Uses of Social Determinants of Health Data to Address Cardiovascular Disease and Health Equity: A Scoping Review.

Background Cardiovascular disease is the leading cause of morbidity and mortality worldwide. Prior research suggests that social determinants of health have a compounding effect on health and are associated with cardiovascular disease. This scoping review explores what and how social determinants of health data are being used to address cardiovascular disease and improve health equity. Methods and Results After removing duplicate citations, the initial search yielded 4110 articles for screening, and 50 studies were identified for data extraction. Most studies relied on similar data sources for social determinants of health, including geocoded electronic health record data, national survey responses, and census data, and largely focused on health care access and quality, and the neighborhood and built environment. Most focused on developing interventions to improve health care access and quality or characterizing neighborhood risk and individual risk. Conclusions Given that few interventions addressed economic stability, education access and quality, or community context and social risk, the potential for harnessing social determinants of health data to reduce the burden of cardiovascular disease remains unrealized.

Stakeholder Perspectives on Data-Driven Solutions to Address Cardiovascular Disease and Health Equity in New York City.

Introduction: There is growing recognition of the importance of addressing the social determinants of health in efforts to improve health equity. In dense urban environments such as New York City, disparities in chronic health conditions (e.g., cardiovascular disease) closely mimic inequities in social factors such as income, education, and housing. Although there is a wealth of data on these social factors in New York City, little is known about how to rapidly use available data sources to address health disparities. Methods: Semistructured interviews were conducted with key stakeholders (N=11) from across the public health landscape in New York City (health departments, healthcare delivery systems, and community-based organizations) to assess perspectives on how social determinants of health data can be used to address cardiovascular disease and health equity, what data-driven tools would be useful, and challenges to using these data sources and developing tools. A matrix analysis approach was used to analyze the interview data. Results: Stakeholders were optimistic about using social determinants of health data to address health equity by delivering holistic care, connecting people with additional resources, and increasing investments in under-resourced communities. However, interviewees noted challenges related to the quality and timeliness of social determinants of health data, interoperability between data systems, and lack of consistent metrics related to cardiovascular disease and health equity. Conclusions: Future research on this topic should focus on mitigating the barriers to using social determinants of health data, which includes incorporating social determinants of health data from other sectors. There is also a need to assess how data-driven solutions can be implemented within and across communities and organizations.

Variance of US Hospital Characteristics by Safety-Net Definition.

This cross-sectional study examines whether characteristics of hospitals differ across 5 frequently used safety-net hospital definitions using 2020 data.

Firearm Laws Enacted by Municipalities in 6 States With Diverse Policy Frameworks.

INTRODUCTION: Firearm violence is a public health crisis. Municipalities are frequently prevented from adopting firearm-related laws because of state preemption-when the state limits local authority to enact laws on a specific topic. Yet, it is unknown the extent to which municipalities enact firearm-related laws under varying preemption regimes, the content of such laws, and how municipal laws relate to the state's firearm-policy framework. METHODS: A purposeful sample of 6 states with diverse preemption laws were chosen; 3 with robust preemption: South Carolina, Maryland, and Arizona; 1 with moderate preemption: Nebraska; and 2 without preemption: Connecticut and New York. Using Lexis+, municipal codes as of December 31, 2020 were identified, and the policy topics were evaluated and compared with the state's policy framework. Counties representing the municipalities identified were characterized using public use data. RESULTS: In total, 613 municipal policies were identified, covering 56 topics. The number of policy topics enacted by at least 1 municipality in the state included 18 for Arizona, 21 for Connecticut, 24 for Maryland, 25 for Nebraska, 40 for New York, and 28 for South Carolina. The most common policy identified was restricting public discharge in community-centered locations. Local laws in preemption states replicated state requirements or were consistent with savings clauses expressly allowing local action. New York City, a municipality in a state without preemption, enacted laws covering the most policy topics of the municipalities identified. CONCLUSIONS: When not constrained by state preemption, local lawmakers actively passed firearm-related legislation. Many such laws are specific to local contexts and may reflect local lawmakers' responsiveness to constituent concerns.

Association between COVID-19 vaccine hesitancy and trust in the medical profession and public health officials.

