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Dynamics and mechanisms of neuron migration in the adult songbird brain
(2025) Shvedov, Naomi R.; Scott, Benjamin B.
Throughout the life of the songbird, new neurons are born in the walls of the lateral ventricle and then disperse extensively throughout the forebrain where they integrate into circuits involved in the learning and production of birdsong. Still, little is known about how populations of neurons navigate through the songbird brain. Here, I leveraged advancements in optical imaging, genetics, and electron microscopy (EM) connectomics to study populations of migratory neurons in the adult zebra finch. In my first experiment, I used in vivo imaging to track large populations of migrating neurons in the living adult songbird brain. I showed that migratory neuron dynamics in and around song nucleus HVC were well described by a diffusion model and could sufficiently populate the song nucleus in a simulation. In my second experiment, I used a fully reconstructed, EM connectomics dataset from the zebra finch basal ganglia to study neuron migration. From this data, I generated a library of segmented cells that appeared to be migratory neurons, and then quantitatively characterized their surrounding microenvironment. These putative migratory neurons were found distributed throughout synapse-rich tissue, contacting various features of mature circuits such as dendrites, axons, and mature neuron somas. I observed that migrating neurons seemed to perturb nearby structures, and hypothesized neuronal “tunneling” as a potential feature of neuron migration. In our third experiment, we characterized three-photon microscopy in transgenic zebra finches, and evaluated the possibility of studying neurogenesis in the deep-brain of living songbirds. In our fourth experiment, we transplanted zebra finch brain tissue into an immunodeficient mouse brain to test the capacity of immature zebra finch neurons to migrate in different brain environments.
All together, these findings suggest a specialized migratory strategy in the adult brain in which immature neurons do not rely on particular scaffolds, but instead tunnel through mature brain tissue, pushing aside synapses and mature cell bodies in their migratory path as they disperse in a diffusive-like, multidirectional manner. In the final chapter, I synthesize these data and propose a comprehensive model of neuron migration in which migrating neurons independently “diffuse” through the brain, stochastically interact with surrounding structures, and then functionally integrate into existing circuitry through an interaction of both cell-intrinsic and local signaling factors.
Animal models for investigating coronavirus heterotypic immunity
(2025) Sanders, Nathan Lee; Mizgerd, Joseph P.; Saeed, Mohsan
Endemic coronaviruses (CoVs) such as OC43 circulate seasonally and, while usually mild, represent the 6th leading cause of viral pneumonia. Additionally, multiple zoonotic spillovers of CoVs have occurred in the last 25 years to cause severe pneumonia, most recently the coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome (SARS)-CoV-2. Coronaviruses therefore continue to pose significant public health burdens, and although significant advances have been made in understanding SARS-CoV-2, the immune response to endemic CoVs remains poorly understood. While most studies of immune memory are focused on defense against a subsequent infection with the same pathogen, this memory can cross-react with related pathogens in a phenomenon termed heterotypic immunity. Studies with other respiratory pathogens have implicated memory lymphocytes that establish long-term residency in the lung as critical in heterotypic immunity. Accumulating observational evidence from human studies suggests that remodeling of the immune landscape induced by prior endemic CoV infection influences outcomes of subsequent SARS-CoV-2 infection. Prior to 2020 no animal models existed for any of the four endemic CoVs, so the degree to which endemic CoVs produce lung-resident memory and the potential contributions of this to heterotypic immunity is unknown. In these studies, we utilized both rodents and non-human primates to model sequential infection of OC43 followed by SARS-CoV-2. In the mouse we focus on developing an OC43 model and how OC43 remodels the lung-resident environment, while in the macaque we focus on systemic and local inflammation generated during the subsequent SARS-CoV-2 infection.
In the mouse, OC43 was rapidly cleared but produced significant weight loss, leukocyte influx, and a robust type I interferon (IFN)-dependent production of IFN-γ. After two OC43 infections, lungs contained antigen-specific resident memory T and B lymphocytes and specific IgG and IgA. The addition of the immunostimulatory molecule cyclic-di-GMP (CDG) significantly increased generation of resident memory in lymphoid aggregates around lung vasculature and promoted Th1/Th17 polarization. The T cells and antibodies, with or without CDG, were specific to OC43 and did not cross-react with structural proteins of SARS-CoV-2.
