As people get older, they often feel less energetic, mobile or active. This may be due in part to a decline in mitochondria, the tiny powerhouses inside of our cells, which provide energy and regulate metabolism. In fact, mitochondria decline with age not only in humans, but in many species. Why they do so is not well understood. Scientists at the Max Planck Institute for Biology of Ageing in Cologne set out to understand how mitochondrial function is diminished with age and to find factors that prevent this process. They found that communication between mitochondria and other parts of the cell plays a key role.

For their studies, the scientists used the simple roundworm, Caenorhabditis elegans, an important model system for aging research. Over half the genes of this animal are similar to those found in humans, and their mitochondria also decline with age. From their research, the scientists found a nuclear protein called NFYB-1 that switches on and off genes affecting mitochondrial activity, and which itself goes down during aging. In mutant worms lacking this protein, mitochondria don’t work as well and worms don’t live as long.

Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. “We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity,” says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains.

A pre-print study reveals that young blood plasma given to older mice reduced aging by an average of 54% across multiple tissues; and had an impact on other signs of aging, such as cellular senescence, fat accumulation, and behavioural measures.

“We’ve wondered if it might be possible to simply rewind the aging clock without inducing pluripotency,” said Vittorio Sebastiano, assistant professor at Stanford University and senior author of the Nature Communications article. “Now we’ve found that tightly controlling the exposure to these proteins can promote rejuvenation in multiple human cell types, including stem cells. This has profound implications for regeneration and restoration of cell functionality of aged tissues.”

MOUNTAIN VIEW, Calif., March 25, 2020 /PRNewswire/ — A study published in the respected Nature Communications journal highlights the promise of technology being developed by Turn Biotechnologies to treat age-related health conditions.

The study by researchers at the Stanford University School of Medicine found that old human cells can be induced into a more youthful and vigorous state when they are exposed to a rejuvenating treatment that triggers the limited expression of a group of proteins known as Yamanaka factors, which are important to embryonic development.

An international team of scientists, led by University of Helsinki reported that vitamin B3, niacin, has therapeutic effects in progressive muscle disease. Niacin delayed disease progression in patients with mitochondrial myopathy, a progressive disease with no previous curative treatments.

Vitamin B3 forms have recently emerged as potent boosters of energy metabolism in rodents. These vitamins are precursors for NAD⁺, a molecular switch of metabolism between fasting and growth modes.

As fasting has been shown promote health and longevity in for example mice, a variety of “NAD boosters” are being developed. However, whether actual NAD⁺ deficiency exists in human disease, and whether NAD⁺ boosters could have curative effects in patients with degenerative diseases, has remained elusive.