One's personal physician, national and state or local public health officials, and the broader medical profession play important roles in encouraging vaccine uptake for COVID-19. However, the relationship between trust in these experts and vaccine hesitancy has been underexplored, particularly among racial/minority groups where historic medical mistrust may reduce uptake. Using an April 2021 online sample of US adults (n = 3041) that explored vaccine hesitancy, regression models estimate levels of trust in each of these types of experts and between trust in each of these experts and the odds of being COVID-19 vaccine takers vs refusers or hesitaters. Interaction terms assess how levels of trust in the medical profession by race/ethnicity are associated with vaccine hesitancy. Trust in each expert is positively associated with trust in other experts, except for trust in the medical profession. Only trust in one's own doctor was associated with trust in the medical profession, as measured by factor scores derived from a validated scale. Lower levels of trust in experts were significantly associated with being either a hesitater or a refuser compared to being a taker. Black respondents had higher odds of being either a hesitater or a refuser compared to white respondents but the interaction with trust was insignificant. For Hispanic respondents only, the odds of being a hesitater declined significantly when trust in the medical profession rose. Mistrust in the medical profession, one's doctor and national experts contributes to vaccine hesitancy. Mobilizing personal physicians to speak to their own patients may help.

Do alcohol policies affect everyone equally? An assessment of the effects of state policies on education-related patterns of alcohol use, 2011-2019.

BACKGROUND: Public policies are a powerful tool to change behaviors that may harm population health, but little is known about how state alcohol policies affect different population groups. This study assesses the effects of a comprehensive measure of the state alcohol regulatory environment (the State Alcohol Policy Score or SAPS) on heavy drinking-a risk factor for premature death-on different population groups, defined by levels of educational attainment, then by race/ethnicity, and sex. METHODS: We pool each state's Behavioral Risk Factor Surveillance Survey (BRFSS) 2011-2019 and use robust Poisson regression analyses that control for individual-level factors, state-level factors (1 year lagged SAPS score for each state, state fixed effects), and year fixed effects to assess the relationship between SAPS and heavy drinking behaviors by education group. Interaction terms test whether education moderates the relationship by race/ethnicity and gender. RESULTS: SAPS scores increased 2010-2018, but substantial gaps persist between states. A 10 % increase in a state's alcohol policy score is associated with a 2 % lower prevalence in current drinking (APR=0.97, 95 % CI=0.97-0.97, p < 0.0011) although not for those with a high school education or less. A 10 % increase in the SAPS was associated with a 3 % lower prevalence of heavy drinking; interaction terms in models reveal that a 10 % increase in the SAPS was associated with a lower prevalence of heavy drinking among those with less than a college education. CONCLUSION: Narrowing gaps in alcohol policies between states may reduce heavy drinking among those with lower educational attainment.

Determinants of the COVID-19 vaccine hesitancy spectrum.

Vaccine hesitancy remains an issue in the United States. This study conducted an online survey [N = 3,013] using the Social Science Research Solution [SSRS] Opinion Panel web panelists, representative of U.S. adults age 18 and older who use the internet, with an oversample of rural-dwelling and minority populations between April 8 and April 22, 2021- as vaccine eligibility opened to the country. We examined the relationship between COVID-19 exposure and socio-demographics with vaccine intentions [eager-to-take, wait-and-see, undecided, refuse] among the unvaccinated using multinomial logistic regressions [ref: fully/partially vaccinated]. Results showed vaccine intentions varied by demographic characteristics and COVID-19 experience during the period that eligibility for the vaccine was extended to all adults. At the time of the survey approximately 40% of respondents were unvaccinated; 41% knew someone who had died of COVID-19, and 38% had experienced financial hardship as a result of the pandemic. The vaccinated were more likely to be highly educated, older adults, consistent with the United States initial eligibility criteria. Political affiliation and financial hardship experienced during the pandemic were the two most salient factors associated with being undecided or unwilling to take the vaccine.

Drosophila Model for Gut-Mediated Horizontal Transfer of Narrow- and Broad-Host-Range Plasmids.