In the macaque, OC43 infection produced no clinical signs of disease and was cleared by 3 days post-infection. Despite this asymptomatic (or at most mild) infection, prior OC43 decreased SARS-CoV-2 viral load and was sufficient to abrogate the serum inflammatory cytokine signature (IFN-β, IL-6, IL-8, IL-17, GM-CSF, and CCL2) that was observed in both naïve macaques. OC43-experienced macaques also had evidence of quicker pulmonary inflammation, more lung T cells, and decreased germinal center activity in draining lymph nodes compared to naïve counterparts after SARS-CoV-2.
Together, these studies demonstrate that OC43 infection remodels the lung immune landscape, including generation of lung-resident memory lymphocytes, and this can be boosted by immunostimulants. In the Balb/c inbred mouse line, the T cells and antibodies generated do not cross-react with SARS-CoV-2 structural proteins and experienced mice are not protected from SARS-CoV-2. In contrast, naïve macaques have greater markers of systemic and local inflammation after a mild SARS-CoV-2 compared to experienced macaques. The contrasting results underscore the need for human-like models to accomplish relevant host-pathogen interactions in the study of heterotypic adaptive immunity. These studies contribute to our understanding of CoV immune responses by establishing a mouse model of OC43 homotypic immunity and a primate model of CoV heterotypic immunity for future mechanistic investigations.
Striatal dynamics facilitate sensorimotor transformations through associative learning
(2025) Rodriguez Morales, Gabriela Alejandra; Howe, Mark; Hasselmo, Michael E.
Instrumental behaviors can be defined as actions that, often elicited by external stimuli, are taken in pursuit of particular goals or rewards. To engage in appropriate instrumental behaviors, it is necessary to distinguish and discriminate relevant stimuli and associate them with appropriate actions. This process, known as sensorimotor transformations, requires the brain to transform the perceived stimulus into a motor-related signal that can modify behavior. The basal ganglia, a set of subcortical nuclei, is particularly well positioned to perform these transformations. The striatum, its main input nucleus, receives and integrates sensory, motor and cognitive inputs from a multitude of cortical, subcortical and limbic regions. The output from the striatum can then directly modulate action through a series of pathways that interconnects it with other subcortical structures and eventually with cortex. The dorsomedial region of the striatum (DMS) is one of particular interest since it receives direct projections from somatosensory associative and motor cortices. Within the basal ganglia field, the involvement of the dorsomedial striatum in instrumental behaviors has been focused, primarily, in action-outcome associations. Studies looking into reward-based action selection have been extensive, from single action behavioral paradigms i.e. lever pressing, to more complex behaviors like dual port, magazine entries. However, there is an increasing need to incorporate more ethological behaviors that incorporate the critical interaction between stimuli, actions and outcomes. In an effort to expand on this literature, this study puts forward an investigation into the cell-type specific role of the dorsomedial striatum during sensory-guided instrumental behavior. To that end, my thesis puts forth four studies that link the activity of the striatum to the necessary sensorimotor transformations that produce instrumental behaviors. The first study utilized bilateral optogenetic inhibition of the DMS while expert mice performed a two-choice, visually guided task. Findings from this experiment established the necessity of the striatum in the performance of these behaviors. Additionally, we demonstrated that the computations occurring in this region during task performance were not only motoric but associative in nature. Here, we propose the DMS as a locus for visually guided action selection.
In the second study, we utilized two-photon imaging of DMS activity to assess the functional dynamics of the two main striatal pathways, the direct and indirect pathways. Our study demonstrates that learning of the stimulus-action associations governing the task reshapes the intrinsic cue-evoked activity of cells from the direct (dSPNs) and indirect (iSPNs) pathways. This learning effect creates cue-evoked movement information in SPNs, providing evidence of the sensorimotor transformations that produce appropriate instrumental actions. The third study investigates how the activity of individual cue-responsive cells changes with learning by comparing isolated cue responses across different stages of learning. This study poses the emergence of lateralized preferences in cells from both pathways as the source for these transformations. Altogether, these studies propose that learning reshapes the individual preference for lateralized movement of individual cells, leading to stimulus-evoked movement direction representation. We suggest these representations play an active role in instrumental action-selection.
