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science on tHe cutting edge
“These findings could lead to new ways to treat brain While researchers found neuronal IL-1R1 in
disorders tied to inflammation. In terms of behavioral brain regions related to mood, affect and cognition,
implications, our results support the hypothesis that an unexpected finding is that IL-1R1 is expressed in
nIL-1R1 signaling influences emotional and cognitive neurons in the sensory system. Using high-tech spatial
behavior.” transcriptomics, they identified that neuronal IL-1R1
Results reveal that nIL-1R1 expression is most regulates gene pathways involved in synapse organization
prominent in the somatosensory and glutamatergic without triggering typical inflammation. This suggests
systems, areas that had previously been understudied that IL-1R1 has a role in synaptic formation and can
‘Ding-Dong’: A Study Finds in this context. Among the brain regions identified modify neural circuits and their function.
as expressing nIL-1R1, the dentate gyrus (DG) was
“With the most detailed mapping of neuronal IL-1R1
Specific Neurons With An consistently highlighted, reaffirming its role as a key site expression in the mouse brain to date, this study brings an
for neuronal IL-1R1 expression. The study also pinpoints
unprecedented level of clarity to how IL-1 signaling impacts
Immune Doorbell the thalamic relay centers and various sensory cortical the neural circuits that govern behavior,” said Randy D.
regions, suggesting that IL-1 signaling could play a Blakely, Ph.D., co-author, executive director of the FAU
By Gisele Galoustian significant role in sensory processing. Stiles-Nicholson Brain Institute, the David J.S. Nicholson
Interleukin-1 (IL-1) is a key molecule involved in “This new discovery opens up questions about Distinguished Professor in Neuroscience, and a professor of
inflammation and plays an important role in both healthy whether immune signals influence our sensory processing biomedical science in FAU’s Schmidt College of Medicine.
and diseased states. In disease, high levels of IL-1 in the and whether IL-1R1-mediated alterations of sensory “The findings open the door to new pathways of exploration,
brain are linked to neuroinflammation, which can disrupt signals contribute to cognitive issues, anxiety or offering critical insights into the mechanisms underlying
the body’s stress response, cause sickness-like behaviors, depression,” said Dan Nemeth, Ph.D., first author and a both normal and disrupted behavioral states seen in stress-
worsen inflammation by activating brain immune cells, postdoctoral fellow, FAU Schmidt College of Medicine related disorders, depression and anxiety.”
and allow immune cells from the body to enter the brain. and Stiles-Nicholson Brain Institute. “Furthermore, this
It also can lead to brain damage by causing support cells study shows that neurons do not signal the same way other
to produce harmful molecules. Elevated IL-1 levels are IL-1R1-expressing cells do.” Science On The Cutting Edge on page 17
associated with mood disorders, such as depression, and
problems with memory and thinking.
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and somatosensory cortex.
Conversely, in normal conditions without inflammation,
IL-1 has essential roles in the brain. It helps regulate
there’s an infection or injury, and in immune cells, it signals Your family dentist in Your family dentist in
hormone activity, supports healthy sleep patterns, and
improves cognitive functions such as memory and learning.
IL-1R1 is like a doorbell on cells that gets rung when
the body to start an immune response. However, neurons
that express IL-1R1 are not thought to induce inflammation,
suggesting that these cells may actually integrate immune
Now, a new study by Florida Atlantic University Palm Beach GardensPalm Beach Gardens
signals into neural ones. It has yet to be revealed where or
how IL-1R1 (Interleukin-1 Receptor Type 1) may control
or modify normal brain function.
provides the most detailed and comprehensive mapping of
neuronal IL-1R1 (nIL-1R1) expression in the mouse brain
to date, resolving long-standing inconsistencies. Previous
research has suggested that IL-1 signaling in neurons is
involved in sickness behaviors, anxiety, and changes in Cosmetic & Comprehensive
sleep, but the exact neural circuits involved have not been
well-defined.
The study, published in the Journal of Neuroinflammation, Restorative Dentistry
narrows down the specific neuronal populations and
neurotransmitter systems that could mediate these effects.
Researchers were able to tag neuronal populations that Implant Dentistry & Orthodontics / Clear Aligners
express nIL-1R1 using a clever cell tagging approach,
offering new insights into the functional roles of this
glutamatergic neurons influences cognitive and social- Eduardo Marmelstein Lima, D.D.S.
receptor in the central nervous system (CNS).
Previous studies conducted by the FAU Quan
Laboratory, reveal that chronic IL-1 signaling in
avoidance behaviors, particularly in the context of
neuroinflammation and stress-related disorders. This
supports the idea that nIL-1R1 could play a crucial role in 10887 N. Military Trail, Suite 6
conditions such as chronic stress, depression and anxiety in
the unique neural circuits described by the current study. Palm Beach Gardens, FL 33410
Using genetically modified mice, researchers
identified neurons in certain brain areas such as the
somatosensory cortex, hippocampus and others, which (561) 622-2815
have neuronal IL-1R1. Most of these neurons use
glutamate (a neurotransmitter for signaling), while some
use serotonin (important for mood). They found that these
IL-1R1-positive neurons are involved in circuits that
control sensory processing, mood regulation and memory. University of Texas Health and Science Center at San Antonio, Texas
“Our study shows how certain neurons are connected
to immune signals and may help explain how inflammation Residency and Masters in Orthodontics - Brazil
contributes to sensory, mood and memory disorders,” said Implant fellowship training - Brazil
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science, FAU Schmidt College of Medicine, and an
investigator in the FAU Stiles-Nicholson Brain Institute.