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Neural crest cells arise early in the development of vertebrates, migrate extensively through the embryo, and differentiate to give rise to a wide array of diverse derivatives. Their contributions include a large proportion of our peripheral nerves, the melanocytes that provide skin color and protection from damaging UV light, as well as many different cell types in our face, including muscle, bone, cartilage and tooth-forming cells.

An international team of scientists has for the first time shown that mitochondria, the batteries of the cells, are essential for ageing.

Ironically, antiaging product advertisements often promise to “slow down the clock.” But abolishing the circadian clock—for example, by knocking out Bmal1, a core clock gene—accelerates aging and shortens the life span in mice. As a result, Bmal1 knockout mice often serve as a model system in studies of the role of circadian rhythms in the aging process. Now Yang et al. show that the developmental timing of Bmal1 expression influences the circadian clock’s effects on aging and survival.

As brain cells age they lose the fibers that receive neural impulses, a change that may underlie cognitive decline. Researchers at the University of California, Irvine recently found a way to reverse this process in rats. The study was published Feb. 3, 2016 in The Journal of Neuroscience. Researchers caution that more studies are needed, but the findings shed light on the mechanisms of cognitive decline and identify potential strategies to stem it.

Researchers have revealed a list of proteins most associated with aging and age-related disease including Alzheimer's. The team has found that short and highly charged proteins are most vulnerable to oxidation, which damages proteins in aging cells.

The many paths to immortality in post-Soviet Russia

The aging processes in brain cells that are thought to underlie cognitive decline may be reversible, according to research published in The Journal of Neuroscience. Researchers believe they have found a way to regenerate the fibers that receive neural impulses.

Caloric restriction (CR) is known to retard aging and delay functional decline as well as the onset of diseases in most organisms. Ghrelin is secreted from the stomach in response to CR and regulates energy metabolism. We hypothesized that in CR ghrelin has a role in protecting aging-related diseases.

The risk of dementia is slightly higher in people with minimal exposure to benzodiazepines but not with the highest level of exposure. These results do not support a causal association between benzodiazepine use and dementia.

As brain cells age they lose the fibers that receive neural impulses, a change that may underlie cognitive decline. Researchers at the University of California, Irvine recently found a way to reverse this process in rats. The study was published Feb. 3, 2016 in The Journal of Neuroscience. Researchers caution that more studies are needed, but the findings shed light on the mechanisms of cognitive decline and identify potential strategies to stem it.