Lastly, our final study aims to propose a mechanism for how the co-activation of the direct and indirect pathways selects and invigorates instrumental actions. We utilized the reliability of activation of individual cells across trials as an overall measure for levels of activation in both pathways. Comparison of dSPN and iSPN reliability show the emergence of a learning-related imbalance that favors the activation of the direct pathway. In accordance with classical model of basal ganglia function, we propose that after learning, higher levels of activation in the direct pathway ensure the selection of the appropriate lateralized response. Altogether, the body of work presented here proposes a model in which the striatum acquires the ability to select actions based on sensory stimuli through the imbalanced recruitment of cue-responsive SPNs that encode lateralized movement prior to the initiation of locomotion.
Adapting to uncertainty: living with chronic pain
(2025) Pereira, Cora; Barnes, Linda; Laird, Lance
OBJECTIVE: This research is rooted in the conviction that People Living with Chronic Pain (PLWCP) experience high degrees of uncertainty that manipulate daily long-term life plans. Uncertainty provokes multiple responses, including (1) legitimizing one’s experience (2) making sense of one's experience (3) changing one’s ongoing life course. I inquire about the day-to-day experience of PLWCP within the Greater Boston area seeking care in medical institutions applying the biopsychosocial model for care and treatment. Individual illness narratives offer a window into the lived experiences of chronic pain in the face of perpetual uncertainty. METHODS: Methods included autoethnographic journal entries, clinical observations in a local chiropractic care setting, and two in-depth interviews to triangulate data and understand shared relationships.
RESULTS: PLWCP dealt with layered uncertainty as (1) seeking legitimacy, (2), meaning making in the form of Explanatory Models, and (3) adapting to uncertainty. Uncertainty creates a permanent limitation that is ever-present and unpredictable, thus limiting the capabilities of one’s life in compounding ways.
CONCLUSION: PLWCP share experiences of uncertainty that constitute a permanently ‘disabled’ life. Further inquiry and research are needed to uncover and identify the structurally reinforced culture and attitudes that marginalize people living with chronic pain. Further inquiry will identify cultural barriers that limit individuals who are disabled from chronic pain and provide more inclusive support and solutions for those adapting their lives to uncertainty.
Investigating autonomic arousal and auditory motor control mechanisms across health and disease
(2025) Tomassi, Nicole; Stepp, Cara
Current investigations of speech production and auditory motor control mechanisms are limited by specificity in scope and paradigms bound to the laboratory environment. Despite attempts to isolate certain speech-related behaviors, heterogeneity exists in the research, especially when clinical populations are the focus of study, making it difficult to draw group-level conclusions and apply findings to the clinical setting. We propose to take a holistic approach to understand speech while leveraging variability to investigate individualistic characteristics that may contribute to certain speech production and auditory motor control behavior across health and disease. In studies 1 and 2 we utilized altered auditory feedback and physiological measures of the autonomic nervous system during cognitive loading tasks to understand the role of autonomic arousal in sensorimotor adaptation of suprasegmental (study 1) and segmental (study 2) aspects of speech in adults with typical speech. We also investigated a range of speech acoustic measures relating to auditory-perceptual aspects of speech in a cognitive loading task without altered auditory feedback to compare how changes in sensorimotor adaptation relate to these downstream changes in speech production in response to increased cognitive demand. We found that autonomic arousal was related to increased sensorimotor adaptation of suprasegmental and segmental features of speech, which suggests a potential role for state-based involvement in these higher-order processes. We also found that changes in sensorimotor adaptation of voice were related to changes in fundamental frequency during running speech without altered auditory feedback, indicating a potential relationship between speech adaptation and production mechanisms when cognitive resources are taxed. In study 3, we used electrodermal measures of autonomic activity and acoustic measures related to auditory-perceptual features of speech in a range of cognitively stressful speaking tasks to investigate the role of autonomic arousal in vocal hyperfunction. We found no effect of group on autonomic measures, indicating typical autonomic regulation in speakers with VH, compared to controls. We found significant effects of autonomic arousal on acoustic measures, demonstrating a role for arousal in speech. In study 4 we used altered auditory feedback, initial production variability, and within-production change in acoustic variance to investigate auditory feedback control in persons with Parkinson’s disease. We compared reflex responses from the altered auditory feedback paradigm with the measures of acoustic variability to determine if these more ecologically valid features of speech could reliably predict auditory feedback control mechanisms. We found no relationship in the suprasegmental features of speech; however, we found that reflex responses and initial production variability were related in the segmental features in speakers with and without Parkinson’s disease. More research is necessary to validate this result and explore the potential mechanism driving the relationship between speech stability and reliance on auditory feedback control in older adults. Through these studies, we implemented a multifaceted approach for understanding speech production and adaptation and investigated individual acoustic variability as a factor in auditory feedback control mechanisms.
