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Fertility treatment enables involuntary childless people to have genetically related children, something that, for many, is a valuable life project. In this paper, I respond to two sets of objections that have been raised against expanding state‐funded fertility treatment provision for existing treatments, such as in vitro fertilisation (IVF), and against funding new treatments, such as uterine transplantation (UTx). Following McTernan, I refer to the first set of objections as the 'one good among many' objection. It purports that it is unjustifiable for the state to prioritise the funding of the life project of becoming a parent through fertility treatment provision over the funding of other life projects that people might have. Following Lotz, I refer to the second set of objections as the 'norm‐legitimation' objection. It maintains that the provision of costly forms of fertility treatment, such as UTx, would legitimise problematic social norms concerning genetic relatedness, reproduction and parenting, and that states should not engage in such a legitimation. In response to these objections, I defend the view that (reproductive) preferences ought to be taken more seriously when discussing fertility treatment provision and parental projects, and that not doing so can be costly, especially for women. The approach defended in this paper seeks to avoid disregarding and policing preferences and to reconcile their fulfilment with political projects aimed at improving the material and social conditions of sub‐fertile people: people who, for social or biological reasons (or an intersection of the two), are unable to reproduce unassisted. [ABSTRACT FROM AUTHOR]

The first section of this paper sets the record straight regarding many of Debouwere's (2024, Review of Education, 12, e3445) specific criticisms. The second section discusses the magnitude of the SES‐achievement relationship, specifically Debouwere's (2024) contention that the correlation is strong around 0.5 or 0.6 compared to observed correlations mostly between 0.2 and 0.3. The third section deals with five issues that Debouwere (2024) raises in his paper: (1) the stability of SES vis‐à‐vis cognitive ability; (2) the accuracy of children's reports of parents' socioeconomic characteristics; (3) whether teachers discriminate by students' SES; (4) the importance of cognitive ability for educational differentiation (i.e., tracking and streaming); and (5) SES effects on student achievement, controlling for prior achievement. The fourth section discusses the role of genetics in student achievement. Meta‐analyses and other studies indicate that about 50%–70% of the variance in student achievement is attributable to genetics (i.e., the heritability). The high heritability of student achievement accounts for its high stability, its strong correlations with cognitive ability and the weak effects of SES, net of prior achievement or cognitive ability. [ABSTRACT FROM AUTHOR]

In May 2015, my mother was diagnosed with stage IV pancreatic cancer and passed away three months later at the age of 78. Two years later, my older brother, only 53 at the time, was also diagnosed with pancreatic cancer. He passed away 15 months later. With this news, we engaged in the genetic retelling of family histories and connections, drawing genealogical maps on pieces of paper that reminded me of teaching Anthro 101 and starkly reimagined which relatives 'mattered' in our lives. As an anthropologist interested in subject formation and spatiality informed by a Foucauldian analytic, I have been propelled into exploring what it means to become 'high risk' (as a biologically related daughter and sister), subject to new regimes of surveillance and self‐management espoused by the field of precision medicine. This paper addresses this experience and thus contributes to questions of subject formation within the already‐existing truth‐making practices of genetic probability and personalized risk management. [ABSTRACT FROM AUTHOR]

Background: Sleep problems are regularly reported in people with intellectual disabilities. Recent years have seen a substantial increase in studies comparing sleep in people with intellectual disabilities to control participants, with an increase in the use of validated, objective measures. Emerging patterns of differences in sleep time and sleep quality warrant pooled investigation. Methods: A systematic search was conducted across three databases (Ovid Embase, PsycInfo and Medline) and returned all papers comparing sleep in people with intellectual disabilities to a control group, published since the last meta‐analysis on the topic. A quality framework was employed to rate the risk of bias across studies. Separate meta‐analyses of sleep duration and sleep quality were conducted. Subgrouping compared findings for those studies with participants with genetic syndromes or neurodevelopmental conditions and those with heterogeneous intellectual disability. Results: Thirteen new papers were identified and combined with those from the previous meta‐analysis to provide 34 papers in total. Quality of studies was generally rated highly, though sampling provided risk of bias and adaptive functioning was rarely measured. People with intellectual disability associated with genetic syndromes or neurodevelopmental conditions sleep for shorter time periods (standardised mean difference =.26) and experience worse sleep quality (standardised mean difference =.68) than their peers. People with intellectual disability of heterogeneous origin show no difference in sleep time but have poorer sleep quality. There was some evidence that age moderated these effects. Conclusions: People with intellectual disability have poorer sleep than those without. Subtle patterns suggest that aetiology of intellectual disability moderates the topography of these difficulties, with further work needed to differentiate common and distinct mechanisms across groups. [ABSTRACT FROM AUTHOR]

