INTRODUCTION: The correlation between musical training and academic performance has been explored through several different venues of research in the fields of music, mathematics, and neuroanatomy. Previous research has shown evidence that a correlation between musical abilities and improved performance in academic subjects such as reading, math, and IQ. However, the precise mechanisms by which music influences academic performance as well as how the processing of them may vary, remain unclear. The ability to play music is related to the development and enhancement of executive functioning skills, which are crucial in completing mathematical tasks (Janurik 2019). Executive functions are a set of cognitive processes that are largely associated with the prefrontal cortex and include working memory, attention shifting, decision making, and cognitive flexibility. The aim of this study is to determine the cognitions w/ music which music enhances executive functions, how this translates to performance in various mathematical subjects, and if this connection can be seen by differential activation of areas within the prefrontal cortex. METHODS: Eight male and female adults between the ages of eighteen and twenty-nine in the Boston area were recruited in this IRB- approved study. Their experience in musical training and mathematical knowledge was assessed, as well as their highest education level. Four subjects were determined to be musicians and four were determined to be non-musicians from their score on a music competence assessment, as well as their reported experience with musical training. Testing was the same for all subjects and the music assessment tested ear training, reading music, and rhythm. Participants also completed a math assessment that tested abilities in geometry, algebra, and sudoku. While completing the assessments, a functional near-infrared spectroscopy (fNIRS) headband was worn that measured activity in the prefrontal cortex bilaterally. Activity will be determined by looking at the area under the curve of the difference between concentration of oxygenated and deoxygenated hemoglobin in the right and left dorsolateral prefrontal cortex (DLPFC), ventrolateral prefrontal cortex (VLPFC), orbitofrontal cortex (OFC), and inferior fronto-lateral cortex (IFLC) for each task. RESULTS: Of the eight enrolled in the study, four participants were determined to be musicians and four determined to be non-musicians based on a self reported questionnaire as well as performance on a standardized musical and mathematical assessment. Musicians showed a significant difference in consumption of oxygen in the left VLPFC during the algebra task (p=0.043). Scores on both the musical and mathematical assessment predicted activation of the left hemisphere for the geometry task (p< 0.038), right DLPFC for the sudoku task (p< 0.020), and activation of the right DLPFC for the sudoku task (p< .038). Score on the music assessment predicted activation of the right DLPFC for the geometry task (p< 0.020). Correlations between all of the variables tested were also determined. CONCLUSION: Participants with a higher score on the music assessment predicted activation of the left hemisphere with specialized use of the right DLPFC for geometry and sudoku problems when compared to non-musicians. Musicians showed significantly differential activation of the left VLPFC during the algebra task. A correlation was found between left hemispheric activation during the geometry task and activation of the right DLPFC for the rhythm task. These results indicate that musicians use different cognitive processes in solving various problems when compared to non-musicians. / 2025-03-08T00:00:00Z

Early life adversity (ELA) during critical periods of early development increases the risk of neuropsychiatric disorders. Adversity such as abuse, neglect and poverty can lead to activation of the immune system and alter the development of the brain. ELA can also impact the regulation of neuronal networks by microglia, the innate immune cells of the brain. This neuro-immune dysregulation can result in neurodevelopmental disorders such as autism spectrum disorder (ASD), schizophrenia (SZ) and others. We are also investigating the functions of toll-like receptor 7 (TLR7), a sensor of single-stranded viruses such as influenza and rubella that is highly conserved between humans and rodents. Immune activation induced by in utero administration of the TLR7 agonist imiquimod activates the immune system and is characterized by a phenotype of fragmented social behavior and reduced anxiety-like behavior with a sex bias for males. While it is a strong risk factor, maternal immune activation alone does not always lead to offspring developmental disorders, but it seems to increase the susceptibility to other risk factors. Previous research has shown that a mouse model of ELA resulted in sex-specific alterations in behaviors that are relevant to the clinical manifestations of neurodevelopmental disorders. In this study, we employed a two-hit model of early-life resource deprivation, stress in the form of limited bedding and nesting (LBN) in combination with maternal immune activation via in utero TLR7 stimulation. We then investigated the ability of this two-hit paradigm to induce neural and behavioral alterations and investigate offspring communicative, social, and perseverative behaviors, along with brain proteomic alterations. / 2026-03-07T00:00:00Z

