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Bara, A.

Publications and source records attributed to Bara, A..

4 recordsLinked to original sources

Designing AI-programmable therapeutics with the EDEN family of foundation models

The ability to interpret, modify, and design DNA has driven many of the most significant advances in modern medicine, from diagnostics, biologics, and vaccines to cell and gene therapies. However, the inherent complexity of biological systems means that most modern medicines are still engineered using bespoke, labor-intensive processes. To address the need for a generalisable and programmable approach to therapeutic design, we introduce the EDEN (environmentally-derived evolutionary network) family of metagenomic foundation models, including a 28 billion parameter model trained on 9.7 trillion nucleotide tokens from BaseData1. This dataset, at the time of training, contained more than 10 billion novel genes from over 1 million new species, and is intentionally enriched for environmental and host-associated metagenomes, phage sequences, and mobile genetic elements, enabling the model to learn from diverse and novel cross-species evolutionary mechanisms and apply them to key challenges in human health. EDEN achieves state-of-the-art performance across a series of predictive and generative genomic and protein benchmarks. To demonstrate the models broad applicability across biology, we evaluate EDENs capacity for programmable therapeutic design by challenging a single architecture to design biological novelty across three distinct therapeutic modalities, disease areas and biological scales: (i) large gene insertion, (ii) antibiotic peptide design, and (iii) microbiome design. First, we demonstrate AI-programmable Gene Insertion (aiPGI), in which EDEN designs de novo large serine recombinases (LSRs) capable of inserting large pieces of DNA at desired target sites in the human genome when prompted only on 30 nucleotides of DNA sequence from the desired target site. In low-N experimental validation, EDEN generated multiple active recombinases for all tested disease-associated genomic loci (ATM, DMD, F9, FANCC, GALC, IDS, P4HA1, PHEX, RYR2, USH2A) and 4 potential safe harbor sites in the human genome. EDEN achieves an overall functional hit rate of 63.2% across diverse DNA prompts when prompted on only 30bp of DNA from outside the training data. 50% of EDEN-generated LSRs were active in human cells, achieving therapeutically relevant levels of CAR insertion in primary human T cells. We also show that EDEN can generate active bridge recombinases when prompted on the associated guide RNA alone, with sequence identities to training and public data as low as 65%. These results pave the way for a new generation of cell and gene therapies by opening the door to rapid, programmable and site-specific integration of large genetic payloads without double-strand breaks. This offers an alternative to the safety, efficiency and payload limitations inherent in viral or nuclease-based editing at thousands of currently intractable human therapeutic targets. Second, we use the same model to generate a focused low-N library of novel antimicrobial peptides where 97% showed activity, with top candidates achieving single-digit micromolar potency against critical-priority multidrug-resistant pathogens. Third, to demonstrate that EDEN captures inter-genomic features, we design a gigabase-scale microbiome with over 94,000 synthetic metagenomic assemblies, including prophage genomes and correct cross-species metabolic pathway completions. The EDEN-generated synthetic microbiome covers 9,067 species with a biome-specific taxonomic accuracy of 99%. Over 1,500 of the generated species were outside the fine-tuning dataset while retaining the correct microecological properties and biome association, thus significantly expanding genetic and taxonomic diversity. Together, these results establish a new strategic direction for AI-programmable therapeutics, in which a single foundation model architecture designs candidate therapeutics across diverse modalities and disease areas. This suggests that the combination of billions of years of evolutionary data with specific therapeutic records offers a clear, scaling-driven path to making therapeutic design a predictable engineering discipline. O_FIG O_LINKSMALLFIG WIDTH=141 HEIGHT=200 SRC="FIGDIR/small/699009v2_ufig1.gif" ALT="Figure 1"> View larger version (59K): org.highwire.dtl.DTLVardef@68c20borg.highwire.dtl.DTLVardef@19b8e8corg.highwire.dtl.DTLVardef@1ab9362org.highwire.dtl.DTLVardef@1592cb7_HPS_FORMAT_FIGEXP M_FIG C_FIG

genomics↗

Sex-specific maturational trajectory of endocannabinoid plasticity in the rat prefrontal cortex

