INQUIRY

INQUIRY • Volume 19, 2015
However at concentrations below 3.5%, protists swelled in
size and more contaminating organisms were observed. It
was concluded that optimal salt conditions for laboratory
growth is between 3.5% and 5.5%. These results will help
optimize conditions for growing and maintaining this protist
in the laboratory and will thereby facilitate future work
aimed at characterizing this protist species and investigating
its possible symbiotic relationship with the green sea urchin.
The Temporal Requirement of Nicotinic Acetylcholine
Receptor Subunits Regulating Sleep
Charalambia Louka, Neural Science
Sponsor: Professor Nicholas Stavropoulos, Neuroscience
and Physiology, NYU School of Medicine
Sleep is a crucial animal behavior that impacts health by
affecting metabolism, learning and memory, immunity and
many other bodily functions. Despite the importance of sleep
in our everyday lives, the brain mechanisms that regulate
sleep are still not well understood. Drosophila melanogaster,
the fruit fly, is a model organism whose sleep state shares
key similarities with mammalian sleep and can be used to
identify genes that function within the brain to regulate
sleep. Previous studies in this lab have shown that genes
encoding for the nicotinic acetylcholine receptor subunits
play a role in sleep regulation. To further characterize the
temporal requirement of these genes, this study investigated
whether their expression functions to assemble brain circuits
involved in sleep regulation during fly development or if
the activity of these genes plays a role in regulating sleep
in the adult fly brain on a day-to-day basis. To answer this
question, a conditional genetic system was used to control
the expression of these genes at different times of the fly
life cycle. Understanding how these genes work is critical
in piecing together a more comprehensive model of sleep
regulation that will eventually allow the molecular mechanisms
underlying sleep in humans to be understood.
AD Takes Its Toll: Stimulation of the Toll-like Receptor
9 to Reduce Amyloid Beta Deposition in Alzheimer’s
Disease
Helen Lyo, Biology
Sponsors: Professor Henrieta Scholtzova, Neurology, NYU
School of Medicine; Professor Thomas Wisniewski, Neurology,
NYU School of Medicine
Alzheimer’s Disease (AD) is the 6 th leading cause of
death in the U.S. and the most common cause of dementia.
It is characterized by memory and cognitive decline over
time, of which there is no effective cure. The neuropathology
of AD is associated with the presence of amyloid beta
in the vessels and parenchyma and the formation of tau
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