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Category: genetics – Page 9

CRISPR’s efficiency triples with DNA-wrapped nanoparticles

EVANSTON, IL. — With the power to rewrite the genetic code underlying countless diseases, CRISPR holds immense promise to revolutionize medicine. But until scientists can deliver its gene-editing machinery safely and efficiently into relevant cells and tissues, that promise will remain out of reach.

Now, Northwestern University chemists have unveiled a new type of nanostructure that dramatically improves CRISPR delivery and potentially extends its scope of utility.

Called lipid nanoparticle spherical nucleic acids (LNP-SNAs), these tiny structures carry the full set of CRISPR editing tools — Cas9 enzymes, guide RNA and a DNA repair template — wrapped in a dense, protective shell of DNA. Not only does this DNA coating shield its cargo, but it also dictates which organs and tissues the LNP-SNAs travel to and makes it easier for them to enter cells.

New system delivers CRISPR machinery more safely and effectively into cells.

Satiation variability prediction using AI for obesity treatment

Meal size and termination is regulated by a process called satiation, which varies widely among adults with obesity.

The researchers assessed calories to satiation (CTS) and integrated a machine learning genetic risk score (CTSGRS) to predict obesity treatment outcomes.

High CTS or CTSGRS identified individuals who responded better to phentermine-topiramate, whereas low CTS or CTSGRS predicted greater weight loss with liraglutide, highlighting personalized obesity therapy.

Heterochronic myeloid cell replacement reveals the local brain environment as key driver of microglia aging

Aging, the key risk factor for cognitive decline, impacts the brain in a region-specific manner, with microglia among the most affected cell types. However, it remains unclear whether this is intrinsically mediated or driven by age-related changes in neighboring cells. Here, we describe a scalable, genetically modifiable system for in vivo heterochronic myeloid cell replacement. We find reconstituted myeloid cells adopt region-specific transcriptional, morphological and tiling profiles characteristic of resident microglia. Young donor cells in aged brains rapidly acquired aging phenotypes, particularly in the cerebellum, while old cells in young brains adopted youthful profiles. We identified STAT1-mediated signaling as one axis controlling microglia aging, as STAT1-loss prevented aging trajectories in reconstituted cells. Spatial transcriptomics combined with cell ablation models identified rare natural killer cells as necessary drivers of interferon signaling in aged microglia. These findings establish the local environment, rather than cell-autonomous programming, as a primary driver of microglia aging phenotypes.

Claire Gizowski, Galina Popova, Heather Shin, Wendy Craft, Wenjun Kong, Bernd J Wranik, Yuheng C Fu, Tzuhua D Lin, Baby Martin-McNulty, Po-Han Tai, Kayla Leung, Nicole Fong, Devyani Jogran, Agnieszka Wendorff, David Hendrickson, Astrid Gillich, Andy Chang, Oliver Hahn are current or former employees of Calico Life Sciences LLC. The remaining authors declare no competing interest.

Diet, Supplements Of A Longevity Scientist (Blood Test #5 In 2025)

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Researchers uncover critical genetic drivers of the gut’s ‘nervous system’ development

Vanderbilt researchers, including those from the Vanderbilt Brain Institute, have made significant strides in understanding how the enteric nervous system—sometimes called the “brain” of the gut—forms and functions.

In a study published in Cellular and Molecular Gastroenterology and Hepatology, the lab of principal investigator, Michelle Southard-Smith, sheds light on how the SOX10 protein contributes to the development of gut cells that play a role in gastrointestinal motility, or how food moves through the digestive system.

The paper is titled “Single Cell Profiling in the Sox10Dom Hirschsprung Mouse Implicates Hox genes in Enteric Neuron Trajectory Allocation.”

New insights into the epigenetic processes via which neuroinflammation causes memory loss

Neuroinflammation, a prolonged activation of the brain’s immune system prompted by infections or other factors, has been linked to the disruption of normal mental functions. Past studies, for instance, have found that neuroinflammation plays a central role in neurodegenerative diseases, medical conditions characterized by the progressive degradation of cells in the spinal cord and brain.

When inflammation is taking place, cells release proteins that act as signals between immune cells, also known as cytokines. While some studies have linked a specific cytokine called interleukin-1 (IL-1) to changes in brain function, the mechanisms through which it could contribute to a decline in mental capabilities remain poorly understood.

Researchers at the University of Toulouse INSERM and CNRS recently carried out a study involving mice aimed at better understanding these mechanisms. Their paper, published in Nature Neuroscience, particularly focused on neuroinflammation elicited by the parasite Toxoplasma gondii (T. gondii), which is responsible for a well-known illness called toxoplasmosis.

How an autism-linked mutation reduces vasopressin and alters social behavior

A team of researchers has identified for the first time the mechanism linking a mutation in the Shank3 gene with alterations in social behavior. Using a mouse model carrying this autism-associated mutation, the study shows that vasopressin, a brain hormone essential for social relationships, is not properly released in the lateral septum.

The team is from the Cognition and Social Interactions laboratory, led by Félix Leroy at the Institute for Neurosciences, a joint center of the Spanish National Research Council (CSIC) and the Miguel Hernández University (UMH) of Elche.

The work, published in Nature Communications, demonstrates that the proper release of vasopressin in this region regulates social behaviors through two distinct receptor pathways: one controlling sociability and the other controlling social aggression, and that selective activation of these receptors can reverse deficits in social interaction without triggering unwanted aggressive responses.

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