Lifeboat Foundation: Safeguarding Humanity
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Category: life extension – Page 276

Circa 2010

In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits, and impairments in disorders such as Alzheimer’s disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and β-amyloid likely contribute to impaired neurogenesis in AD. Since factors such as exercise, enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seem promising.

There is a progressive decline in the regenerative capacity of most organs with increasing age, resulting in functional decline and poor repair from injury and disease. Once thought to exist only in high turnover tissues, such as the intestinal lining or bone marrow, it now appears that most tissues harbor stem cells that contribute to tissue integrity throughout life. In many cases, stem cell numbers decrease with age, suggesting stem cell aging may be of fundamental importance to the biology of aging (for review, see Ref. [1]). Therefore, understanding the regulation of stem cell maintenance and/or activation is of considerable relevance to understanding the age-related decline in maintaining tissue integrity, function, and regenerative response.

The adult brain contains neural stem cells (NSCs) that self-renew, proliferate and give rise to neural progenitor cells (NPC) that exhibit partial lineage-commitment. Following several cycles of proliferation, NPC differentiate into new neurons and glia. NSCs are increasingly acknowledged to be of functional significance and harbor potential for repair of the diseased or injured brain. The dramatic decline in neurogenesis with age is thought to underlie impairments in learning and memory, at least in part. Aging is also the greatest risk factor for Alzheimer’s disease (AD), a neurodegenerative disease characterized by progressive loss of memory and cognitive decline. Alterations in neurogenesis have been described extensively in animal models of AD, and key proteins involved in AD pathogenesis are shown to regulate neurogenesis.

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To date, there have been no metrics for accurately assessing individuals’ inflammatory status in a way that could predict these clinical problems and point to ways of addressing them or staving them off, Furman said. But now, he said, the study has produced a single-number quantitative measure that appears to do just that.

You’re as old as your immune system.

Investigators at the Stanford University School of Medicine and the Buck Institute for Research on Aging have built an inflammatory-aging clock that’s more accurate than the number of candles on your birthday cake in predicting how strong your immune system is, how soon you’ll become frail or whether you have unseen cardiovascular problems that could become clinical headaches a few years down the road.

In the process, the scientists fingered a bloodborne substance whose abundance may accelerate cardiovascular aging.

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A serving of mushrooms is just 0.08 kg of CO2 emissions—only lentils have a lower per serving CO2 emission level.

One common question J.P. and I get over and over again is about the problem of overpopulation—if human life extension is a humanitarian goal worth pursuing, won’t there be an inevitable environmental crisis? One worse than what we’re already facing?

When we covered the ethics of life extension we partially answered this question based on what we know about population and consumption trends now (tl;dr: we’re more likely to face a crisis of under population than overpopulation). That said, it’s practically impossible to be able to fully forecast environmental trends 50200, and further years into the future. We noted, “Spanners actually need to address it because we will have to continue living through the consequences of climate change if we don’t.”

In other words, if you’re interested in indefinitely extending your own life, sustainable eating should be a priority today because you’ll most likely be alive in the trash-filled, resource-scarce world of tomorrow.

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Ageing is an incredibly complicated process, so much so that we do not yet understand exactly how complicated it is. It is in fact so complicated, that it could actually be incredibly simple. Confused? Well, imagine if you were a structural engineer who was trying to understand why a building collapsed. From an initial inspection of the rubble, it may be extremely difficult to work out exactly what went wrong. Was the building made from inferior materials? Was it built incorrectly? Was its destruction deliberate? Did it just fall apart due to age? All of these are possible, but what was the true cause for its destruction? Well, that is the same mystery we are trying to solve in longevity research. We can see the damage that is caused by ageing, but what is the cause? Is it a general accumulation of damage, or are there single points of failure which have knock on effects that affect the entire body? A cascade failure if you will.

