Student Research Spotlight January 3, 2019
Jade McLain (DO '22)
McLain recently earned a biomedical sciences degree from GA-PCOM and presented her
neuroscience research at the Alzheimer’s Association International Conference.
Jade McLain (DO ’22) grew up in Coral Springs, Florida. She graduated from Florida
State University in 2014 with a major in Psychology and a minor in Chemistry. She
recently completed a master’s degree in biomedical sciences from Georgia Campus – Philadelphia College of Osteopathic Medicine (GA-PCOM) with a concentration in research focused on neuroscience. In July of 2018, she was
offered the opportunity to present this work at the Alzheimer’s Association International
Conference in Chicago, Illinois. Jade is currently a first-year medical student at PCOM in Philadelphia. She is interested in pursuing a career in Neurology.
What are you studying?
I worked under Harold Komiskey, PhD, professor of neuroscience, physiology, and pharmacology to determine the effects
of several experimental conditions on the accumulation of hyperphosphorylated tau
protein in glial cells. Neurodegenerative diseases like Alzheimer’s and Parkinson’s
disease share a pathology beginning with tau hyperphosphorylation and subsequent accumulation
in neural tissues. Recent literature indicates that patients with diabetes are more
likely to develop neurodegenerative diseases in older age, suggesting a correlation
between glucose metabolism and neurodegenerative disease pathology. Also, as humans
age, levels of an endogenous steroid hormone called dehydroepiandrosterone hormone
(DHEA) decline, which might be associated with the onset of these pathological symptoms.
Our work focused on determining if a correlation exists between glucose manipulation,
DHEA administration and tau hyperphosphorylation by utilizing rat hippocampal astrocytes
as an experimental model.
What prompted you to pursue research?
I was introduced to neurodegenerative disease at a young age. My grandmother was diagnosed
with Progressive Supranuclear Palsy (PSP), and it affected my family drastically.
She was such a vibrant person, and to witness a disease like this change everything
about her was extremely difficult. We went from physician to physician, ultimately
having to face the fact that there was no cure and the best we could do was keep her
comfortable. She passed away within a year of her diagnosis, and I wanted to ensure
that future families do not endure what we did. The physicians who cared for her inspired
me to pursue medicine and use immense compassion and diligence in doing so. Her life
and memory are what drew me towards neuroscience research with Dr. Komiskey.
What experience do you have conducting research?
Prior to this project, I had not previously participated in a research project. The
master’s program provided us with a research course the summer before we started our
thesis projects. We learned about safety precautions in the lab, how to perform sterile
procedures and how to perform common tasks like cell culture and maintenance. After
the course, I was much more comfortable in the lab, though I still had much to learn
regarding the care for our astrocytes!
What are your responsibilities in this research project?
I conducted the project, beginning with culturing the astrocytes which were treated
with varying amounts of glucose media (DMEM) to induce a state of glucose deprivation
in vitro. The steroid hormone DHEA was aliquoted and administered to each condition
to determine what if any potential protective affects it had against the hyperphosphorylation
of tau. Cell viability was determined via WST-8 assay, and hyperphosphorylated tau
was measured via tau-ELISA. Using antibodies specific for hyperphosphorylated tau,
fluorescent images were obtained via confocal microscopy with the aid of Danielle
Warner-McGallagher (DO ’20) to determine the localization of the tau protein and the
accumulation of tau within the cells.
What is the broader impact of your research?
Neurodegenerative diseases can be elusive due to their nature of progression. No cure
exists currently for many of these pathologies. Current literature supports that tau
hyperphosphorylation followed by plaque formation occurs predominantly over other
neurodegenerative disease pathologies. Though the first step of accumulation has been
identified, several isoforms and accumulation patterns of tau exist, making it difficult
to apply results to every condition. Our research specifically examines how glucose
might affect hyperphosphorylation of tau and if DHEA decline contributes to that hyperphosphorylation.
This has implications for patients with glucose metabolism dysfunction as well as
patients suffering from DHEA decline. If future investigation reveals a distinct and
straightforward mechanism of regulation of tau hyperphosphorylation, this would serve
as a target for therapy and/or prevention of neural tissue deterioration and cognitive
decline. Dr. Komiskey’s lab is committed to investigating questions of similar nature
within the realm of neuroscience research.
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