Age-associated alterations in head and neck cancer
(2027) Spinella, Anthony; Varelas, Xaralabos
Head and neck squamous cell carcinomas (HNSCC) are the seventh most common cancers globally and have poor survival rates. Current first-line treatments for HNSCC, which include surgical resection and radiotherapy, result in high post-treatment morbidity while alternative treatment modalities, such as broad-based chemotherapy and immunotherapy, have limited long term efficacy. Thus, there is a need to identify novel factors that mediate the etiology of HNSCC to improve clinical outcomes for patients. One such modulating factor may be aging. The median age of diagnosis for HNSCC is above the age of 65, and older age is associated with increased incidence, reduced survival, and limited treatment efficacy for HNSCC patients. Aging is associated with a multitude of cellular, molecular, and genomic processes that alter the function of tissues, including tumors, such as cellular senescence, reduced immune functions, and altered stromal composition. Despite these tissue modifying features and the largely elderly HNSCC patient population, most pre-clinical cancer models are comprised exclusively of young animals, a discrepancy that likely contributes to the limited efficacy of pharmacological treatments for HNSCC. In these studies, we used carcinogen-induced and syngeneic isograft models of HNSCC orthotopically implanted into the tongues of young (≤16 weeks old; equivalent to approximately a 20-30 year old in human age) and old ((≥75 weeks old; equivalent to approximately a 60-80 year old in human age) mice to elucidate the role of the aged oral tumor microenvironment in modulating oral tumor biology. We observed that older age promotes malignant features in oral lesions. Additionally, we identified an enrichment of an age-associated, immune-evasive carcinoma cell population that coincided with reduced immune infiltration in tumors in old mice, molecular features that corresponded to reduced immune infiltration in human HNSCC. We further identified an age-associated, pro-fibrotic fibroblast population in the aged oral microenvironment that corresponded to elevated collagen deposition and elevated yes-associated protein (YAP) and TEA-domain transcription factor family (TEAD) activity in oral carcinoma cells in old mice. We demonstrated that targeting YAP-TEAD activity restored the immunogenicity of oral carcinoma cells, enhancing immune infiltration and tumor clearance in old mice. In additional studies, we demonstrated that supplementing absent chemokines into the old oral tumor microenvironment can also restore intra-tumoral immune infiltration to promote tumor clearance. Furthermore, we demonstrated that the induction of an age-associated, fibrotic stroma in young mice can partially recapitulate both the growth dynamics and immune-evasive phenotypes in oral carcinoma cells observed in old mice. Overall, these studies highlight the critical importance that aging plays in directing tumor biology in HNSCC, that YAP-TEAD contribute to mediating these dynamics, and that targeting age-associated alterations in the carcinoma cell, immune, or stromal compartments could serve as viable avenues for therapeutic intervention to improve outcomes for older HNSCC patients.
