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Category: genetics – Page 16

Optogenetics, Biohybrid Implants And The Future Of Brain-Computer Interfaces | Dr. Alan Mardinly

Optogenetics, Biohybrid Implants And The Future Of Brain-Computer Interfaces — Dr. Alan Mardinly Ph.D. — CSO & Co-Founder, Science

What if we could restore vision, communicate directly with the brain, and even extend human life—not with machines alone, but with living, engineered biology?

Dr. Alan Mardinly, Ph.D. is the Chief Scientific Officer and Co-Founder of Science Corp. (https://science.xyz/), a neurotechnology company developing next-generation brain interfaces and biohybrid neural implants aimed at restoring human function.

Dr. Mardinly leads the company’s biohybrid program, focused on combining genetically engineered cells with advanced optical hardware to create optogenetic therapies for vision restoration and new types of brain-machine interfaces.

Dr. Mardinly has spent more than 15 years working at the intersection of neuroscience, genetics, and neural engineering.

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A nanoparticle therapy to treat lung cancer and associated muscle wasting at the same time

Researchers at Oregon State University have developed a technique for simultaneously treating lung cancer and a serious muscle-wasting condition that often accompanies it. The study, published in the Journal of Controlled Release, involves lipid nanoparticles delivering therapeutic genetic material to lung tumors.

In a mouse model, scientists led by Oleh Taraula and Yoon Tae Goo of the OSU College of Pharmacy showed that a type of nanocarrier loaded with follistatin messenger RNA is able to accumulate in tumors. Once there, the mRNA triggers cells to produce the follistatin protein, which plays a key role both in inhibiting tumors and promoting muscle tissue growth.

The lipid nanoparticles, or LNPs, can be administered intravenously and reach the lungs courtesy of another protein, vitronectin, that’s found in blood serum. Lipids are fatty acids and similar organic compounds, including many natural oils and waxes. Nanoparticles are tiny pieces of material ranging in size from one-to 100-billionths of a meter.

Cellular reprogramming beyond pluripotency

Aging, once viewed as an irreversible process, is now considered a modifiable process. Recent advances in cellular reprogramming reveal that transient expression of reprogramming factors can reverse molecular hallmarks of aging while preserving somatic cell identity. This ‘partial reprogramming’ rejuvenates tissues, restores regenerative capacity, and, in some models, extends lifespan without the tumorigenic risks of full dedifferentiation. In this review, we summarize genetic and chemical strategies for partial reprogramming, discuss their tissue-specific effects in vivo, and evaluate their implications for tissue regeneration and age-related disease. We further examine key challenges for clinical translation, including safety, delivery strategies, and temporal control of reprogramming.

What keeps vision cells alive?

Clear patterns emerged: two kinase inhibitors consistently protected cones over extended periods.

The researchers identified inhibitors of casein kinase 1 (CK1) that protected cones, heat shock protein 90 (HSP90) inhibitors that saved cones in the short term but damaged them in the longer term, and broad histone deacetylase (HDAC) inhibition by many compounds that significantly damaged cones.

The protective effects held across different stress conditions and were further confirmed in a mouse model of retinal degeneration, supporting their broader relevance.

Beyond identifying protective pathways, the study makes a comprehensive dataset publicly available, covering the compounds tested, their molecular targets, and their effects on human cone survival. This resource will guide the development of therapies aimed at preserving central vision and enable a systematic assessment of potential retinal toxicity. ScienceMission sciencenewshighlights.

Scientists have identified genetic pathways and compounds capable of protecting cone photoreceptors from the degeneration that underlies conditions like age-related macular degeneration.

Cone photoreceptors, concentrated in the macula, are essential for reading, recognizing faces, and perceiving colors. Their death, as it happens in many inherited retinal diseases and macular degeneration, leads to the loss of central vision. Despite decades of research, no approved therapies can halt this process. This new study, conducted by researchers addresses this unmet need using a human-based experimental system.

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Cellular and molecular mechanisms of astrocyte plasticity in learning and memory

Astrocyte plasticity in learning and memory.

Neuronal hallmark features of learning and memory, such as activity dependent plasticity, circuit-level modulation, and gene regulatory mechanisms, are also observed in astrocytes.