Genetic relatedness figures heavily in contemporary ethical debates on egg freezing, although the arguments lack empirical‐based evidence. Rather than adding another theoretical view on the moral relevance of genetic connections, this paper instead proposes an empirically grounded perspective based on two independent qualitative interview‐based studies conducted in Belgium and France. Three themes emerge from our empirical data: (1) prioritizing family building; (2) centering the gestational experience of motherhood; and (3) identifying the complexities and limitations of adoption. These themes suggest that the relationship between egg freezing, genetics, biological motherhood, and adoption is highly complex and less straightforward than what is often assumed in the egg freezing debate. Our study provides more detailed insights into women's ambivalent experiences regarding those reproductive options. We discuss the ethical implications of our empirical findings and hold that pursuing genetic desire is not necessarily the main moral reason why women freeze their eggs. [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Bridi et al papers. To view these articles, visit https://doi.org/10.1111/apt.18099 and https://doi.org/10.1111/apt.18129 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Bridi et al papers. To view these articles, visit https://doi.org/10.1111/apt.18099 and https://doi.org/10.1111/apt.18123 [ABSTRACT FROM AUTHOR]

Societal Impact Statement: Studies that show how empire influenced the development of plant genetics add to the established history of genetics and 20th‐century agricultural science. One approach to broadening this history is to consider the contributions of students studying abroad and their greater careers back home. Research agendas differed between and within institutions, much as they do today. This article explores the postgraduate education of an Indian groundnut breeder. It highlights the structural challenges faced by researchers at agricultural departments who sought promotion through education and examines the consequences for plant breeding and for farmers. Summary: Through the biography of V.K. Badami, this article contributes to debates about genetics and plant breeding in the history of science. Badami, an accomplished breeder in the Mysore Department of Agriculture, took a leave to study genetics at the University of Cambridge. His professors nearly failed him, yet Badami's groundnut breeding experiments proved influential for Indian farmers as well as advances in crop science. This history adds to the thesis that academic genetics varied in support of professional plant breeding by comparing institutional expections between Mysore and Cambridge.The argument is developed by reading Badami's student records along with his groundnut breeding experiments in South India.The study connects the disciplinary history of genetics to plant breeding for the British empire.Badami's experience at Cambridge is indicative of the power relationship between academic genetics and imperial plant breeding in the early 20th century. In this case, his commitments as an Indian agricultural officer conflicted with the discipline's devotion to quantitative analysis. [ABSTRACT FROM AUTHOR]

