Register to attend HERE ! (please note: you MUST register with your college or UK DRI email or you will not receive the links to the sessions!)
If you are a teacher or student from one of our participating schools or outreach programmes please see our separate info page.
Every week throughout Black History Month, Women of the Wohl are hosting 2 speakers who identify as Black researchers in neuroscience and neuro-related research areas. They will showcase their work from a broad range of different neuroscience areas to the King’s College London and UK DRI research community in a 1 hour online seminar on Microsoft Teams. Come along to hear from a wide range of different areas within neuroscience, from institutions around the world and from different career stage researchers!
Each seminar is then followed by a 1 hour informal Q&A discussion aimed at students (undergraduate, masters, PhD) and early career stage researchers, as well as our attending A Level students from London schoools. Although the Q&A discussions are organised with these groups in mind, all other staff are welcome to attend if you wish. Anyone is also completely welcome to just stay for the hour of talks, as your schedules permit. The Q&A session will be an opportunity to ask the speakers anything about their career journey and their lived experience working in research, in a relaxed, informal setting. All King’s College London and UK DRI staff and students are welcome to attend these events: all career levels and all race and gender identities are welcome.
Each event will be chaired by the friendly Women of the Wohl team via audio/video and in the Teams chat function. We will be making sure everyone is treated with respect, feels welcome, safe, & comfortable and that everyone gets a fair chance to speak and ask their questions. You will be able to ask your questions using audio or the chat function in Microsoft Teams. We understand that not everyone finds it easy to ask questions in front of an audience or think of questions on the spot, which is why we’ve also created the option for you to anonymously submit your career-related questions for our speakers in advance here.
How do I register to attend?
If you would like to attend the seminar series you need to register via Eventbrite here. YOU MUST REGISTER USING YOUR KING’S COLLEGE or UK DRI EMAIL OTHERWISE YOU WILL NOT BE SENT THE LINKS TO THE ONLINE SESSIONS. This is so that we can ensure only King’s College and UK DRI staff and students attend, to ensure online safeguarding of our A-level student attendees. You only need to register once for the entire event series and you will be sent the Microsoft Teams link for each week’s meeting.
Session 1 – Thurs 8 Oct
Masters Student, King’s College London
I’m Rebekah, a Jamaican Neuroscience graduate with interests in neurodegeneration and dementia research, specifically frontotemporal dementia and amyotrophic lateral sclerosis (FTD/ALS). I previously studied BSc Neuroscience at University College London (UCL), where I conducted research with Prof Stephanie Schorge and Dr Emma Clayton at the UCL Institute of Neurology. My work investigated synaptic dysfunction in frontotemporal dementia caused by a rare mutation in the gene, CHMP2B. I have recently completed the MSc Neuroscience in Neurodegeneration at King’s College London, working in the lab of Dr Sarah Mizielinska at the UK Dementia Research Institute. There, I investigated disease mechanisms in FTD/ALS caused by C9orf72 mutation and I hope to pursue a PhD in this area. I love all things science communication, widening participation and Jamaican culture (of course!). I am the Miss Jamaica UK 2019-2020 titleholder, an ambassadorial role which allows me to connect with the global Jamaican diaspora.
Twitter @rcsmikle | LinkedIn @rebekahsmikle
Synaptopathy in Frontotemporal Dementia?