The prefrontal cortex (PFC) develops until early adulthood in rodents and humans, but how synaptic plasticity evolves throughout postnatal development is not known. Here, we used a cross-sectional approach to establish the postnatal maturational trajectories of intrinsic properties and synaptic plasticity in the PFC of rats of both sexes. We found that while layer 5 PFC pyramidal neurons from rats of both sexes displayed similar current-voltage relationships, rheobases and resting potentials across all age groups, excitability was lower in female adults compared to the other developmental stages. NMDAR-dependent long-term potentiation and mGluR2/3-mediated long-term depression (LTD) were equally expressed at the juvenile, pubescent and adult developmental stages in animals of both sexes. However, the developmental course of endocannabinoid (eCB)-mediated LTD was sexually dimorphic. First, eCB-LTD emerged during the juvenile period in females. However, although CB1Rs were functional in both sexes at all developmental stages, eCB-LTDs first emerged during pubescence in male. Second, eCB-LTD engaged distinct receptors in males and females depending on their developmental stages. Female rats employ both CB1R and TRPV1R to produce eCB-LTD at the juvenile stage but solely CB1R at pubescence followed by only TRPV1R at adulthood. In contrast, in pubescent and adult males eCB-LTD always and exclusively depended on CB1R. Pharmacological blockade of 2AGs principal degrading enzyme allowed incompetent male juvenile synapses to express eCB-LTD. The data reveal different maturational trajectories in the PFC of male and female rats and provide new cellular substrates to the sex-specific behavioral and synaptic abnormalities caused by adolescent exposure to cannabinoids.

neuroscience↗

Sex differences in the behavioral and synaptic consequences of a single exposure to cannabinoid at puberty and adulthood

Heavy cannabis consumption among adolescents is associated with significant and lasting neurobiological, psychological and health consequences that depend on the age of first use. Chronic exposure to cannabinoid (CB) agonists during adolescence alters social behavior and prefrontal cortex (PFC) activity in adult rats. However, sex differences on social behavior as well as PFC synaptic plasticity after acute CB activation remain poorly explored. Here, we determined the consequences of a single CB activation differently affects PFC in males and females by assessing social behavior and PFC neuronal and synaptic functions in rats during pubertal or adulthood periods, 24h after a single in-vivo cannabinoid exposure (SCE). During puberty, SCE reduced play behavior in females but not males. In contrast, SCE impaired sociability in both sexes at adulthood. General exploration and memory recognition remained normal at both ages and both sexes. At the synaptic level, SCE ablated endocannabinoid-mediated long-term depression (eCB-LTD) in the PFC of females of both ages and heightened excitability of PFC pyramidal neurons at adulthood, while males were spared. In contrast, SCE was associated to impaired long-term potentiation in adult males. Together, the data indicate behavioral and synaptic sex differences in response to a single in-vivo exposure to cannabinoid at puberty and adulthood.

neuroscience↗

Sex specific endophenotypes of in-utero cannabinoid exposure

Cannabinoids can cross the placenta, thus may interfere with fetal endocannabinoid signaling during neurodevelopment, causing long-lasting deficits. Despite increasing cannabis consumption during pregnancy, the protracted consequences of prenatal cannabinoid exposure (PCE) remain incompletely understood. Here we report sex-specific differences in behavioral and neuronal deficits in the adult progeny of rat dams exposed to low doses of cannabinoids during gestation. In males, PCE reduced social interaction, ablated endocannabinoid long-term depression (LTD) and heightened excitability of prefrontal cortex pyramidal neurons, while females were spared. Group 1 mGluR and endocannabinoid signaling regulate emotional behavior and synaptic plasticity. Notably, sex-differences following PCE included levels of mGluR1/5 and TRPV1R mRNA. Finally, positive allosteric modulation of mGlu5 and enhancement of anandamide levels restored LTD and social interaction in PCE adult males. Together, these results highlight marked sexual differences in the effects of PCE and introduce strategies for reversing detrimental effects of PCE.

neuroscience↗