Horizontal gene transfer (HGT) is a driving force of microbial evolution. The gut of animals acts as a potent reservoir for the lateral transfer of virulence, fitness, and antimicrobial resistance genes through plasmids. Reduced-complexity models for the examination of host-microbe interactions involved in plasmid transfer are greatly desired. Thus, this study identifies the use of Drosophila melanogaster as a model organism for the conjugation of plasmids of various incompatibility groups in the gut. Enterobacteriaceae conjugation pairs were identified in vitro and used for oral inoculation of the Drosophila gut. Flies were enumerated for the donor, recipient, and transconjugant populations. Each donor-recipient pair was observed to persist in fly guts for the duration of the experiment. Gut concentrations of the donors and recipients were significantly different between male and female flies, with females generally demonstrating increased concentrations. Furthermore, host genetics significantly altered the concentrations of donors and recipients. However, transconjugant concentrations were not affected by host sex or genetics and were detected only in the IncPε and IncI1 plasmid groups. This study demonstrates Drosophila melanogaster as a model for gut-mediated plasmid transfer. IMPORTANCE Microbial evolution in the gut of animals due to horizontal gene transfer (HGT) is of significant interest for microbial evolution as well as within the context of human and animal health. Microbial populations evolve within the host, and factors from the bacteria and host interact to regulate this evolution. However, little is currently known about how host and bacterial factors regulate plasmid-mediated HGT in the gut. This study demonstrates the use of Drosophila and the roles of sexual dimorphism as well as plasmid incompatibility groups in HGT in the gut.

Identification of conserved transcriptome features between humans and Drosophila in the aging brain utilizing machine learning on combined data from the NIH Sequence Read Archive.

Aging is universal, yet characterizing the molecular changes that occur in aging which lead to an increased risk for neurological disease remains a challenging problem. Aging affects the prefrontal cortex (PFC), which governs executive function, learning, and memory. Previous sequencing studies have demonstrated that aging alters gene expression in the PFC, however the extent to which these changes are conserved across species and are meaningful in neurodegeneration is unknown. Identifying conserved, age-related genetic and morphological changes in the brain allows application of the wealth of tools available to study underlying mechanisms in model organisms such as Drosophila melanogaster. RNA sequencing data from human PFC and fly heads were analyzed to determine conserved transcriptome signatures of age. Our analysis revealed that expression of 50 conserved genes can accurately determine age in Drosophila (R2 = 0.85) and humans (R2 = 0.46). These transcriptome signatures were also able to classify Drosophila into three age groups with a mean accuracy of 88% and classify human samples with a mean accuracy of 69%. Overall, this work identifies 50 highly conserved aging-associated genetic changes in the brain that can be further studied in model organisms and demonstrates a novel approach to uncovering genetic changes conserved across species from multi-study public databases.

RNA Sequencing Reveals Key Metabolic Pathways Are Modified by Short-Term Whole Egg Consumption.

Eggs are protein-rich, nutrient-dense, and contain bioactive ingredients that have been shown to modify gene expression and impact health. To understand the effects of egg consumption on tissue-specific mRNA and microRNA expression, we examined the role of whole egg consumption (20% protein, w/w) on differentially expressed genes (DEGs) between rat (n = 12) transcriptomes in the prefrontal cortex (PFC), liver, kidney, and visceral adipose tissue (VAT). Principal component analysis with hierarchical clustering was used to examine transcriptome profiles between dietary treatment groups. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis as well as genetic network and disease enrichment analysis to examine which metabolic pathways were the most predominantly altered in each tissue. Overall, our data demonstrates that whole egg consumption for 2 weeks modified the expression of 52 genes in the PFC, 22 genes in VAT, and two genes in the liver (adj p < 0.05). Additionally, 16 miRNAs were found to be differentially regulated in the PFC, VAT, and liver, but none survived multiple testing correction. The main pathways influenced by WE consumption were glutathione metabolism in VAT and cholesterol biosynthesis in the PFC. These data highlight key pathways that may be involved in diseases and are impacted by acute consumption of a diet containing whole eggs.

Whole egg consumption increases gene expression within the glutathione pathway in the liver of Zucker Diabetic Fatty rats.