Astrocytic calcium displays plastic, activity-dependent recruitment and refinement (akin to neuronal activity) across neuronal subtypes, brain regions, and behavioral paradigms, and Designer Receptors Exclusively Activated by Designer Drugs (DREADDs)-mediated manipulations highlight astrocytic recruitment of circuit-specific neurons.

Astrocyte peripheral processes display activity-dependent plasticity and are able to discriminate between neuronal subtypes, circuits, and even individual synapses.

Single-cell RNA sequencing reveals molecularly defined subtypes of astrocytes that display unique transcriptional responses to learning and memory and implicates potential ‘ensemble’-like networks of astrocytes. sciencenewshighlights ScienceMission https://sciencemission.com/astrocyte-plasticity

Learning and memory arise from coordinated activity-dependent plasticity across neural circuits and brain regions. Astrocytes are increasingly recognized as active contributors to learning and memory via their roles in sensing, integrating, and responding to contextual information. Astrocytes modulate synaptic transmission, engage in circuit-specific signaling, and display context-dependent calcium dynamics that influence behavior. In this review, we focus on astrocyte functions across rodent models that display plasticity traditionally ascribed to neurons, including activity-dependent molecular and structural plasticity, circuit-level modulation, ensemble-like networks, and transcriptional, translational, proteomic, and epigenetic plasticity.

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New genetic risk score better predicts diabetes, obesity and downstream complications

Type 2 diabetes (T2D) and obesity are metabolic conditions with many causes, including overlapping and distinct genetic features. A polygenic risk score (PRS) can capture multiple genetic risk factors to provide an estimate for whether a person may develop a complex medical condition and how they might fare long-term.

Building stronger genetic risk scores By integrating genetic findings from several of the world’s largest biobanks, investigators from Mass General Brigham built metabolic PRSs for predicting obesity and T2D, which outperformed existing disease-prediction models and predicted downstream morbidity and clinical interventions. Findings are published in Cell Metabolism.

“Our intention was to not only capture the risk of being diagnosed with obesity or diabetes, but also to better predict health consequences across the life course by integrating many aspects of metabolic function,” said co-first author Min Seo Kim, MD, MSc.

Designed to remember

In a new Science study, researchers report that specific regions dense in cytosine and guanosine dinucleotides are epigenetically modified during inflammation to enable gene expression and that these changes persist during the animal’s lifetime.

The finding has implications for understanding how the genome determines the longevity of memory, which affects tissue fitness.

Learn more in a new Science Perspective.

Specific DNA sequence features encode the persistence of epigenetic memory of inflammation.

Guillaume Blot and Przemyslaw Sapieha Authors Info & Affiliations

Science

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Advancements in organoid models emulating metastatic niches

Metastatic niche in organoid models.

The mortality rate of cancer patients remains high, mainly due to the lack of metastasis-tailored treatments, highlighting the need for alternative experimental approaches that capture metastatic development in a human context.

Human-induced pluripotent stem cell derived organoids cocultured with cancer cells (‘chimeroids’) have the potential to emulate aspects of colonized organ specific microenvironments and offer an alternative platform for target identification and drug discovery, as these models are amenable to scalable genetic and chemical perturbation screens.

Conceptually, organoid models have progressed from epithelial-only organoids to multilineage, niche enriched systems incorporating stromal, vascular, and tissue-resident immune components, thereby bringing in vitro models closer to organ-specific metastatic microenvironments.

Yet no single organoid model fully recapitulates the entire complexity of an organ in vivo; thus, model selection must be driven by the specific scientific question, ensuring that the relevant stage of metastatic development and organ microenvironment are appropriately represented. ScienceMission sciencenewshighlights https://sciencemission.com/organoid-models-emulating-metastatic-niches

Metastases cause most cancer-related deaths, underscoring the need for therapies targeting metastatic stages, including the tumor microenvironment. Yet translating biological insights into treatments remains difficult. Preclinical metastasis research largely relies on rodent models, which have species-specific limitations and are incompatible with large-scale perturbation screens in a human context. Human organoids aim to emulate organ microenvironments in vitro and, when cocultured with cancer cells, can provide complementary models. These ‘chimeroids’ may enable scalable studies of cancer–microenvironment interactions and support genetic and pharmacological screens to discover new targets, offering insights into the final, often lethal step of metastasis—tissue colonization.

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