Characterising presynaptic dysfunction of mutant CHMP2B
Frontotemporal dementia is the second most common form of early-onset dementia and senile neurodegenerative disease. One rare subtype is caused by a mutation in the gene CHMP2B. CHMP2B is a subunit of the endosomal sorting complexes required for transport (ESCRT) and CHMP2B mutation causes defects in certain protein degradation pathways. The ESCRT pathway is involved in degradation of synaptic vesicle proteins, and preliminary data by E. Clayton and S. Schorge demonstrates that several synaptic proteins accumulate in brains of aged mutant CHMP2B mice compared to age-matched controls. Synaptic vesicle protein accumulation would inevitably cause synaptic dysfunction, an effect not well studied in frontotemporal dementia. This project aimed to characterise this probable ‘synapto-pathogenic’ feature of CHMP2B-frontotemporal dementia, by investigating the subcellular localisation of mutant CHMP2B protein and examining the relative synaptic vesicle protein levels at early postnatal stages. Using immunofluorescence microscopy in mouse cortical neurons transfected with mutant CHMP2B DNA, we found that mutant CHMP2B forms puncta which co-localise with presynaptic marker SV2. Wildtype CHMP2B shows diffuse staining, but also co-localises with SV2. Cycloheximide chase and subsequent western blot were conducted to inhibit protein synthesis in protein lysates and isolate levels of the synaptic vesicle proteins synapsin, synaptophysin and SV2 remaining after protein degradation. While no significant difference was found between mutant lysates and wildtype controls, a surprising trend of increased protein accumulation in wildtype and decreased protein accumulation in mutant samples was observed. Additionally, an SV2 isoform not observed in wildtype samples accumulated in mutant samples. These findings demonstrate that mutant CHMP2B is localised to the presynaptic terminal, but point to the need for further investigation of its mechanism of action, including isoform-specific protein degradation. Understanding the pathogenic agency of mutant CHMP2B at the synapse will be useful for identifying therapeutic targets in CHMP2B-frontotemporal dementia.
Senior Research Assistant & PhD Student, University of Oxford
Connor Scott is a neuroscientist at the University of Oxford, working in the Ansorge Lab in the Nuffield Department of Clinical Neurosciences. In his lab, he works both as a senior research assistant while completing his studies as a PhD student. His research topics include glioblastoma, neurodegeneration, and LCM proteomics. In 2012, he graduated with a BSc in Biomedical Sciences at the University of Greenwich. After his undergraduate studies, he volunteered in several laboratories before receiving a job offer from the University of Oxford in 2013. After working as a scientist for 3 years, he started his PhD project and is aiming to complete it in the next few months.
During his studies, Connor was the Middle Common Room President of his Oxford college, and has a keen interest in public engagement, science communication, and education.
Twitter: @ConnorScott_OX | Website: connorscott.info
Investigating the Human Betz Cell
Classifying neurons and understanding neuronal selective vulnerability is paramount to understanding disease and discovering potential cures. The human Betz cell is the largest cell in the human body, and although first described in 1874 there has not been comprehensive research into the nature of the cell, despite its obvious morphology and clear involvement in amyotrophic lateral sclerosis. Using post mortem human brains as material, my PhD aims to discover unique insights into the Betz cell by using laser capture microdissection coupled with mass spectrometry or RNA sequencing to discover a Betz cell biochemical signature that will aid in future research, discover potential biomarkers, and help explain their vulnerability in disease.
Session 2 – Wed 14 Oct
Erin C. Hanlon, PhD
University of Chicago
Erin C. Hanlon, Ph.D. is a Research Associate Professor in the Department of Medicine, Section of Adult and Pediatric Endocrinology, Diabetes, and Metabolism, at the University of Chicago. She received her undergraduate degree at Duke University and her PhD in Neuroscience from the University of Wisconsin-Madison. As a behavioral neuroscientist, her primary research interests have included the detrimental effects of sleep loss and how sleep benefits health, with particular focus on the links between sleep deficiency, obesity, and diabetes. Specifically, she has focused on the effect of sleep restriction on brain reward and feeding systems as well as peripheral metabolic systems in both rodent and human models.
Sleep Deficiency: A Pathway to Obesity
Dr. Hanlon’s most recent studies have identified a 24hr rhythm in circulating endocannabinoid (eCB) levels, a system that has garnered much attention in recent years for its involvement in the regulation of hedonic food intake. Dr. Hanlon has shown that this rhythm is altered by sleep loss suggesting the involvement of the eCB system and hedonic eating in the excess food intake observed following sleep restriction. Further, she demonstrated that obese individuals have a misaligned endocannabinoid rhythm, suggesting that circadian disruption in the eCB system may constitute a circadian-mediated mechanism contributing to the underlying pathophysiology of obesity.
