Lifeboat Foundation

Let’s face it, getting older sucks, and not because of all the extra candles on the birthday cake. Getting cake and presents every year is great, but the loss of health and independence isn’t a particularly good birthday present. (Wow, what’d I get this year? Just what I didn’t want: sarcopenia and hearing loss!)

Given the downsides of aging, it really is surprising how little people talk about it beyond the odd grumble or even as a joke. Normally, it’s to complain about the aches and pains that gradually appear as the years roll by, as we find it harder to walk up the stairs and “bright-eyed and bushy-tailed” turns into “cloudy-eyed and with an aching back”.

That’s not even the serious side of aging, which involves the gradual loss of independence and the age-related diseases that first rob us of our quality of life before they get around to killing us. The serious part is the horror of Alzheimer’s and the loss of self that it brings, the heart disease that cripples us, the frailty that steals our independence, and the lurking threat of cancer that rises dramatically as we age.

RAADfest is the largest event in the world where practical and cutting-edge methods to reverse aging are presented for all interest levels, from beginner to expert.

Chronic inflammation, which results when old age, stress or environmental toxins keep the body’s immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer’s and Parkinson’s to diabetes and cancer.

Now, scientists at the University of California, Berkeley, have identified a molecular “switch” that controls the immune machinery responsible for chronic inflammation in the body. The finding, which appears online Feb. 6 in the journal Cell Metabolism, could lead to new ways to halt or even reverse many of these age-related conditions.

“My lab is very interested in understanding the reversibility of aging,” said senior author Danica Chen, associate professor of metabolic biology, nutritional sciences and toxicology at UC Berkeley. “In the past, we showed that aged stem cells can be rejuvenated. Now, we are asking: to what extent can aging be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases.”

Researchers at Albany Medical College in New York have discovered that a specific type of immune cell accumulates in older brains, and that activating these cells improves the memory of aged mice. The study, which will be published on February 5, 2020, in the Journal of Experimental Medicine (JEM), suggests that targeting these cells might reduce age-related cognitive decline and combat aging-associated neurodegenerative disease in humans.

The brain is highly susceptible to aging, with cognitive functions, such as learning and memory, gradually declining as we get older. Much of the body’s immune system also deteriorates with age, resulting in increased susceptibility to infection and higher levels of inflammation. In their new JEM study, however, a team of researchers led by Qi Yang and Kristen L. Zuloaga at Albany Medical College reveal that aging-related changes in a class of immune cell known as group 2 innate lymphoid cells (ILC2s) could allow doctors to combat the effects of aging on the brain.

ILC2s reside in specific tissues of the body and help to repair them when they are damaged. Recently, for example, ILC2s in the spinal cord were shown to promote healing after spinal cord injury. “However, whether ILC2s also reside in other parts of the central nervous system, and how they respond to aging, was unknown,” Yang says.

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US biotech companies are working towards plasma therapies to tackle age-related diseases in humans.

Researchers from SENS Research Foundation, including Matthew O’Connor and Amutha Boominathan, have published a new study showing how codons play an important role in getting copies of mitochondrial genes placed in the cellular nucleus to express themselves correctly [1].

A possible solution to mitochondrial diseases

Mitochondrial disease is not a single disease; in fact, it is a group of rare and related conditions that are thought to affect perhaps 1 in 5000 people. These are caused due to mutations in the genes involved in the process of aerobic respiration, one of the main functions of our mitochondria.

Both genetically altered and naturally long-lived mammals are more resistant to toxic compounds that may cause cancer and age-associated diseases than their shorter-lived counterparts. The mechanisms by which this stress resistance occurs remain elusive. We found that longer-lived rodent species had markedly higher levels of signaling activity of the multifunctional regulator nuclear factor erythroid 2-related factor (Nrf2) and that this increase in cytoprotective signaling appeared to be due to species differences in Kelch-like ECH-Associated Protein 1 (Keap1) and β-transducin repeat-containing protein (βTrCP) regulation of Nrf2 activity. Both of these negative regulators of Nrf2-signaling activity are significantly lower in longer-lived species. By targeting the proteins that regulate Nrf2 rather than Nrf2 itself, we may be able to identify new therapies that impact aging and age-associated diseases such as cancer.

The preternaturally long-lived naked mole-rat, like other long-lived species and experimental models of extended longevity, is resistant to both endogenous (e.g., reactive oxygen species) and environmental stressors and also resists age-related diseases such as cancer, cardiovascular disease, and neurodegeneration. The mechanisms behind the universal resilience of longer-lived organisms to stress, however, remain elusive. We hypothesize that this resilience is linked to the activity of a highly conserved transcription factor, nuclear factor erythroid 2-related factor (Nrf2). Nrf2 regulates the transcription of several hundred cytoprotective molecules, including antioxidants, detoxicants, and molecular chaperones (heat shock proteins). Nrf2 itself is tightly regulated by mechanisms that either promote its activity or increase its degradation.