Objective: Infantile seizures cause great concern for both doctors and parents. In addition to modern neuroimaging and genetics, clinical tools helpful in predicting the course of the disease are needed. We prospectively studied the incidence, electroclinical characteristics and etiologies of epilepsy syndromes with onset before the age of 12 months and looked for prognostic determinants of outcome by age 24 months. Methods: From February 2017 through May 2019, we recruited all eligible infants diagnosed with epilepsy at our unit. Data on electroclinical studies, genetic investigations and drug response were gathered prospectively. The infants were given a structured neurological examination (Hammersmith Infantile Neurological examination [HINE] and Griffiths scales) at predetermined intervals until age 24 months at which age neurocognitive evaluation with Bayley scales was performed. Results: Included were 60 infants (27 female). The mean onset age of epilepsy was 5.3 (±2.5 standard deviation) months. The incidence of epilepsy in the population‐based cohort was 131 (95% confidence interval 99–172)/100 000. Epilepsy syndrome was identified in 80% and etiology in 58% of infants. Self‐limited infantile epilepsy was the second most common syndrome (incidence 18/100 000) after infantile epileptic spasms syndrome. PRRT2 was the most common monogenic cause. At age 24 months, 37% of the infants had drug‐resistant epilepsy (DRE) and half had a global developmental delay (GDD). Abnormal first HINE was the strongest predictor of GDD, followed by DRE and identified etiology. DRE was associated with structural etiology and GDD. Those with normal first HINE and good response to treatment had favorable outcomes, irrespective of the identified etiology. Significance: Our results support a high incidence of self‐limited epilepsy in infancy and PRRT2 as the genetic cause in the first year of life. Notwithstanding the advances in etiological discovery, we want to highlight the importance of clinical evaluation as standardized neurological examination with HINE proved a valuable tool in prognostication. Plain Language Summary: One in every 700–800 babies develop epilepsy within the first year after birth. Our study identified an epilepsy syndrome in 80% and the cause of epilepsy in 60% of the participants. By age 2 years, over one‐third of the children still experienced seizures, and almost half faced significant developmental delay. Structural brain abnormalities increased the likelihood of difficult epilepsy and developmental challenges. Babies whose epilepsy was caused by a gene defect varied widely in development and response to medications. Babies with normal neurological examination at first visit, especially if their seizures stopped quickly, had favorable development. [ABSTRACT FROM AUTHOR]

Trimethylamine N‐oxide (TMAO) is a circulating microbiome‐derived metabolite implicated in the development of atherosclerosis and cardiovascular disease (CVD). We investigated whether plasma levels of TMAO, its precursors (betaine, carnitine, deoxycarnitine, choline), and TMAO‐to‐precursor ratios are associated with clinical outcomes, including CVD and mortality. This was followed by an in‐depth analysis of their genetic, gut microbial, and dietary determinants. The analyses were conducted in five Dutch prospective cohort studies including 7834 individuals. To further investigate association results, Mendelian Randomization (MR) was also explored. We found only plasma choline levels (hazard ratio [HR] 1.17, [95% CI 1.07; 1.28]) and not TMAO to be associated with CVD risk. Our association analyses uncovered 10 genome‐wide significant loci, including novel genomic regions for betaine (6p21.1, 6q25.3), choline (2q34, 5q31.1), and deoxycarnitine (10q21.2, 11p14.2) comprising several metabolic gene associations, for example, CPS1 or PEMT. Furthermore, our analyses uncovered 68 gut microbiota associations, mainly related to TMAO‐to‐precursors ratios and the Ruminococcaceae family, and 16 associations of food groups and metabolites including fish‐TMAO, meat‐carnitine, and plant‐based food‐betaine associations. No significant association was identified by the MR approach. Our analyses provide novel insights into the TMAO pathway, its determinants, and pathophysiological impact on the general population. Highlights: Exploration of microbiome‐related metabolites (trimethylamine N‐oxide [TMAO], choline, betaine, l‐carnitine, and deoxycarnitine) in 7834 participants from five population cohorts.Cardiovascular risk was associated with elevated choline concentrations, but not with TMAO concentrations.Characterization of the genetic architecture behind metabolite concentration variability.Identification of gut microbial taxonomic abundance associated with metabolite's plasma concentration levels.Fish intake is the major dietary driver of TMAO concentrations, and betaine is related to grains and vegetable intake. [ABSTRACT FROM AUTHOR]