Jillian E. Franks
University of Missouri-St. Louis
Jillian E. Franks hopes to inspire the next generation of scholars and researchers and create a learning environment that recognizes and celebrates the differences inherent in humanity. Training as a social neuroscientist, Jillian has a Bachelor of Science degree in Neuroscience from Rhodes College in Memphis, Tennessee with a minor in theater. Currently, she is a graduate student at the University of Missouri-St. Louis in the Social Neuroscience and Intergroup Relations Lab. Her early interest in the brain was sparked by a Christmas gift of a toy brain. Overtime, Jillian has participated in programs that support students from historically underrepresented communities interested in science and technology.
During graduate study, Jillian was awarded a Graduate School Minority Master’s Recruitment Fellowship, was second author on a mini-review published in the Journal of Neuroscience Research, and presented research on the effects of sexist comments made toward women STEM majors. Her proposed Master’s Thesis project examines same-race memory bias for skin tone modified emoji faces. Research interests also include neural synchronization, empathy, and cooperation in interracial dyads.
Competing as a high school and college swimmer, Jillian enjoys a leisurely lap around the pool and loves live theatre. Jillian desires to unite her passion for neuroscience and theatre by taking an interdisciplinary approach to the study of acting.
The Other-Race Effect and Emojis: A Memory and ERP Study Using Diverse Emojis
Other-race-effect or own-race-bias is a well-documented phenomenon in memory. Findings suggest that humans are better at recognizing and remembering faces of their own race than other races. Previous research suggests that these results are due to a lack of interracial contact or exposure to other racial groups. Evidence from previous studies has demonstrated that individuals process own-race faces differently than other-race faces, paying more attention to more salient features that become better encoded. While there is empirical support for both hypotheses, it has yet to be studied if the other-race effect for memory extends to people-emojis. Emojis are digital pictures used for electronic communication of emotions, expressions, and meaning. The current studies set out to determine if the other-race effect for recognition memory can be extended to emojis, specifically the category of “people” emojis. Black and White participants will view both light/medium-light skin tone and dark/medium-dark skin tone emojis. Participants will be tested on own-race bias in recognition memory of people-emojis and how it relates to cooperation. In the second study, own-race bias recognition memory and the event-related potentials, P100 and N170, associated with early facial detection and structural encoding, will be examined. It is predicted that both groups will demonstrate own-race bias when recalling emojis.
Session 3 – Wed 21 Oct
University of Cape Town
I am currently doing my Master’s degree in Neuropsychology at the University of Cape Town (UCT). I’m hoping to become a clinical neuropsychologist and open my own memory clinic one day that also provides services to underserved rural communities in South Africa. My research interest lie in cross-cultural neuropsychology, particularly in the development of tests that take context and cultural differences into consideration. I am also interested in epilepsy research, rehabilitation and ways in which to increase quality of life in patients with incurable neurological disorders.
While I was completing my Honours degree in Psychology in 2019, I also worked as a tutor in the Psychology Department at UCT and as a research assistant for two independent studies. One study investigated non-adherence to HIV medication in a local clinic, and entailed the collection of both qualitative and quantitative data. The other study was quantitative and focused on the neuropsychological functioning and MRI findings in patients with HIV in order to understand how HIV encephalopathy affects their memory and behaviour.
In my spare time I enjoy exploring different art galleries and museums because I love the intersection of art with history.
‘Detecting Cultural Influences on Social Cognition: The South African-Adapted NEmo Test Battery’
The psychological construct of social cognition comprises several distinct forms of mental processing that are essential for healthy interpersonal relations. Two separate and hierarchically inferior constructs, emotion recognition and theory of mind (ToM), are central to social cognition and have been the subject of intense neuroscientific study. Although these constructs are universal, numerous studies have shown that cultural-linguistic influences might affect expression of social cognitive abilities in these domains. Given the importance of intact emotion recognition and ToM for adaptive functioning, it is imperative for local research to describe possible cultural and linguistic influences on their expression and to ensure that tools used to assess them are contextually appropriate. In this study, I evaluated a South African-adapted version of the NEmo battery, a newly developed battery by the Swiss Epilepsy Centre. The tasks on the NEmo test battery were translated from their original German into English, and South African faces and voices replaced the original Swiss faces and voices as stimuli for the emotion recognition tasks. South African university students (N = 40; age M = 22.14 ± 3.84 years) completed the NEmo test battery and other standardized cognitive tests. English-speakers and Afrikaans-speakers performed significantly better on tasks assessing ToM than Xhosa-speakers. This suggests that culture influences the expression of this construct. Future research needs to ensure these tasks are adapted to Xhosa to ensure that social cognition is reliably measured in this language group.
