Justice Department Orders Three NSF Diversity Programs Ended: The U.S. Justice Department has ruled that three long-running National Science Foundation programs aimed at increasing participation by historically underrepresented groups violate constitutional protections against race- and sex-based discrimination. The affected initiatives include the Louis Stokes Alliances for Minority Participation, Alliances for Graduate Education and the Professoriate, and a program supporting Hispanic-Serving Institutions, together accounting for more than $100 million in congressional appropriations. DOJ said four other NSF workforce programs remain lawful and two could continue with modifications. The opinion relies heavily on recent Supreme Court decisions restricting the use of race in admissions and other government programs. Critics warn the ruling could weaken efforts to broaden participation in science, while some legal experts say it still leaves room for race- and sex-neutral strategies targeting socioeconomic, geographic, or disability-related barriers. (Science)

Congo Ebola Outbreak Becomes Country’s Deadliest: The Democratic Republic of the Congo is experiencing its deadliest Ebola outbreak on record, with 2,325 deaths and nearly 5,000 cases reported in just three months. The outbreak, caused by the Bundibugyo strain, has surpassed the country’s 2018–2020 epidemic and now carries a case-fatality rate of roughly 46%. Unlike some other Ebola strains, Bundibugyo currently lacks an effective vaccine or approved therapeutic, raising concerns that the epidemic could continue accelerating. During the week of August 3–9 alone, officials recorded 579 cases and 304 deaths, the highest weekly totals so far. Health workers are also being infected, with at least 155 confirmed cases among them. The United Nations has committed an additional $30.5 million as international officials warn that rapid intervention is increasingly urgent. (CIDRAP)

Narcolepsy Drug Targets Disorder at Its Source: The FDA has approved oveporexton (Orzeyful), the first narcolepsy treatment designed to address the disorder’s underlying biology rather than merely suppress its symptoms. Type 1 narcolepsy is associated with loss of orexin-producing neurons in the hypothalamus, disrupting the brain’s ability to regulate sleep and wakefulness. Oveporexton mimics orexin by activating its receptors, helping stabilize those circuits. In two phase III trials involving 273 people, patients taking the drug showed improved daytime alertness, nighttime sleep, cataplexy, sleep paralysis, and hallucinations. Researchers say orexin agonists could represent a new therapeutic class, with companies developing similar compounds. Scientists are also exploring whether orexin-targeting drugs might eventually help treat fatigue, ADHD, Parkinson’s disease, multiple sclerosis, anxiety, addiction, and other neurological conditions. (Nature)

Alzheimer’s Risk Gene Directly Disrupts Neuronal Synapses: Researchers have identified PLCG2 as a potentially important genetic link between Alzheimer’s disease risk and the breakdown of synaptic function. Using high-content screening in neuronal cultures, the team found that reducing PLCG2 expression disrupted dendritic structure and synaptic activity in mouse neurons. The effect carried over to human neuronal cultures, where PLCG2 downregulation impaired synapses while increasing amyloid-beta levels and tau phosphorylation, two major Alzheimer’s hallmarks. Very rare loss-of-function variants in PLCG2 were associated with roughly tenfold higher Alzheimer’s risk. Single-nucleus RNA sequencing also showed altered pathways tied to neuronal and synaptic function. The findings suggest that PLCG2 is not simply an immune-related Alzheimer’s risk gene, but may act directly within neurons to influence disease vulnerability and progression. (Nature)

Heart Failure Subtypes Have Distinct Genetic Blueprints: A large multi-ancestry genome-wide association study has mapped genetic differences between the two major forms of heart failure: reduced ejection fraction and preserved ejection fraction. Researchers analyzed 38,781 cases of reduced-EF heart failure, 38,163 preserved-EF cases and more than 526,000 controls drawn from European, African, Hispanic and Asian ancestry groups. They identified 46 significant loci for reduced-EF disease, including nine previously unknown, and three loci for preserved-EF disease, one of them novel. Several signals appeared specifically in participants of African ancestry and were rare in European populations. A broader analysis of more than 200,000 heart-failure cases uncovered 136 loci. Follow-up analyses highlighted vascular, metabolic and TGF-beta/Smad signaling pathways, underscoring the value of diverse populations for understanding cardiovascular genetics. (Nature)

Hidden Mutation Helps Tuberculosis Resist Key Antibiotic: Genomic surveillance has uncovered another route by which Mycobacterium tuberculosis can become resistant to antibiotics. Researchers combined population genomics with laboratory genetics and identified frequent mutations in a gene called idsA2 among clinical strains. Disrupting idsA2 altered isoprenoid metabolism and reduced bacterial susceptibility to several drugs, with the strongest effect seen for ethambutol. The mutations doubled the drug concentration needed to inhibit growth and often appeared after mutations in embB, a well-known ethambutol-resistance gene. When both mutations were present, their effects multiplied, producing high-level resistance. Lipid analyses suggested that idsA2 mutations redirect metabolic resources toward decaprenyl phosphate compounds, helping explain the mechanism. Adding idsA2 variants to genetic resistance tests could improve the accuracy of identifying ethambutol-resistant tuberculosis and guide treatment choices. (PLOS)