This article summarizes the Special Issue of Evolutionary Applications focused on "Advances in Salmonid Genetics." Contributions to this Special Issue were primarily presented at the Coastwide Salmonid Genetics Meeting, held in Boise, ID in June 2023, with a focus on Pacific salmonids of the west coast region of North America. Contributions from other regions of the globe are also included and further convey the importance of various salmonid species across the world. This Special Issue is comprised of 22 articles that together illustrate major advances in genetic and genomic tools to address fundamental and applied questions for natural populations of salmonids, ranging from mixed‐stock analyses, to conservation of genetic diversity, to adaptation to local environments. These studies provide valuable insight for molecular ecologists since salmonid systems offer a window into evolutionary applications that parallel conservation efforts relevant and applicable beyond salmonid species. Here, we provide an introduction and a synopsis of articles in this Special Issue, along with future directions in this field. We present this Special Issue in honor of Fred Utter, a founder and leader in the field of salmonid genetics, who passed away in 2023. [ABSTRACT FROM AUTHOR]

Background: Photo‐ageing is a form of skin ageing which affects the entire face. A photo‐aged skin has a diverse variety of wrinkles and dyspigmentation all over the face. Here, we discuss photo‐ageing on the Chinese skin evaluated using a photo‐numeric scale developed and validated on Caucasian skin (i.e., Caucasian scale) and evaluated using a photo‐numeric scale developed and validated on Korean skin (i.e., Korean scale). The Korean scale can be subdivided into two scales that separately address the wrinkling and dyspigmentation constituents of photo‐ageing. Aim: As there are currently no photo‐ageing scales for Chinese skin, the main objective of this study is to adapt existing photo‐ageing photo‐numeric scales for use on ethnic Chinese skin. Method: Three trained assessors studied facial photo‐ageing on 1,081 ethnic Chinese young adults from the Singapore/Malaysia Cross‐sectional Genetics Epidemiology Study (SMCGES) cohort. Results: All assessors are highly internally consistent (Weighted Kappa (κw) values≥0.952). We found that the Caucasian scale and Korean scale give nearly synonymous results for the wrinkling constituent of photo‐ageing (R2 = 0.9386). The two scales are strongly concordant (Spearman's Rank Correlation (ρ) value: 0.62 ± 0.06, p = 1.31×10−84). A weak‐to‐moderate inter‐scalar level of agreement (Cohen's Kappa (κ) values: 0.38 ± 0.05, p = 8.87×10−53) persists and is statistically significant after accounting for agreements due to chance. When tested on ethnic Chinese skin, both scales detect photo‐ageing consistently (Area under curve [AUC] values: 0.76‐0.84). Additionally, the Korean scale for the dyspigmentation constituent of photo‐ageing is concordant with both the Caucasian scale (R2 = 0.7888) and the Korean scale for the wrinkling constituent of photo‐ageing (R2 = 0.7734). Conclusion: Our results show that the Caucasian scale is suitable for capturing photo‐ageing on Chinese skin, especially wrinkle variations. The Korean dyspigmentation scale supplements the Caucasian scale to capture dyspigmentation patterns on Chinese skin that may be absent on Caucasian skin. Currently, photo‐ageing scales for Chinese skin are absent. When developed, these photo‐ageing scales must be properly validated for their ability to capture photo‐ageing of the entire face. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Alzheimer's disease (AD) is the predominant dementia globally, with heterogeneous presentation and penetrance of clinical symptoms, variable presence of mixed pathologies, potential disease subtypes, and numerous associated endophenotypes. Beyond the difficulty of designing treatments that address the core pathological characteristics of the disease, therapeutic development is challenged by the uncertainty of which endophenotypic areas and specific targets implicated by those endophenotypes to prioritize for further translational research. However, publicly funded consortia driving large‐scale open science efforts have produced multiple omic analyses that address both disease risk relevance and biological process involvement of genes across the genome. METHODS: Here we report the development of an informatic pipeline that draws from genetic association studies, predicted variant impact, and linkage with dementia associated phenotypes to create a genetic risk score. This is paired with a multi‐omic risk score utilizing extensive sets of both transcriptomic and proteomic studies to identify system‐level changes in expression associated with AD. These two elements combined constitute our target risk score that ranks AD risk genome‐wide. The ranked genes are organized into endophenotypic space through the development of 19 biological domains associated with AD in the described genetics and genomics studies and accompanying literature. The biological domains are constructed from exhaustive Gene Ontology (GO) term compilations, allowing automated assignment of genes into objectively defined disease‐associated biology. This rank‐and‐organize approach, performed genome‐wide, allows the characterization of aggregations of AD risk across biological domains. RESULTS: The top AD‐risk‐associated biological domains are Synapse, Immune Response, Lipid Metabolism, Mitochondrial Metabolism, Structural Stabilization, and Proteostasis, with slightly lower levels of risk enrichment present within the other 13 biological domains. DISCUSSION: This provides an objective methodology to localize risk within specific biological endophenotypes and drill down into the most significantly associated sets of GO terms and annotated genes for potential therapeutic targets. [ABSTRACT FROM AUTHOR]