Nutrigenomic evidence supports the idea that Type 2 Diabetes Mellitus (T2DM) arises due to the interactions between the transcriptome, individual genetic profiles, lifestyle, and diet. Since eggs are a nutrient dense food containing bioactive ingredients that modify gene expression, our goal was to examine the role of whole egg consumption on the transcriptome during T2DM. We analyzed whether whole egg consumption in Zucker Diabetic Fatty (ZDF) rats alters microRNA and mRNA expression across the adipose, liver, kidney, and prefrontal cortex tissue. Male ZDF (fa/fa) rats (n = 12) and their lean controls (fa/+) (n = 12) were obtained at 6 wk of age. Rats had ad libitum access to water and were randomly assigned to a modified semi-purified AIN93G casein-based diet or a whole egg-based diet, both providing 20% protein (w/w). TotalRNA libraries were prepared using QuantSeq 3' mRNA-Seq and Lexogen smallRNA library prep kits and were further sequenced on an Illumina HighSeq3000. Differential gene expression was conducted using DESeq2 in R and Benjamini-Hochberg adjusted P-values controlling for false discovery rate at 5%. We identified 9 microRNAs and 583 genes that were differentially expressed in response to 8 wk of consuming whole egg-based diets. Kyto Encyclopedia of Genes and Genomes/Gene ontology pathway analyses demonstrated that 12 genes in the glutathione metabolism pathway were upregulated in the liver and kidney of ZDF rats fed whole egg. Whole egg consumption primarily altered glutathione pathways such as conjugation, methylation, glucuronidation, and detoxification of reactive oxygen species. These pathways are often negatively affected during T2DM, therefore this data provides unique insight into the nutrigenomic response of dietary whole egg consumption during the progression of T2DM.

Roles of Regulatory RNAs in Nutritional Control.

Small RNAs (sRNAs), including microRNAs (miRNAs), are noncoding RNA (ncRNA) molecules involved in gene regulation. sRNAs play important roles in development; however, their significance in nutritional control and as metabolic modulators is still emerging. The mechanisms by which diet impacts metabolic genes through miRNAs remain an important area of inquiry. Recent work has established how miRNAs are transported in body fluids often within exosomes, which are small cell-derived vesicles that function in intercellular communication. The abundance of other recently identified ncRNAs and new insights regarding ncRNAs as dietary bioactive compounds could remodel our understanding about how foods impact gene expression. Although controversial, some groups have shown that dietary RNAs from plants and animals (i.e., milk) are functional in consumers. In the future, regulating sRNAs either directly through dietary delivery or indirectly by altered expression of endogenous sRNA may be part of nutritional interventions for regulating metabolism.

Drosophila enabled promotes synapse morphogenesis and regulates active zone form and function.

BACKGROUND: Recent studies of synapse form and function highlight the importance of the actin cytoskeleton in regulating multiple aspects of morphogenesis, neurotransmission, and neural plasticity. The conserved actin-associated protein Enabled (Ena) is known to regulate development of the Drosophila larval neuromuscular junction through a postsynaptic mechanism. However, the functions and regulation of Ena within the presynaptic terminal has not been determined. METHODS: Here, we use a conditional genetic approach to address a presynaptic role for Ena on presynaptic morphology and ultrastructure, and also examine the pathway in which Ena functions through epistasis experiments. RESULTS: We find that Ena is required to promote the morphogenesis of presynaptic boutons and branches, in contrast to its inhibitory role in muscle. Moreover, while postsynaptic Ena is regulated by microRNA-mediated mechanisms, presynaptic Ena relays the output of the highly conserved receptor protein tyrosine phosphatase Dlar and associated proteins including the heparan sulfate proteoglycan Syndecan, and the non-receptor Abelson tyrosine kinase to regulate addition of presynaptic varicosities. Interestingly, Ena also influences active zones, where it restricts active zone size, regulates the recruitment of synaptic vesicles, and controls the amplitude and frequency of spontaneous glutamate release. CONCLUSION: We thus show that Ena, under control of the Dlar pathway, is required for presynaptic terminal morphogenesis and bouton addition and that Ena has active zone and neurotransmission phenotypes. Notably, in contrast to Dlar, Ena appears to integrate multiple pathways that regulate synapse form and function.

The conserved microRNA miR-34 regulates synaptogenesis via coordination of distinct mechanisms in presynaptic and postsynaptic cells.

