Tattoo ink stays with you for life. Researchers are now asking how these pigments interact with the immune system and whether long-term exposure matters.
Category: biotech/medical – Page 174
New mouse model of virus-driven liver cancer may boost diagnosis and treatments
Liver cancer is one of the world’s deadliest cancers, and most cases are linked to chronic viral hepatitis. Yet scientists have lacked an animal model that faithfully recapitulates how the disease unfolds in people, from initial infection with a virus to liver inflammation, scarring, and cancer. Now, researchers at The Rockefeller University have developed that model, as described in the Journal of Hepatology.
By infecting ordinary laboratory mice with an engineered version of Norway rat hepacivirus (NrHV)—a close relative of hepatitis C virus (HCV)—and tracking the animals over 18 months, the team documented the progression from chronic viral hepatitis to spontaneous liver cancer.
“This model fills a critical gap that has long existed in the field,” says Charles M. Rice, whose Laboratory of Virology and Infectious Disease helmed the study. “For the first time, we have a system in which natural chronic viral infection drives liver cancer in an immunologically healthy animal, opening the door to studies and preclinical trials that simply weren’t possible before.”
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.
First-in-class molecules dial down inflammation without compromising immunity
Scripps Research scientists have developed a new class of drug compounds that reduce harmful inflammation while leaving the body’s ability to fight infections intact—a long-sought goal in treating autoimmune diseases. The compounds, called ENDOtollins, work by interrupting a “molecular handshake” between two proteins inside immune cells. The research, published in Nature Chemical Biology, could lead to more targeted treatments for conditions like lupus, rheumatoid arthritis and juvenile arthritis, which together affect more than 15 million Americans.
“A key component of our approach is to begin by understanding the biological mechanisms at play,” says Sergio D. Catz, professor at Scripps Research and senior author. “By accomplishing this first, we can more easily target the pathway driving inflammation without affecting other important processes.”
New Alzheimer’s Treatment Strategy Reverses Cognitive Decline in Mice
Researchers have developed a novel compound that could transform the way we treat Alzheimer’s disease, offering not just a new weapon but potentially a new strategy for battling the most common form of dementia worldwide.
While current drugs for Alzheimer’s mostly focus on removing amyloid-beta plaques associated with the disease, the new compound takes a fundamentally different approach, instead targeting a specific enzyme to therapeutically reprogram the epigenome of neurons – a series of molecular marks that can be added to or removed from DNA, to change the way genes work.
Monoclonal antibody drugs such as lecanemab and donanemab, which target amyloid-beta proteins, help somewhat to slow the progression of the disease when treatment is started early, but there is still no proven way to reverse cognitive decline from Alzheimer’s in humans.