Lifeboat Foundation

Stem cells can be classified based on their ability to specialize. Totipotent stem cells can become any tissue in the body, pluripotent stem cells can become any cell type except for a complete organ, and multipotent stem cells can only differentiate into specific tissue types.

Induced pluripotent stem cells (iPSCs) show promise in treating retinal degenerative diseases. They are created by reprogramming adult cells using Yamanaka factors, allowing them to revert to an embryonic state. These cells provide a virtually unlimited cell source for research and potential therapies.

Scientists are researching several diseases and drug development applications for these cells, highlighting the characteristics that make them an ideal therapy for macular degeneration.

More than 20 years ago, the human genome was first sequenced. While the first version was full of “holes” representing missing DNA sequences, the genome has been gradually improved in successive rounds. Each has increased the quality of the genome and, in so doing, resolved most of the blank spaces that prevented us from having a complete reading of our genetic material.

The fundamental difficulty researchers faced in reading the genome from end to end is the enormous number of repeated sequences that populate it. The 20,000 or so genes we humans have occupy barely 2% of the entire genome. The remaining 98% is essentially made up of these families of repeated sequences, mobile elements known as transposons and retrotransposons, and—to a lesser but functionally important extent— gene expression regulatory sequences. These function as switches that determine when and where genes are turned on and off.

In March 2022, a major revision of the genome was published in the journal Science. An international consortium of researchers known as “T2T” (telomere to telomere, which are the ends of chromosomes) used a novel strategy based a type of cell (CHM13) that retains only one copy of each chromosome.

A promising, more durable fuel cell design could help transform heavy-duty trucking and other clean fuel cell applications. Consisting of nanowires that are less susceptible to corrosion than other designs, the innovative electrode—the heart of a polymer electrolyte-membrane fuel cell—could usher in a new era for fuel cells, which use hydrogen as emission-free power for vehicles.

“In real-world terms, this means that we can have a more durable fuel cell that will provide high fuel economy over a longer lifetime,” said Jacob Spendelow, a scientist with the Los Alamos National Laboratory team that described its results in the journal Advanced Materials. “This work demonstrates that we can get rid of conventional carbon-based catalyst supports, eliminating the degradation problems associated with carbon corrosion, while still achieving high fuel cell performance.”

The improved durability makes this fuel cell a promising candidate for use in heavy-duty trucking applications, which require fuel cell lifetimes of more than 25,000 hours.

Dan Buettner’s Blue Zones research has transformed his lifestyle: He’s made physical activity a habit of his daily life and started eating more beans.

The incidence of cancer increases exponentially as we age. Unlike most age-related diseases, which generally cause cell and tissue degeneration and loss of function, cancer cells must acquire different, albeit aberrant, functions to progress to lethal disease. One link between age-related cancer and degeneration could be an inflammatory tissue environment driven by MTOR in senescent cells.

In her groundbreaking 2010 research perspective paper, The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression, Dr. Judith Campisi from the Buck Institute for Research on Aging highlighted the tumor-promoting aspects of senescent cells. Campisi’s research showcased the significant ability of senescent cells to reshape the cellular landscape around them, crafting what scientists term the ‘microenvironment.’

Far from being an inert backdrop, this microenvironment serves as a dynamic stage upon which cells interact and potentially pave the way for disease progression, particularly cancer.

Scientists have recently reviewed the available literature to examine the critical roles played by mitochondria in maintaining homeostasis. The review summarized the involvement of mitochondria in age-related disease progression and highlighted its potential as a therapeutic target of these diseases. This review has been published in Experimental & Molecular Medicine.

Mitochondria is a cytoplasmic organelle in most eukaryotic cells and is enclosed by two phospholipid membranes: the inner mitochondrial membrane (IMM) and outer mitochondrial membrane (OMM). These membranes separate functionally compartmentalized structures, i.e., matrix and intermembrane space. Mitochondria contain a unique genetic code, mitochondrial DNA (mtDNA).

During evolution, most mitochondrial genes were lost or translocated to nuclei. However, genes that remained in mtDNA encode for essential translational apparatus, i.e., ribosomal RNAs and transfer RNAs. In addition, these genes also encode proteins that are key components of oxidative phosphorylation system (OXPHOS) complexes embedded in the IMM.

NIH-funded study suggests reducing exposure to airborne particulates may decrease dementia risk.

Higher rates of new cases of dementia in a population over time — known as incident dementia — are linked to long-term exposure to fine particulate matter (PM2.5) air pollution, especially from agriculture and open fires, according to a study funded by the National Institutes of Health and published in JAMA Internal Medicine. Scientists found that 15% of older adults developed incident dementia during the average follow-up of 10 years.

“As we experience the effects of air pollution from wildfires and other emissions locally and internationally, these findings contribute to the strong evidence needed to best inform health and policy decisions,” said Richard J. Hodes, M.D., director, National Institute on Aging (NIA), part of NIH. “These results are an example of effectively using federally funded research data to help address critical health risks.”

“A major highlight of the work is our approach to achieve longevity: using computers to simulate the natural aging system and guide the design and rational engineering of the system to extend lifespan,” Hao told Motherboard. “This is the first time this computationally-guided engineering-based approach has been used in aging research. Our model simulations actually predicted that an oscillator can double the lifespan of the cell, but we were happily surprised that it actually did in experiments.”

The study is part of a growing corpus of mind-boggling research that may ultimately stave off some of the unpleasant byproducts of aging until later in life, while boosting life expectancy in humans overall. Though countless hurdles have to be cleared before these treatments become a reality, Hao thinks his team’s approach could eventually be applied to humans.

“I don’t see why it cannot be applied to more complex organisms,” Hao said. “If it is to be introduced to humans, then it will be a certain form of gene therapy. Of course it is still a long way ahead and the major concerns are on ethics and safety.”

Researchers at the University of Rochester have successfully exported a longevity gene from naked mole rats to mice – a transfer that resulted in both improved health and an extension of the mouse’s lifespan [1].

Longevity. Technology: Naked mole rats, which are known for their long lifespans and exceptional resistance to age-related diseases, have been a focus of longevity research for some time. By introducing a specific gene responsible for improved cellular repair and protection into mice, the Rochester researchers have created promising opportunities to better understand the mechanisms behind aging and potentially increase human lifespan.

“Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals,” says Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester [2].