University of California San Diego
Alyx Shepherd is the research coordinator for the Women Inflammation and Tau Study (WITS) at UCSDs Altman Clinical and Translation Research Institute. She obtained her undergraduate degree from California State University of Fullerton in three years with a double major in Anthropology and Ethnic Diversities Studies and the goal of becoming an archaeologist. However, an unexpected and life-altering health condition set her on her somewhat unconventional and mostly kismet path toward medicine and neuroscience research.
Her experience in research has been primarily Alzheimer’s and dementia; as well as TBI, fMRI, and neurorehabilitation. These fields of research hold her interest because of the vital necessity for breakthroughs in these areas for underrepresented and marginalized communities. She has spent time as a student at the University of Chiang Mai in Thailand studying the displaced hill tribes of Northern Thailand and teaching inner-city high school students in Medellin, Colombia.
She is the creator and host of the Angry Black Woman Podcast, a podcast that highlights the black American Experience and integrates mental health and mindfulness. In her free time, she enjoys studying foreign languages, writing short screenplays, gardening and long hikes with her pup.
‘Diversity-Focused Recruitment in Neuroscience Research and the Potential Impact on Data Quality’
Pathways to research and medicine can be obscure and this is markedly true for underrepresented populations. It is imperative to not only diversify researchers but also ensure diversity-focused recruitment by embedding diversity and inclusion into research culture. Research has shown that preventative approaches to cognitive decline include social interaction and diet and exercise. My work as a research assistant and office manager at a neurological office piqued my interest in therapeutic interventions in Alzheimer’s. Fostering that interest, I joined a study that aimed to study how Internet-based conversational Engagement impacted the cognitive functions of socially isolated older adults. The study was written to recruit an 80% African American population in an area that simply could not support these numbers. This was something that immediately stood out to me when I began the study and it remained the constant concern throughout.
Methods: In this 12-Month long study eligible participants were randomized to either the intervention or control group. The intervention group received 30-Minute video calls 4 days a week for 6 months then 2 days a week for 6 months to study completion. The control group received 1 weekly phone call that included a fun-fact as a retention method to keep them engaged in the study.
The preliminary results of the study were promising in terms of the main cognitive aims and were expected to continue this trend. The concerns for diversity arose when it became evident that while chat-staff was well trained in the intervention methods they were not trained to work with diverse populations. Thus, many of them found it difficult to connect with the African American participants that were recruited. I raised my concerns about the impact this would have on both our African-American participants and overall study data with the principal investigator and we outlined a plan for how to address these concerns. The need for diversely trained researchers is highlighted here and needs to continue to be highlighted across disciplines, borders, and school curriculums.
Session 4 – Wed 28 Oct
University of Oxford
Hello! My name is Zeinab (Zai for short, she/her). I completed my undergraduate degree at King’s College London in 2018. Currently, I’m a DPhil (PhD) student at the University of Oxford (Department of Physiology, Anatomy and Genetics). I am working in Professor Elizabeth Fisher’s lab, which is a collaboration between MRC Harwell and the UCL Institute of Neurology. Using an interdisciplinary approach, my project is trying to uncover the role of lipid metabolism in ALS-FTD pathophysiology.
I am the Postgraduate Equality and Diversity officer at Corpus Christi College. My goal is to improve representation at Oxbridge and in neuroscience through outreach and science communication. In my spare time, I enjoy exploring new walking routes and reading!
‘A new in vivo model of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD)‘
Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease which is characterised by progressive muscle weakness and subsequent motor defects, due to degenerative changes of upper and lower motor neurons in the brain and spinal cord. Traditionally, ALS was believed to spare cognitive functions. However, ~50% of ALS patients develop cognitive and behavioural impairments, whilst ~15% of patients develop frontotemporal dementia (FTD). ALS and FTD are now considered parts of the same spectrum disorder.