Micro(mi)RNA-based post-transcriptional regulatory mechanisms have been broadly implicated in the assembly and modulation of synaptic connections required to shape neural circuits, however, relatively few specific miRNAs have been identified that control synapse formation. Using a conditional transgenic toolkit for competitive inhibition of miRNA function in Drosophila, we performed an unbiased screen for novel regulators of synapse morphogenesis at the larval neuromuscular junction (NMJ). From a set of ten new validated regulators of NMJ growth, we discovered that miR-34 mutants display synaptic phenotypes and cell type-specific functions suggesting distinct downstream mechanisms in the presynaptic and postsynaptic compartments. A search for conserved downstream targets for miR-34 identified the junctional receptor CNTNAP4/Neurexin-IV (Nrx-IV) and the membrane cytoskeletal effector Adducin/Hu-li tai shao (Hts) as proteins whose synaptic expression is restricted by miR-34. Manipulation of miR-34, Nrx-IV or Hts-M function in motor neurons or muscle supports a model where presynaptic miR-34 inhibits Nrx-IV to influence active zone formation, whereas, postsynaptic miR-34 inhibits Hts to regulate the initiation of bouton formation from presynaptic terminals.

FOXO Regulates Neuromuscular Junction Homeostasis During Drosophila Aging.

The transcription factor foxo is a known regulator of lifespan extension and tissue homeostasis. It has been linked to the maintenance of neuronal processes across many species and has been shown to promote youthful characteristics by regulating cytoskeletal flexibility and synaptic plasticity at the neuromuscular junction (NMJ). However, the role of foxo in aging neuromuscular junction function has yet to be determined. We profiled adult Drosophila foxo- null mutant abdominal ventral longitudinal muscles and found that young mutants exhibited morphological profiles similar to those of aged wild-type flies, such as larger bouton areas and shorter terminal branches. We also observed changes to the axonal cytoskeleton and an accumulation of late endosomes in foxo null mutants and motor neuron-specific foxo knockdown flies, similar to those of aged wild-types. Motor neuron-specific overexpression of foxo can delay age-dependent changes to NMJ morphology, suggesting foxo is responsible for maintaining NMJ integrity during aging. Through genetic screening, we identify several downstream factors mediated through foxo-regulated NMJ homeostasis, including genes involved in the MAPK pathway. Interestingly, the phosphorylation of p38 was increased in the motor neuron-specific foxo knockdown flies, suggesting foxo acts as a suppressor of p38/MAPK activation. Our work reveals that foxo is a key regulator for NMJ homeostasis, and it may maintain NMJ integrity by repressing MAPK signaling.

A transgenic resource for conditional competitive inhibition of conserved Drosophila microRNAs.

Although the impact of microRNAs (miRNAs) in development and disease is well established, understanding the function of individual miRNAs remains challenging. Development of competitive inhibitor molecules such as miRNA sponges has allowed the community to address individual miRNA function in vivo. However, the application of these loss-of-function strategies has been limited. Here we offer a comprehensive library of 141 conditional miRNA sponges targeting well-conserved miRNAs in Drosophila. Ubiquitous miRNA sponge delivery and consequent systemic miRNA inhibition uncovers a relatively small number of miRNA families underlying viability and gross morphogenesis, with false discovery rates in the 4-8% range. In contrast, tissue-specific silencing of muscle-enriched miRNAs reveals a surprisingly large number of novel miRNA contributions to the maintenance of adult indirect flight muscle structure and function. A strong correlation between miRNA abundance and physiological relevance is not observed, underscoring the importance of unbiased screens when assessing the contributions of miRNAs to complex biological processes.

QIL1 is a novel mitochondrial protein required for MICOS complex stability and cristae morphology.

The mitochondrial contact site and cristae junction (CJ) organizing system (MICOS) dynamically regulate mitochondrial membrane architecture. Through systematic proteomic analysis of human MICOS, we identified QIL1 (C19orf70) as a novel conserved MICOS subunit. QIL1 depletion disrupted CJ structure in cultured human cells and in Drosophila muscle and neuronal cells in vivo. In human cells, mitochondrial disruption correlated with impaired respiration. Moreover, increased mitochondrial fragmentation was observed upon QIL1 depletion in flies. Using quantitative proteomics, we show that loss of QIL1 resulted in MICOS disassembly with the accumulation of a MIC60-MIC19-MIC25 sub-complex and degradation of MIC10, MIC26, and MIC27. Additionally, we demonstrated that in QIL1-depleted cells, overexpressed MIC10 fails to significantly restore its interaction with other MICOS subunits and SAMM50. Collectively, our work uncovers a previously unrecognized subunit of the MICOS complex, necessary for CJ integrity, cristae morphology, and mitochondrial function and provides a resource for further analysis of MICOS architecture.

miR-8 controls synapse structure by repression of the actin regulator enabled.