Leveraging Marburg virus model systems to elucidate filovirus gene expression illuminates VP30 interplay with genomic regulatory sequences
(2025) Suder, Ellen Lee Macdonald; Mühlberger, Elke
Viruses of the family Filoviridae, including Marburg virus (MARV) and Ebola virus (EBOV), carry out a plethora of complex processes in the course of infection using only a few, multifunctional proteins. Critical among these processes is the expression of viral genes and regulation thereof, which is not yet thoroughly understood. The phosphoprotein VP30, specific to the filoviruses, performs necessary functions in gene expression, partially through interactions with genomic regulatory sequences. While indispensable for rescue of infectious virus from cDNA of any filovirus genus, the requirement for VP30 in other facets of gene expression varies between filovirus genera. Minigenome systems modeling transcription and replication of MARV minigenomes function independently of VP30, whereas EBOV systems require VP30 for transcriptional activation at the start of the first gene, a dependence also present in filoviruses of the cuevavirus genus. The inability of filovirus polymerases to initiate transcription at sites internal to the genome has restricted the extent to which VP30 function can be assessed in EBOV model systems, due to the impact of the immediate transcriptional defect in the absence of VP30 on all potential subsequent transcriptional events. To elucidate further transcriptional roles of VP30 in filovirus gene expression with potential application across genera, we leveraged the VP30-independence of MARV transcriptional activation by generating MARV systems modeling transcriptional re-initiation and viral particle production, as well as a novel application of targeted protein degradation for inducible depletion of MARV VP30 at different stages of infection. Furthermore, by dissecting the discrepancy between VP30 interactions with a regulatory sequence in the untranslated region of the respective nucleoprotein genes of EBOV and MARV, we built a VP30-independent EBOV minigenome system using MARV sequence elements and identified two nucleotides primarily responsible for the dependence of EBOV transcription on VP30. Surprisingly, this effect appeared more specific to the sequence than to the stem-loop structure already implicated in VP30 regulation of EBOV transcription.
966BIn addition to filovirus gene expression, this work describes the application of multiple approaches to visualize and quantify viral infection in the investigation of viruses for which reagents are not yet available, including detection of a novel filovirus and antiviral drug testing in specialized cell types early in the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Role of vascular smooth muscle Interleukin-11 in aortic aneurysm development
(2025) Alton, Bardayson Karim; Seta, Francesca; Herscovitz, Haya
BACKGROUND: The formation of aortic aneurysms (AAs) presents a significant cardiovascular risk, with limited treatment options. Our laboratory examined wild-type (WT) and BCL11B knockout (BSMKO) mice treated with Angiotensin II (AngII) for a period of 7 days. The BSMKO mice given AngII exhibited aneurysm formation, while the WT mice did not show this response. RNA sequencing of entire aortas from BSMKO mice and WT mice given this AngII treatment revealed that Interleukin-11 (IL-11) was the most significantly increased in BSMKO aortas compared to the WT aortas. This research aims to validate these findings in vascular smooth muscle cells (VSMCs) and identify the molecular pathways connecting the knockout of BCL11B to IL-11 expression and AA development via AT1 receptors and PIEZO1 channels. METHODS: To simulate these BSMKO conditions, aortic VSMCs were pharmacologically treated with AngII and Yoda1. This treatment is expected to enhance calcium influx via AT1 receptors and PIEZO1 channels, resulting in increased activity of the calcium-dependent phosphatase calcineurin (PP2B). PP2B then dephosphorylates the inactive, phosphorylated nuclear factor of activated T-cells (NFAT), facilitating the activation and nuclear translocation of NFAT2, which may promote IL-11 transcription. Western blot analysis was performed to assess IL-11 and NFAT2 levels in VSMCs after exposure to AngII (100 μM), Yoda1 (20 μM), and their combination over 24 hours. IL-11 and NFAT2 expression levels were analyzed using ImageJ. RESULTS: Western blot analysis revealed that AngII treatment alone resulted in variable IL-11 expression, with some instances of upregulation and others where no significant increase was observed (n=6; p = 0.9226) compared to control. Yoda1 treatment led to a slight, non-significant increase in IL-11 levels (n=4; p = 0.0896). However, co-treatment with AngII and Yoda1 consistently produced the highest IL-11 expression, showing a statistically significant increase compared to the control (n=3; p = 0.0162). Additionally, Western blot analysis indicated an upregulation of NFAT2 in all treatment conditions compared to control, suggesting that AngII and PIEZO1 activation triggered calcium-related events culminating in NFAT2 activation, consistent with our hypothesis. CONCLUSION: Our results suggest that calcium entry through AT1 receptors and PIEZO1 channels enhances IL-11 expression in VSMCs, potentially via the calcium-dependent PP2B/NFAT2 pathway. By linking mechanosensitive calcium signaling to IL-11 expression, which has been linked to apoptosis or inflammation of VSMCs, this research offers new insights into the underlying molecular mechanisms of AA formation. Future research should explore whether targeting PIEZO1, AT1 receptors, or PP2B/NFAT2 signaling could serve as a therapeutic strategy to prevent AAs.
