Fan1 heterozygous (one copy deleted) as the second experimental model to observe for any differences.
Why study Rett Syndrome and Fan 1?
Personally, my response to this question usually comes from the complexity of Rett Syndrome. No two people with Rett Syndrome are the same. An identical MeCP2 gene alteration can be associated with very different symptom severity in different people. The substantial health impact and the limited treatment options available for people living with Rett Syndrome are important reasons to study Rett syndrome. By understanding Rett Syndrome at the genetic level, researchers might be able to link and relate certain cell functions to other diseases and potentially find cures for them. Research has also shown that Fan1 is involved in other neurodevelopmental disorders such as Huntington’s disease and might be a potential key player in our scientific journey to predict, prevent, and treat these conditions.
Future Directions and Goals
The results of my summer research found no significant morphological difference between the phenotypes, but we have to understand the keyword ‘morphological’. In this study, we only looked at the overall shape and size of the cerebral cortex and did not analyze cellular differences which is one of our major future directions. There are six layers of the cerebral cortex that are all comprised of different and similar cells whose proportions are different based on the layer of the cortex we are analyzing. There is much left to learn about the relationship between Fan1 and Rett Syndrome.
To conclude, my summer research experience was nothing short of amazing and I learnt so much. I learned new skills like mouse handling (which was initially a bit of a challenge for me because I was absolutely terrified), and I was able to meet amazing people whom I worked with over the summer. I also now understand how important communicating science with the general public is. It is an important part of our job as scientific researchers to demystify topics that the public is hesitant to talk about or is even unaware of, as this is a way to close the knowledge gap that sometimes happens between science research and the public.
Note of Thanks
I want to say thank you to Dr. Robert Beattie and all the members of the Beattie Lab. I also want to say thank you to the ENRRICH Research Theme for their support.
References
Enikanolaiye, A., Ruston, J., Zeng, R., Taylor, C., Schrock, M., Buchovecky, C.M., Shendure, J., Acar, E., and Justice, M.J. 2020. Suppressor mutations in Mecp2-null mice implicate the DNA damage response in Rett Syndrome pathology. Genome Res 30(4): 540–552. doi:10.1101/gr.258400.119.
Published November 1, 2024
About the Author
Tia graduated from the University of Winnipeg in 2024 with a B.A. Honours degree in Psychology. She has been with the Hearts and Minds lab since Fall 2023 and began her new position as a research coordinator in Summer 2024. Her research interests involve addressing the needs of underrepresented populations within Canada through the implementation of eMental Health interventions.
About the Author
Adebola Adeniji is an undergraduate student at the University of Manitoba majoring in Microbiology. She worked as a summer Research Student under the supervision of Dr. Robert Beattie. She has always had an interest in human genetics, particularly in neuroscience and human-pathogen relationships that disrupt normal brain development.