INTRODUCTION: We aimed to expand the range of the frontotemporal dementia (FTD) phenotypes assessed by the Clinical Dementia Rating Dementia Staging Instrument plus National Alzheimer's Coordinating Center Behavior and Language Domains (CDR plus NACC FTLD). METHODS: Neuropsychiatric and motor domains were added to the standard CDR plus NACC FTLD generating a new CDR plus NACC FTLD‐NM scale. This was assessed in 522 mutation carriers and 310 mutation‐negative controls from the Genetic Frontotemporal dementia Initiative (GENFI). RESULTS: The new scale led to higher global severity scores than the CDR plus NACC FTLD: 1.4% of participants were now considered prodromal rather than asymptomatic, while 1.3% were now considered symptomatic rather than asymptomatic or prodromal. No participants with a clinical diagnosis of an FTD spectrum disorder were classified as asymptomatic using the new scales. DISCUSSION: Adding new domains to the CDR plus NACC FTLD leads to a scale that encompasses the wider phenotypic spectrum of FTD with further work needed to validate its use more widely. Highlights: The new Clinical Dementia Rating Dementia Staging Instrument plus National Alzheimer's Coordinating Center Behavior and Language Domains neuropsychiatric and motor (CDR plus NACC FTLD‐NM) rating scale was significantly positively correlated with the original CDR plus NACC FTLD and negatively correlated with the FTD Rating Scale (FRS).No participants with a clinical diagnosis in the frontotemporal dementia spectrum were classified as asymptomatic with the new CDR plus NACC FTLD‐NM rating scale.Individuals had higher global severity scores with the addition of the neuropsychiatric and motor domains.A receiver operating characteristic analysis of symptomatic diagnosis showed nominally higher areas under the curve for the new scales. [ABSTRACT FROM AUTHOR]

Background: Scleroderma, also referred to as systemic sclerosis, is a multifaceted autoimmune condition characterized by abnormal fibrosis and impaired vascular function. Pathologically, it encompasses the persistent presence of inflammation, abnormal collagen buildup, and restructuring of blood vessels in various organs, resulting in a wide range of clinical symptoms. This review incorporates the most recent scientific literature on scleroderma, with a particular emphasis on its pathophysiology, clinical manifestations, diagnostic approaches, and treatment options. Methodology: A comprehensive investigation was carried out on numerous databases, such as PubMed, MEDLINE, Scopus, Web of Science, and Google Scholar, to collect pertinent studies covering diverse facets of scleroderma research. Results: Scleroderma presents with a range of systemic manifestations, such as interstitial lung disease, gastrointestinal dysmotility, Raynaud's phenomenon, pulmonary arterial hypertension, renal complications, neurological symptoms, and cardiac abnormalities. Serological markers, such as antinuclear antibodies, anti‐centromere antibodies, and anti‐topoisomerase antibodies, are important for classifying diseases and predicting their outcomes. Discussion: The precise identification of scleroderma is crucial for promptly and correctly implementing effective treatment plans. Treatment approaches aim to improve symptoms, reduce complications, and slow down the progression of the disease. An integrated approach that combines pharmacological agents, including immunosuppressants, endothelin receptor antagonists, and prostanoids, with nonpharmacological interventions such as physical and occupational therapy is essential for maximizing patient care. Conclusion: Through the clarification of existing gaps in knowledge and identification of emerging trends, our goal is to improve the accuracy of diagnosis, enhance the effectiveness of therapeutic interventions, and ultimately enhance the overall quality of life for individuals suffering from scleroderma. Ongoing cooperation and creative research are necessary to advance the field and achieve improved patient outcomes and new therapeutic discoveries. [ABSTRACT FROM AUTHOR]