The role of pro-resolving mediators in cancer cachexia
(2025) Akter, Fahmida; Panigrahy, Dipak; Dominguez, M. Isabel
Cancer cachexia is a complex and multifactorial syndrome characterized by persistent inflammation, leading to severe muscle wasting, weight loss, and metabolic dysfunction. Conventional anti-inflammatory approaches have exhibited limited efficacy in effectively managing patient outcomes, emphasizing the importance of targeted therapies that resolve inflammation rather than merely suppressing it. However, special pro-resolving mediators (SPMs) recently described, including Resolvin D1 (RvD1) and Maresins, have emerged as potential candidates to combat inflammation-induced muscle degradation. In this study, the authors investigate the role of SPMs in the control of the key inflammatory pathways, e.g., NF-κB and JAK-STAT signaling, to attenuate cachexia-induced tissue atrophy. SPMs were assessed on systemic cytokine expression, muscle preservation, and tumor-induced inflammation using murine models of pancreatic and gastric cancer.The study results reveal that SPMs suppress the production of proinflammatory cytokines, prevent the degradation of muscle, and promote the resolution of inflammation. Hence, the study suggests that SPMs are potential candidates as therapeutic interventions for cancer cachexia. Nevertheless, many challenges stand between utilizing these insights in clinical applications. The reduced SPMs stability and bioavailability makes SPMs an ideal candidate for advanced delivery systems like nanovesicles (NVs) for improving their stability and therapeutic efficacy. Murine models are also very useful in providing mechanistic insights, but their metabolic and immune responses may not be identical to human responses. Future studies should determine the optimal delivery strategies of SPM, perform long-term in-vivo studies, as well as evaluate their combination with standard cancer treatments like chemotherapy and immunotherapy. Efforts to address these challenges are crucial to leverage SPM-based interventions for improving clinical outcomes for cancer cachexia patients.
A review of digital interventions to improve hypertension outcomes in Black adults
(2025) Anderson, Rachel V.; Symes, Karen; Kalinowski, Jolaade
INTRODUCTION: Hypertension (≥130/80 mmHg) is a risk factor for stroke, heart attack, kidney disease and heart disease. Black adults in the United States have higher rates of hypertension (56%) compared to White (48%) and Hispanic (39%) adults. Controlled blood pressure (BP) is also lower in Black adults (25%) than White adults (32%). Telemedicine and self-management of BP are associated with improved BP outcomes and hypertension management. Despite knowndisparities in hypertension prevalence, telemedicine, and digital health to manage BP is lower among racial/ethnic groups. One study found when analyzing the participants based on race, 70.2% of their White participants reported using digital
health technologies while 11.4% of the Black participants reported using digital health technologies. The purpose of this review was to synthesize the available literature on digital health interventions among Black adults and to describe the impacts on BP management and BP outcomes of these interventions. METHODS: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) as well as the Assessing the Methodological Quality of Systematic Reviews (AMSTAR) was used. A comprehensive search was completedof two databases (PubMed and Scopus). Included studies had interactive digital health interventions, Black adults 18 and over, BP measurements, adults with hypertension and were US based. Covidence software was used to identify duplicates and screen studies. RESULTS: In total, 55 articles were screened and 20 were chosen for full text review. Fourteen intervention studies met the criteria, including five nurse-managed telemonitoring interventions, two pharmacist-led interventions, three tailored interventions, a personally tailored mHealth intervention to improve medication adherence, a change-based counseling intervention, a texting intervention to improve medication adherence, and other two behavioral interventions with digital components. Improvements in medication adherence, reductions in systolic BP and diastolic BP seemed to be most effective in combinational interventions that had components addressing behavior management and education as well as medicationmanagement. CONCLUSION: This systematic review demonstrates the promise of digital health interventions for Black adults with hypertension. More studies are needed to explore the efficacy of combinational management techniques that utilize digital health tools for Black adults with hypertension are warranted. Such interventions could have beneficial outcomes for BP control in Black adults.