TDP-43 is an RNA-binding protein that is implicated in both ALS and FTD pathology. This protein is normally localised in the nucleus and is involved in a number of RNA metabolism processes, including splicing. Cytoplasmic aggregates of TDP-43 protein are found in >90% of ALS cases and in 45% of FTD cases. Currently, there is no physiological TDP-43 model that exhibits both the motor and cognitive defects seen in ALS-FTD. The M323K mouse contains a point mutation in the endogenous TDP-43 gene (Tardbp). Homozygous mice display a mid-to-late life onset neurodegenerative phenotype, mainly motor symptoms (Fratta et al, 2018). However, cognitive testing on these mice has remained to be undertaken.
Methodology: A longitudinal study, consisting of a comprehensive phenotyping pipeline, was conducted on a cohort of M323K female mice (n=9 wild-types and n=9 homozygotes). This study focused on identifying progressive phenotypic changes in homozygous mice; heterozygous mice were omitted since they show minimal neurodegenerative changes. A range of motor, cognitive and metabolic tests were conducted at an early (3-months) and late (1-year) time point.
Results: Preliminary data show that homozygous mice display cognitive deficits from 3-months of age. General well-being tests, such as marble burying and nesting, revealed impairments in normal rodent behaviours, indicating non-specific hippocampal dysfunction. Further in-depth cognitive tests, spontaneous alternation and fear conditioning, revealed learning and memory problems in the homozygous mice at 1-year.
Conclusion: The M323K mouse is an excellent physiological model of ALS-FTD. Its ability to display motor and cognitive phenotypes, which mimic clinical observations, make it a unique and invaluable tool to further understand ALS-FTD TDP-43 pathophysiology.
University of Birmingham
‘Imagi-neering: Investigating changes in corticomotor excitability associated with motor learning induced by imaginary movements in combination with Transcranial Direct Current Stimulation’
Imagined practise and Transcranial Direct Current Stimulation (TDCS) are two intervention methods that have been used separately to enhance motor skill acquisition. Both imagined practise and TDCS are thought to target mechanisms that involve M1, underlying motor learning specifically. Their efficacy as motor learning interventions alone has been proven and has gained support within the literature, particularly within sports performance and neurorehabilitation contexts. There is still room, however, to create consensus on the effectiveness of a motor skill learning intervention that combines imagined practise with TDCS. The main objective of this study is to develop an effective motor learning intervention protocol combining the use of imagined practise and TDCS. The proposed study will evaluate the efficacy of our methodology design by assessing the effects of imagined practise combined with TDCS on M1 corticomotor mechanisms and skill performance outcomes. We will also assess how participants’ perception of their own mental visualisation skills will affect these corticomotor and performance parameters. It is also thought that those who consider themselves better at mental visualisation are better at mental imagery tasks. Yet, it is still to be determined if better visualisers display different improvements in motor learning via imagined practise protocols, including those that are combined with TDCS.
Method: Participants will be asked to perform physically or using imagined practise of a predefined keyboard sequence either with or without TDCS for five consecutive one-hour practise sessions. M1 corticomotor representation size will be assessed using Transcranial Magnetic Stimulation (TMS) via Brainsight® neuronavigation before and after the five practise sessions. Following these sessions, we will consider and compare decreases in activation threshold and the change in size of the corticomotor representation maps produced between groups. Performance accuracy will be assessed via Spike2 programming. We will measure how far before or behind a 60 beat per minute metronome participants play the prescribed keyboard sequence for their final performance. This will be reported as global number of errors and standard deviation from metronome. Mental visualisation skills of the participants will be determined by their scores on the MIQ-3 (Movement Imagery Questionnaire-3).
Results: We expect our protocol design will positively influence our outlined assessment parameters – leading to expansion in M1 corticomotor representation maps, decrease in activation threshold, decrease in global number of errors, and decrease in standard deviation from metronome beat. We expect higher MIQ-3 scores for better visualisers. This will have positive interactions with corticomotor representation map expansion and performance accuracy.
Conclusion: We have designed and developed an intervention combining imagined practise and M1-focussed TDCS that has potential to enhance the motor learning processes underlying the acquisition of a novel motor skill. There is potential for this intervention to be used to improve sports performance and clinical neurorehabilitation outcomes.