Who or what first sparked your interest in science?
It’s hard to pinpoint – science has always been something I remember being interested in, even early in childhood. My mother worked in a hospital and a lot of dinner table conversations included topics related to health and I think that’s probably when I first became interested in science – wondering how the body works and wanting to learn more.
Is there a particular mentor that inspired you to become a scientist or that has significantly influenced your goals in research?
Dr. Liza Leventhal was my first manager out of college, and she was the first scientist who I developed a really close mentoring relationship with. She really opened my eyes to a new career path as a scientist in industry, a path that perhaps I wouldn’t have considered before. She also taught me a lot about how to effectively mentor young scientists and I’ve modeled a lot of how I interact with undergraduates in the lab after her.
Prior to pursuing your graduate work, you had the opportunity to do research in pharmaceutical companies. How critical were those experiences in your decision to pursue a graduate degree and a career in science?
My experience working full-time as a research associate at a pharmaceutical company was absolutely crucial in developing my interest in graduate study. I took on as much responsibility as I could as an associate, but I really wanted more opportunities to design experiments. I felt that graduate school was the best path to have more opportunities to drive research in specific directions.
As a graduate student and postdoctoral fellow, what are some key differences between research in the private sector vs academia?
Industry places a focus on process that I have not seen as much in my experience in academia. The pace of industry is also much faster, and negative data is openly accepted in the pharmaceutical industry in order to keep the pipeline for new therapies open. In academia, the path to discovery can be more ambling with more ability to follow interesting data in a way that doesn’t happen in industry as much. There are pros and cons to both of these differences.
How do you convey to friends and family the significance of your research work? Why is your research important to the general public?
I think I have it pretty easy in this regard – a lot of people see the value of studying Alzheimer’s disease since most people know someone who is affected by the disease, either personally or in a caretaking role. There’s always a lot in the news about the latest Alzheimer’s research (and other neuroscience), and I spend a lot of time acting as the “neuroscience liaison” with my friends and family, which is a role I generally welcome!
What types of activities within academic departments (e.g., teaching, mentoring and committee services) have you participated in and which of these have benefited your career development the most?
As a postdoc, I’ve run the journal club for the unit as a part of service; as a graduate student, I worked on the graduate student council reading travel award applications and on the graduate study committee for the neuroscience graduate program. I’ve also worked as a teaching assistant in graduate school and am currently teaching an undergraduate seminar course on glia in health and disease. I’ve also mentored several undergraduate students in the lab. I would say that I’ve enjoyed teaching and mentoring more than I ever expected, and knowing that about myself has allowed me to pursue a specific career track as I apply for faculty positions that strongly emphasize undergraduate education which I hadn’t placed as much importance on before I started teaching a course independently.
Presenting your work at large meetings may be challenging? From your experience presenting at the recent Nanosymposium on Alzheimer’s Disease and Neuroinflammation-SfN2017, what advice would you give to your peers about how to prepare for such an experience?
Giving a talk at a large meeting is hugely different than a poster presentation. Poster presentations are fun because you get to interact face-to-face with other scientists and get important feedback on your early research. It’s definitely more intimidating to give a talk to a large room because it’s not as much of a dialogue, but you do get to have a larger audience to disseminate your research findings to than with a poster presentation. I think one important thing for preparing for a slide talk is to make sure your slides are simplified and easy for a large audience to follow, and easy for you to explain. Especially a nanosymposium, where there’s only a few minutes to describe your research findings. And of course, part of simplifying your message is practicing and getting feedback early and often! I presented my SfN work at the local SfN meeting, the Boston Area Neuroscience Group (BANG) meeting, and it helped me figure out what parts of my talk I needed to work on before SfN2017.
In your past research experience as a doctoral student, you focused on the role of Ca2+ in neuroinflammation and cognitive dysfunction. How are you bridging your interest in Ca2+ homeostasis with your current postdoctoral work?
I wanted to make sure that during my postdoc I learned something different than what I learned in grad school, but thematically similar. I’ve been able to shape the direction of our research to include a lot more work on microglia and neuroinflammation in Alzheimer’s disease. I’ve also done some interesting work looking at the transcriptional consequences of over-activation of neuronal phosphatase calcineurin, which is upregulated during calcium dysregulation in Alzheimer’s disease. I’ve been able to pivot my graduate research in two different directions, focusing on calcium dysregulation and microglia-mediated neuroinflammation separately.
Your recent studies showed that while microglia incorporate and process Tau seeds, there are factors that limit this activity. What mechanisms may underscore such limitation in microglial Tau processing?
This is an area of active interest in my research. Some research has shown that tau is toxic to microglia, but the mechanisms of this weren’t examined. Due to the insoluble nature of tau seeds, it’s also likely that the microglia are simply unable to process it fast enough to keep up. Another interesting possibility is that microglia are breaking the tau down, but into specific species of tau, since we see lots of different cleavages in the brain, with different cleavages present in different diseases as well as in the presence of amyloid, so perhaps microglia are part of this process. I’m excited for the opportunity to examine some of these possibilities!
Select Publications by Dr. Sarah Hopp:
Hopp SC, D’Angelo HM, Royer SE, Kaercher RM, Crockett AM, Adzovic L, Wenk GL. (2015) Calcium dysregulation via L-type voltage dependent calcium channels and ryanodine receptors underlies memory deficits and synaptic dysfunction during chronic neuroinflammation. J Neuroinflammation. 12, 56.
Hopp SC, D’Angelo HM, Royer SE, Kaercher RM, Adzovic L, Wenk GL. (2014) Differential rescue of spatial memory deficits in aged rats by L-type voltage dependent calcium channel and ryanodine receptor antagonism. Neuroscience. 280: 10-8.
Hopp SC, Royer SE, D’Angelo HM, Kaercher RM, Fisher DA, Wenk GL. (2015) Differential neuroprotective and anti-inflammatory effects of L-type voltage dependent calcium channel and ryanodine receptor antagonists in the substantia nigra and locus coeruleus. J Neuroimmune Pharmacol. 10(1): 35-44.
Adzovic L, Crockett AM, D’Angelo HM, Lynn AE, Kaercher RM, Royer SE, Hopp SC, Wenk GL. (2015) Insulin improves spatial memory and attenuates chronic neuroinflammation in the hippocampus of young but not aged brains. J. Neuroscience. J Neuroinflammation. 12, 63.
Hopp SC, Royer S, Brothers HM, Kaercher RM, Bardou I, Wenk GL. (2014) Age associated alterations in the time-dependent profile of pro- and anti-inflammatory proteins within the hippocampus in response to acute exposure to interleukin-1β. J. Neuroimmunology. 267(1-2): 86-91.
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