Of the many different changes that occur during the ageing process, one of the most well-known and understood is the decreased capacity for our body to produced chemical energy, which has a knock-on effect throughout the body. This results in a general decrease in our ability to carry out cellular functions and will therefore effective everything from muscle strength to DNA replication and repair. This decrease in energy output has been linked to defects in our mitochondria, but in addition to these physical defects that occur in these small organisms, we now know that they also suffer a decreased capacity to carry out their function due to lacking a critical coenzyme called Nicotinamide adenine dinucleotide (NAD). Anyone who has taken a high school level biology class will probably recognise this enzyme as part of the electron transport chain in respiration.

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“Deep in the forests of Germany, nestled neatly into the hollowed-out shells of acorns, live a smattering of ants who have stumbled upon a fountain of youth. They are born workers, but do not do much work. Their days are spent lollygagging about the nest, where their siblings shower them with gifts of food. They seem to elude the ravages of old age, retaining a durably adolescent physique, their outer shells soft and their hue distinctively tawny. Their scent, too, seems to shift, wafting out an alluring perfume that endears them to others. While their sisters, who have nearly identical genomes, perish within months of being born, these death-defying insects live on for years and years and years,” Katherine J. Wu writes.

A parasite gives its hosts the appearance of youth, and an unmatched social power in the colony.

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Zoledronate is a biophosphonate, a drug used to strengthen bones and reduce the risk of osteoporosis-related bone fractures. It is well-absorbed into the bones, so it only needs to be administered through infusion once a year.

A 2010 study had found that people who were given zoledronate after experiencing hip fractures showed slightly reduced all-cause mortality compared to a control group. Patients who took the drug were at significantly lower risk for heart arrhythmias and pneumonia.

As this is a drug that is already being given to people, the choice to go back to genetically modified fruit flies, a much simpler model of aging, may seem counterintuitive. The team chose to test these insects for two principal reasons. The first is that Drosophila flies are a common subject of studies on basic aging pathways, which the researchers wished to explore. The second is simpler: Drosophila flies lack bones, making the bone-affecting properties of zoledronate irrelevant to the study.

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The Retrobiome, Cancer, And Aging — Roswell Park Comprehensive Cancer CtrThe Retrobiome, Cancer, And Aging — Dr. Andrei Gudkov, PhD, DSci, Roswell Park Comprehensive Cancer Center, joins me on Progress, Potential, And Possibilities Cornell University College of Veterinary Medicine #Cancer #Vaika #Genome #DnaDamage #ImmunoSenescence #Pets #Dogs #Health #Lifespan #LifeExtension #Inflammaging #Longevity #Aging #Oncology

Dr Andrei Gudkov, PhD, DSci, is a preeminent cancer researcher who serves as Senior Vice President, Research Technology and Innovation, Chair of the Department of Cell Stress Biology, and a member of the senior leadership team for National Cancer Institute (NCI) Cancer Center Support Grant at Roswell Park Comprehensive Cancer Center (https://www.roswellpark.org/andrei-gudkov).

Dr. Gudkov is responsible for building on the basic and translational research strengths of the Cell Stress Biology program in DNA damage and repair, photodynamic therapy, thermal and hypoxic stress and immune modulation.

Dr. Gudkov assists the President & CEO in developing and implementing strategic plans for new scientific programs and enhancing collaborations in research programs with regional and national academic centers as well as with industry.

Before joining Roswell Park, Dr. Gudkov served as chair of the Department of Molecular Genetics at Lerner Research Institute, Cleveland Clinic Foundation, and Professor of Biochemistry at Case Western University. He earned his doctoral degree in Experimental Oncology at the Cancer Research Center, USSR and a Doctorate of Science (D.Sci) in Molecular Biology at the Moscow State University, USSR. He has authored or co-authored over 135 scientific articles and holds 27 patents.

Continue reading “Dr. Andrei Gudkov, PhD — The Retrobiome, Cancer, And Aging — Roswell Park Comprehensive Cancer Ctr” | >