Fungi adapt to their surroundings, modifying their behaviors and composition under different conditions like nutrient availability and environmental stress. This perspective examines how a basic understanding of fungal genetics and the different ways that fungi can be influenced by their surroundings can be leveraged toward the production of functional mycelium materials. Simply put, within the constraints of a given genetic script, both the quality and quantity of fungal mycelium are shaped by what they eat and where they grow. These two levers, encompassing their global growth environment, can be turned toward different materials outcomes. The final properties of myco‐materials are thus intimately shaped by the conditions of their growth, enabling the design of new biobased and biodegradable material constructions for applications that have traditionally relied on petroleum‐based chemicals.This perspective highlights aspects of fungal genetics and environmental adaptation that have potential materials science implications, along the way touching on key studies, both to situate the state of the art within the field and to punctuate the viewpoints of the authors. Finally, this work ends with future perspectives, reinforcing key topics deemed important to consider in emerging myco‐materials research. [ABSTRACT FROM AUTHOR]

Tolerance occurs when, following an initial experience with a substance, more of the substance is required subsequently to induce identical behavioral effects. Tolerance is not well‐understood, and numerous researchers have turned to model organisms, particularly Drosophila melanogaster, to unravel its mechanisms. Flies have high translational relevance for human alcohol responses, and there is substantial overlap in disease‐causing genes between flies and humans, including those associated with Alcohol Use Disorder. Numerous Drosophila tolerance mutants have been described; however, approaches used to identify and characterize these mutants have varied across time and labs and have mostly disregarded any impact of initial resistance/sensitivity to ethanol on subsequent tolerance development. Here, we analyzed our own, as well as data published by other labs to uncover an inverse correlation between initial ethanol resistance and tolerance phenotypes. This inverse correlation suggests that initial resistance phenotypes can explain many 'perceived' tolerance phenotypes, thus classifying such mutants as 'secondary' tolerance mutants. Additionally, we show that tolerance should be measured as a relative increase in time to sedation between an initial and second exposure rather than an absolute change in time to sedation. Finally, based on our analysis, we provide a method for using a linear regression equation to assess the residuals of potential tolerance mutants. These residuals provide predictive insight into the likelihood of a mutant being a 'primary' tolerance mutant, where a tolerance phenotype is not solely a consequence of initial resistance, and we offer a framework for understanding the relationship between initial resistance and tolerance. [ABSTRACT FROM AUTHOR]