Breathing is a lifelong activity that involves the coordination of several rhythmic behaviors. This dissertation investigates the neural origins of two of these breathing rhythms: eupnea and sighing. Eupnea, or regular unlabored breathing, occurs on the order of seconds and serves to drive the exchange of oxygen and carbon dioxide between the circulatory system and the environment. Sighs, deep breaths that are typically 2-5 times the volume of a eupneic breath, occur on the order of minutes and are critical in maintaining pulmonary function. Understanding how these rhythms are generated on a cellular and synaptic level is an essential step in preventing numerous pathologies, such as sudden infant death syndrome, and respiratory depression and failure as a consequence of opioids in a clinical setting or as drugs of abuse. First, we uncover the cellular and synaptic mechanisms that couple these two rhythms using electrophysiology and an in vitro breathing model from neonatal mice. Next, using mathematical modeling techniques, we explore how interconnectivity of the neural circuitry may drive the eupnea rhythm. Finally, we layout and test a novel framework for how intracellular calcium oscillations drive the sigh rhythm using a combination of electrophysiology and an in vitro breathing model combined with mathematical modeling. Unraveling the mechanisms that generate the eupnea and sigh rhythms reveals deeper insights into rhythms throughout the brain.

Goal-directed animals must optimize their behavior to address five fundamental questions: ‘What do I need?’, ‘Why do I need it?’, and ‘Where, when, and how do I get it?’. The brain solves this problem by creating internal representations of the animal’s world which are refined as the animal continues to explore its surroundings. These internal representations are thought to form the foundation of episodic memories, personal experiences occurring in a specific spaciotemporal context. The crucial role of the hippocampus in episodic memory formation and spatial navigation has been well documented, as well as the importance of hippocampal place cells in memory and navigation. However, it is still unknown exactly how this system works. In this thesis, we test the hypothesis that spatial decoding of an environment can be explained from cell-pair coactivity relationships and relies crucially on the most anti-coactive cells in the hippocampal CA1 region. In this experiment mice were virally infected so that CA1 principal cells expressed GCaMP6f, a fluorescent calcium sensor used to infer firing activity. A GRIN lens and UCLA miniscope were implanted to record fluorescent CA1 imaging data. Mice were placed in two distinct environments, a circle enclosure and a square enclosure, and were allowed to freely explore. Kendall tau correlations were calculated to rank cells by their participation in anti-cofiring cell pairs. IsoMap dimensionality reduction was computed for each enclosure and 2D manifolds were constructed. The proportion overlap between the manifolds of the circle and the square enclosure was used as a measure of the ability of the mouse to distinguish between each environment. Increasing percentages of anti-cofiring cells were then removed from the model to determine what would happen to the proportion overlap between the manifolds. Data was analyzed using the Kruskal-Wallis equality-of-populations rank test to reveal the following conclusions in support of the hypothesis: the removal of increasing percentages of anti-cofiring cells from the model was correlated with a significant increase in the proportion overlap between manifolds of the circle and square enclosures; anti-cofiring cells became more meaningful with time, indicating that these cells may be uniquely involved in spatial learning; removing the same number of cells at random was not correlated with a significant increase in the proportion overlap between manifolds.

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Increased attention has been given to the gut lately in a number of conditions, from maintaining health via the use of probiotics to treating Autism Spectrum Disorder. Parkinson's Disease has a history with the gut starting with the Braak hypothesis, in which eminent researcher Heiko Braak observed that the spread of Parkinson's (PD) seemed to occur along either olfactory or enteric neurons prior to reaching the substantia nigra in the midbrain, where the classical disease symptoms become evident. Though this finding was largely ignored at the time, the possibility of a gut origin for PD has received interest lately as a growing body of epidemiological and mechanistic research supports a gut-based influence. One key study showed that the presence of a toxin that induces oxidative stress in the intestine is capable of generating protein aggregates that spread to the brain and cause a PD-like pathology. The spread of protein aggregates from gut neurons to the brain has been corroborated in a number of studies. The open question, then, is what type of toxic triggers are capable of causing protein aggregation in the real world, and how do they cause protein aggregation in enteric neurons, which do not directly contact the intestinal lumen? We propose here that the enzyme Nox1 contributes to oxidative stress in the gut and eventually to the protein aggregation that can lead to PD via the generation of endogenous reactive oxygen species. Nox1 functions to generate superoxide radicals and is highly expressed in the colon. Knockdown of NOX1 in the brain has been shown to have a protective effect in a PD mouse model. To bridge a trigger in the intestinal lumen to protein aggregation in enteric neurons, we investigate a class of cells that contact both the intestinal lumen and enteric neurons, known as enteroendocrine cells. Finally, we conduct a small study to explore a possible toxic trigger, high fat diet.

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