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The real power of the biological tool lies in exploring how genomes work.

Birds and bees are just the beginning for a burgeoning technology.

A controversial study has suggested that the neurodegenerative disease might be transferred from one person to another. Now scientists are racing to find out whether that is true.

We are accustomed to treating aging as a set of things that go wrong with the body. But for more than twenty years, there has been accumulating evidence that much of the process takes place under genetic control.

The new drug, called IONIS-HTTRx, silences the gene known to be responsible for the production of a protein which causes Huntington’s

Direct induction of induced hepatocytes (iHeps) from fibroblasts holds potential as a strategy for regenerative medicine but until now has only been shown in culture settings. Here, we describe in vivo iHep formation using transcription factor induction and genetic fate tracing in mouse models of chronic liver disease.

This could explain why obese people have lower mortality rates. For the first time, scientists have discovered a connection between a cell's fat content and its lifespan, which could explain the 'obesity paradox' that's been puzzling scientists for decades: why obese people have the lowest all-cause mortality rates, whereas the rate for those who are fit and lean is higher.

Purpose: Telomere attrition and corresponding cellular senescence of the retinal pigment epithelium contribute to the changes of age-related macular degeneration. Activation of the enzyme telomerase can add telomeric DNA to retinal pigment epithelium chromosomal ends and has been proposed as a treatment for age-related macular degeneration. We report the use of a small molecule, oral telomerase activator (TA)-65 in early macular degeneration. This study, focusing on early macular degeneration, p...

In the fierce debate about CRISPR gene editing, it’s time to give patients a voice.

Muscle stem cells (MuSCs) exhibit distinct behavior during successive phases of developmental myogenesis. However, how their transition to adulthood is regulated is poorly understood. Here, we show that fetal MuSCs resist progenitor specification and exhibit altered division dynamics, intrinsic features that are progressively lost postnatally.