Introduction: Developmental dysplasia of hip (DDH) is a hip joint disorder leading to subsequent osteoarthritis. Previous studies suggested collagen XI alpha 1 (COL11A1) as a potential gene in hip dysplasia and chondrocyte degeneration. However, no genetic association has reported COL11A1‐related cellular therapy as treatment of DDH and joint degeneration. Methods and Results: We report identified genetic association between COL11A1 locus and DDH with genome‐wide association study (GWAS). Further exome sequencing for familial DDH patients was conducted in different populations to identify potential pathogenic Col11A1 variants for familiar DDH. Further studies demonstrated involvement of COL11A1 expression was down‐regulated in femoral head cartilage of DDH patients and Col11a1‐KO mice with induced DDH. Col11a1‐KO mice demonstrated aggravated joint degeneration and severe OA phenotype. To explore the underlying mechanism of Col11a1 in cartilage and DDH development, we generated scRNA‐seq profiles for DDH and Col11a1‐KO cartilage, demonstrating disrupted chondrocyte homeostasis and cellular senescence caused by Col11a1–HIF1α‐mediated glycolysis–OXPHOS shift in chondrocytes. Genetically and biologically inspired, we further fabricated an intra‐articular injection therapy to preventing cartilage degeneration by generating a Col11a1‐over‐expressed (OE) SMSC mini‐organoids. Col11a1‐OE organoids demonstrated superior chondrogenesis and ameliorated cartilage degeneration in DDH mice via regulating cellular senescence by up‐regulated Col11a1/HIF1α‐mediated glycolysis in chondrocytes. Conclusion: We reported association between COL11A1 loci and DDH with GWAS and exome sequencing. Further studies demonstrated involvement of COL11A1 in DDH patients and Col11a1‐KO mice. ScRNA‐seq for DDH and Col11a1‐KO cartilage demonstrated disrupted chondrocyte homeostasis and cellular senescence caused by Col11a1–HIF1α‐mediated glycolysis–OXPHOS shift in chondrocytes. Genetically and biologically inspired, an intra‐articular injection therapy was fabricated to prevent cartilage degeneration with Col11a1‐OE SMSC organoids. Col11a1‐OE organoids ameliorated cartilage degeneration in DDH mice via regulating cellular senescence by up‐regulated Col11a1/HIF1α‐mediated glycolysis in chondrocytes. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Alzheimer's disease (AD) is a complex disease influenced by genetics and environment. More than 75 susceptibility loci have been linked to late‐onset AD, but most of these loci were discovered in genome‐wide association studies (GWAS) exclusive to non‐Hispanic White individuals. There are wide disparities in AD risk across racially stratified groups, and while these disparities are not due to genetic differences, underrepresentation in genetic research can further exacerbate and contribute to their persistence. We investigated the racial/ethnic representation of participants in United States (US)‐based AD genetics and the statistical implications of current representation. METHODS: We compared racial/ethnic data of participants from array and sequencing studies in US AD genetics databases, including National Institute on Aging Genetics of Alzheimer's Disease Data Storage Site (NIAGADS) and NIAGADS Data Sharing Service (dssNIAGADS), to AD and related dementia (ADRD) prevalence and mortality. We then simulated the statistical power of these datasets to identify risk variants from non‐White populations. RESULTS: There is insufficient statistical power (probability <80%) to detect single nucleotide polymorphisms (SNPs) with low to moderate effect sizes (odds ratio [OR]<1.5) using array data from Black and Hispanic participants; studies of Asian participants are not powered to detect variants OR <= 2. Using available and projected sequencing data from Black and Hispanic participants, risk variants with OR = 1.2 are detectable at high allele frequencies. Sample sizes remain insufficiently powered to detect these variants in Asian populations. DISCUSSION: AD genetics datasets are largely representative of US ADRD burden. However, there is a wide discrepancy between proportional representation and statistically meaningful representation. Most variation identified in GWAS of non‐Hispanic White individuals have low to moderate effects. Comparable risk variants in non‐White populations are not detectable given current sample sizes, which could lead to disparities in future studies and drug development. We urge AD genetics researchers and institutions to continue investing in recruiting diverse participants and use community‐based participatory research practices. [ABSTRACT FROM AUTHOR]

The resources for carrying out and analyzing microbial evolution experiments have become more accessible, making it possible to expand these studies beyond the research laboratory and into the classroom. We developed five connected, standards‐aligned yeast evolution laboratory modules, called "yEvo," for high school students. The modules enable students to take agency in answering open‐ended research questions. In Module 1, students evolve baker's yeast to tolerate an antifungal drug, and in subsequent modules, investigate how evolved yeasts adapted to this stressful condition at both the phenotype and genotype levels. We used pre‐ and post‐surveys from 72 students at two different schools and post‐interviews with students and teachers to assess our program goals and guide module improvement over 3 years. We measured changes in student conceptions, confidence in scientific practices, and interest in STEM careers. Students who participated in yEvo showed improvements in understanding of activity‐specific concepts and reported increased confidence in designing a valid biology experiment. Student experimental data replicated literature findings and has led to new insights into antifungal resistance. The modules and provided materials, alongside "proof of concept" evaluation metrics, will serve as a model for other university researchers and K − 16 classrooms interested in engaging in open‐ended research questions using yeast as a model system. [ABSTRACT FROM AUTHOR]