Lifeboat Foundation

Hospital nurseries routinely place soft bands around the tiny wrists of newborns that hold important identifying information such as name, sex, mother, and birth date. Researchers at Rockefeller University are taking the same approach with newborn brain cells—but these neonates will keep their ID tags for life, so that scientists can track how they grow and mature, as a means for better understanding the brain’s aging process.

As described in a new paper in Cell, the new method developed by Rockefeller geneticist Junyue Cao and his colleagues is called TrackerSci (pronounced “sky”). This low-cost, high-throughput approach has already revealed that while newborn cells continue to be produced through life, the kinds of cells being produced greatly vary in different ages. This groundbreaking work, led by co-first authors Ziyu Lu and Melissa Zhang from Cao’s lab, promises to influence not only the study of the brain but also broader aspects of aging and disease across the human body.

“The cell is the basic functional unit of our body, so changes to the cell essentially underlie virtually every disease and the aging process,” says Cao, head of the Laboratory of Single-Cell Genomics and Population Dynamics. “If we can systematically characterize the different cells and their dynamics using this novel technique, we may get a panoramic view of the mechanisms of many diseases and the enigma of aging.”

Hearing diminishes as we age — about 50% of adults 75 and over in the United States have disabling hearing loss.

Age-related hearing loss cannot currently be stopped.

Researchers from the University of Guelph and Tufts.

Continue reading “Omega-3 fatty acids may slow age related hearing loss” »

An analysis of data from the Dunedin Multidisciplinary Health and Development study, a large longitudinal study in New Zealand, showed that participants with a history of antisocial behavior had a significantly faster pace of biological aging. When these individuals reached the calendar age of 45, they were on average 4.3 years older biologically compared to those who had lower levels of antisocial behavior. The study was published in the International Journal of Environmental Research and Public Health.

Antisocial behavior refers to actions that consistently violate social norms, disregard the rights of others, and often involve a lack of empathy or remorse. It involves behaviors such as deceitfulness, aggression, theft, violence, lying, and other behaviors that are harmful, manipulative, or exploitative towards others.

Antisocial behavior is typically associated with youth. This type of behavior starts between the ages of 8 and 14, peaks between 15 and 19, and usually becomes less frequent between the ages of 20 and 29. Although it becomes less common with age, it seems to have a lasting negative impact on health. Studies have shown that individuals who exhibit antisocial behaviors in their youth tend to have worse health outcomes as adults compared to their peers.

Low-grade inflammation contributes to age-related decline and impairment, but the precise pathways responsible for this inflammation and their impact on natural aging have until now remained elusive.

A study headed by researchers at the Swiss Federal Institute of Technology Lausanne (EPFL) has now shown that a molecular signaling pathway known as cGAS/STING plays a critical role in driving chronic inflammation and functional decline during aging. Andrea Ablasser, PhD, and colleagues found that blocking the STING protein suppressed inflammatory responses in human senescent cells and tissues, and reduced aging-related inflammation in multiple peripheral organs and in the brain in mice.

The researchers in addition studied the effects of blocking the STING protein in aged mice. As expected by its central role in driving inflammation, inhibiting STING alleviated markers of inflammation both in the periphery and in the brain. “Notably, various aging-related immune signature genes were significantly attenuated as a result of STING inhibition,” they stated. And importantly, animals receiving STING inhibitors displayed significant enhancements in spatial and associative memory, as well as improved muscle strength and physical endurance.

Continue reading “Signaling Pathway Implicated in Inflammation and Functional Decline during Aging” »

In a groundbreaking study published today in Nature, Australian scientists have resolved a long-standing problem in regenerative medicine. Led by Professor Ryan Lister from the Harry Perkins Institute of Medical Research and The University of Western Australia and Professor Jose M Polo from Monash University and the University of Adelaide, the team developed a new method to reprogram human cells to better mimic embryonic stem cells, with significant implications for biomedical and therapeutic uses.

In a revolutionary advance in the mid-2000s, it was discovered that the non-reproductive adult cells of the body, called ‘somatic’ cells, could be artificially reprogrammed into a state that resembles embryonic stem (ES) cells which have the capacity to then generate any cell of the body.

The ability to artificially reprogram human somatic cells, such as skin cells, into these so-called induced pluripotent stem (iPS) cells provided a way to make an essentially unlimited supply of ES-like cells, with widespread applications in disease modelling, drug screening and cell-based therapies.

A protein involved in wound healing can improve learning and memory in ageing mice1.

Platelet factor 4 (PF4) has long been known for its role in promoting blood clotting and sealing broken blood vessels. Now, researchers are wondering whether this signalling molecule could be used to treat age-related cognitive disorders such as Alzheimer’s disease.

“The therapeutic possibilities are very exciting,” says geneticist and anti-ageing scientist David Sinclair at Harvard University in Boston, Massachusetts, who was not involved in the research. The study was published on 16 August in Nature.

Continue reading “Older mouse brains rejuvenated by protein found in young blood” »

A new editorial paper published in the journal Aging argues that in multicellular organisms, neighboring cells are in constant competition.

The underlying reasons for aging have long remained elusive. However, in 1977, Thomas Kirkwood hypothesized that organisms might gain a fitness advantage by reducing investment in somatic maintenance if this allowed them to invest more resources in more crucial processes such as reproduction. The accumulation of somatic damage was therefore inevitable, and his disposable soma theory has dominated gerontology ever since.

However, as our understanding of aging increases, it is becoming increasingly difficult to align all the aspects of aging with accumulating damage. For example, mutations that increase damage accumulation can also increase longevity, while rejuvenation revelations such as parabiosis and Yamanaka factors indicate that youthfulness can be regained without high energetic cost and despite high levels of damage.

New research hints at a few ways fatty foods affect cells in the brain, a finding that could help explain the link between a high-fat diet and impaired memory – especially as we age.

The Ohio State University study in cell cultures found the omega-3 fatty acid DHA may help protect the brain from an unhealthy diet’s effects by curbing fat-induced inflammation at the cellular source.

Separate experiments using brain tissue from aging mice showed a high-fat diet may lead specific brain cells to overdo cell-signaling management in a way that interferes with the creation of new memories.

Restoration of lost memories.

Prof Bryce Vissel, who leads the Clinical Neuroscience and Regenerative Medicine Initiative (CNRM) at St Vincent’s Centre for Applied Medical Research, and his team, have identified a molecule in the brain that controls loss of nerve cell connections.

This molecule we are calling ‘the switch’ is decreased in the Alzheimer’s brain but no one really understands why, or what role it plays. When ‘encouraged’ or ‘forced’ to be expressed normally again, in our laboratory tests of a mouse model, this molecule can actually rescue its memory.

Continue reading “Alzheimer’s research breakthrough” »