Sequencing Reveals Familial Heart Disease Variants: A small case-control sequencing study in Pakistan has found potentially important genetic variants among young adults with familial cardiovascular disease. Researchers examined 20 patients treated at two tertiary hospitals in Peshawar and compared them with 20 matched healthy controls. Targeted PCR and Sanger sequencing focused on candidate genes previously linked to inherited cardiovascular disorders, including LRP6, MEF2A and CYP27A1. Mutations were detected in 12 of the 20 affected participants. The study is notable because it examines a population with high rates of consanguinity, where recessive and familial variants can become more visible across generations. However, the sample was small, so the findings need validation in much larger cohorts. The authors argue that expanded genomic screening could eventually improve early detection and prevention in high-risk families. (PLOS)

Marmoset Brains Can Contain Their Siblings’ Cells: Marmosets can carry a surprising biological legacy from their littermates: substantial numbers of brain immune cells containing a sibling’s genome. Because marmoset twins and triplets share connected circulation in the womb, stem cells can pass between siblings and persist for life. Researchers used single-cell RNA sequencing and transcribed genetic variants to identify the origin of cells in blood, liver, kidney and multiple brain regions. They found that sibling-derived cells were restricted to blood-forming lineages. In the brain, 20 to 52 percent of microglia and 18 to 64 percent of macrophages could come from a sibling, while neurons, glia and ependymal cells did not show such chimerism. The pattern varied across brain regions, offering researchers a natural experiment for separating genetic effects from local brain-environment effects. (Life Science Network)

Multifunctional Genes Face Strong Evolutionary Constraints: Genes that perform several biological jobs at once may evolve more slowly, but pleiotropy alone does not explain their connection to neurological disease. Researchers examined genes involved in immunity, neuronal function or both across 12 Drosophila species. They compared evolutionary constraint using dN/dS ratios and also measured how broadly genes were expressed across developmental stages. Genes shared between the nervous and immune systems showed stronger purifying selection and less stage-specific expression than immune-only genes, consistent with the idea that multifunctional genes face tighter evolutionary constraints. The team then examined human counterparts of these genes for links to neurological disease. Slower-evolving genes were more often disease-associated, but that relationship was strongest for neuron-specific genes rather than pleiotropic ones. The results complicate simple assumptions about multifunctional genes and disease risk. (OUP Academic)

New Candidate Genes Emerge for Hereditary Cancer: Researchers studying hereditary breast and ovarian cancer have identified additional candidate susceptibility genes in families where standard genetic testing finds no explanation. The team analyzed the full set of genes and patterns of gene activity in blood samples from 134 people with breast cancer, ovarian cancer or both. All had previously tested negative for disease-causing variants in the 13 established high-risk genes used in routine screening, including BRCA1 and BRCA2. The analysis highlighted genes involved in DNA repair and genome stability, including some better known for rare recessive disorders. The results suggest that, in certain cases, carrying an altered copy of one of these genes may contribute to cancer susceptibility. The candidates are not yet established clinical risk genes, but larger sequencing datasets could clarify which variants genuinely increase risk. (Medical Xpress)

Three-Dimensional DNA Maps Expose Crohn’s Risk Genes: A new genomic method is making it possible to connect disease-associated DNA variants with the genes they regulate inside rare immune cells. Researchers adapted promoter-capture Hi-C to work with relatively small numbers of type 3 innate lymphoid cells, or ILC3s, which help maintain gut barriers and regulate inflammation. By mapping the three-dimensional folding of DNA, the team could identify distant enhancers that physically contact gene promoters rather than assuming a risk variant acts on the nearest gene. Combining those maps with genome-wide association data prioritized more than 100 candidate genes linked to Crohn’s disease. One unexpected candidate was CLN3, best known for causing Batten disease. Mouse experiments showed that increasing Cln3 reduced inflammatory gene activity and cytokine production, though the researchers caution that this does not yet prove CLN3 causes inflammatory bowel disease. (Medical Xpress)

Ancient DNA Rewrites Pacific Migration Timeline: Ancient DNA from Fiji and neighboring Pacific islands is sharpening the timeline of one of humanity’s great ocean migrations. Researchers generated genomic data from skeletal remains of 72 people spanning roughly the past 3,000 years, including the first ancient human genomes from Fiji. The results distinguish two major movements into Remote Oceania. An early population related primarily to Southeast Asians moved rapidly through the region, while later Papuan-related ancestry spread more slowly. Genetic dating places Papuan-related ancestry in Vanuatu by about 2,700 years ago, but suggests it took roughly another 500 years to appear farther east in Fiji. The genomes also document later movements that helped create Polynesian “outlier” communities in Vanuatu. The study reveals repeated migration, mixing and social complexity rather than a single wave of Pacific settlement. (Phys.org)

Old Tissue Archives Gain New Genomic Life: Scientists have developed a more precise way to recover molecular information from old, formalin-fixed tissue samples stored in hospitals and pathology archives. Traditional approaches often isolate only cell nuclei from these preserved specimens, losing much of the RNA and other information contained in the rest of the cell. A new method instead recovers more intact whole cells, allowing researchers to capture a richer picture of gene activity and cell identity. Tests on colon and thymus tissue showed especially strong improvements in colon samples, where larger cells retain substantial material outside the nucleus. The approach could transform enormous collections of archived patient tissue into usable resources for genomics and cell biology, enabling researchers to compare gene expression across age, disease and treatment histories without requiring new biopsies or prospective sample collection. (Phys.org)