MicroRNAs (miRNAs) are post-transcriptional regulators of gene expression that play important roles in nervous system development and physiology. However, our understanding of the strategies by which miRNAs control synapse development is limited. We find that the highly conserved miRNA miR-8 regulates the morphology of presynaptic arbors at the Drosophila neuromuscular junction (NMJ) through a postsynaptic mechanism. Developmental analysis shows that miR-8 is required for presynaptic expansion that occurs in response to larval growth of the postsynaptic muscle targets. With an in vivo sensor, we confirm our hypothesis that the founding member of the conserved Ena/VASP (Enabled/Vasodilator Activated Protein) family is regulated by miR-8 through a conserved site in the Ena 3' untranslated region (UTR). Synaptic marker analysis and localization studies suggest that Ena functions within the subsynaptic reticulum (SSR) surrounding presynaptic terminals. Transgenic lines that express forms of a conserved mammalian Ena ortholog further suggest that this localization and function of postsynaptic Ena/VASP family protein is dependent on conserved C-terminal domains known to mediate actin binding and assembly while antagonizing actin-capping proteins. Ultrastructural analysis demonstrates that miR-8 is required for SSR morphogenesis. As predicted by our model, we find that Ena is both sufficient and necessary to account for miR-8-mediated regulation of SSR architecture, consistent with its localization in this compartment. Finally, electrophysiological analysis shows that miR-8 is important for spontaneous neurotransmitter release frequency and quantal content. However, unlike the structural phenotypes, increased expression of Ena fails to mimic the functional defects observed in miR-8-null animals. Together, these findings suggest that miR-8 limits the expansion of presynaptic terminals during larval synapse development through regulation of postsynaptic actin assembly that is independent of changes in synapse physiology.

Retrograde BMP signaling at the synapse: a permissive signal for synapse maturation and activity-dependent plasticity.

At the Drosophila neuromuscular junction (NMJ), the loss of retrograde, trans-synaptic BMP signaling causes motoneuron terminals to have fewer synaptic boutons, whereas increased neuronal activity results in a larger synapse with more boutons. Here, we show that an early and transient BMP signal is necessary and sufficient for NMJ growth as well as for activity-dependent synaptic plasticity. This early critical period was revealed by the temporally controlled suppression of Mad, the SMAD1 transcriptional regulator. Similar results were found by genetic rescue tests involving the BMP4/5/6 ligand Glass bottom boat (Gbb) in muscle, and alternatively the type II BMP receptor Wishful Thinking (Wit) in the motoneuron. These observations support a model where the muscle signals back to the innervating motoneuron's nucleus to activate presynaptic programs necessary for synaptic growth and activity-dependent plasticity. Molecular genetic gain- and loss-of-function studies show that genes involved in NMJ growth and plasticity, including the adenylyl cyclase Rutabaga, the Ig-CAM Fasciclin II, the transcription factor AP-1 (Fos/Jun), and the adhesion protein Neurexin, all depend critically on the canonical BMP pathway for their effects. By contrast, elevated expression of Lar, a receptor protein tyrosine phosphatase found to be necessary for activity-dependent plasticity, rescued the phenotypes associated with the loss of Mad signaling. We also find that synaptic structure and function develop using genetically separable, BMP-dependent mechanisms. Although synaptic growth depended on Lar and the early, transient BMP signal, the maturation of neurotransmitter release was independent of Lar and required later, ongoing BMP signaling.

MicroRNAs shape the neuronal landscape.

The nervous system equips us with capability to adapt to many conditions and circumstances. We rely on an armamentarium of intricately formed neural circuits for many of our adaptive strategies. However, this capability also depends on a well-conserved toolkit of different molecular mechanisms that offer not only compensatory responses to a changing world, but also provide plasticity to achieve changes in cellular state that underlie a broad range of processes from early developmental transitions to life-long memory. Among the molecular tools that mediate changes in cellular state, our understanding of posttranscriptional regulation of gene expression is expanding rapidly. Part of the "epigenetic landscape" that shapes the deployment and robust regulation of gene networks during the construction and the remodeling of the brain is the microRNA system controlling both levels and translation of messenger RNA. Here we consider recent advances in the study of microRNA-mediated regulation of synaptic form and function.