Dear Future Centenarian,
LATEST HEALTHY LIFE EXTENSION HEADLINES
HEAT SHOCK PROTEINS AS BIOMARKERS OF AGING (September 17 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4905
These researchers suggest that heat shock proteins might be used as a biomarker of aging, a way to determine biological age rather than chronological age, and hence predict life span or evaluate the effectiveness of potentially longevity-inducing therapies: “Since their discovery in Drosophila, the heat shock proteins (Hsps) have been shown to regulate both stress resistance and life span. Aging is characterized by increased oxidative stress and the accumulation of abnormal (malfolded) proteins, and these stresses induce Hsp gene expression through the transcription factor HSF. In addition, a subset of Hsps is induced by oxidative stress through the JNK signaling pathway and the transcription factor Foxo. The Hsps counteract the toxicity of abnormal proteins by facilitating protein refolding and turnover, and through other mechanisms including inhibition of apoptosis. The Hsps are up-regulated in tissue-specific patterns during aging, and their expression correlates with, and sometimes predicts, life span, making them ideal biomarkers of aging. The tools available for experimentally manipulating gene function and assaying healthspan in Drosophila provides an unparalleled opportunity to further study the role of Hsps in aging.”
WHY RESEARCHERS ARE INTERESTED IN CALORIE RESTRICTION (September 16 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4903
A great many research groups continue to investigate the biochemistry of calorie restriction, and this paper is a good illustration as to why this is the case: “It is well known that calorie restriction (CR) can retard the aging process in organisms ranging from yeast to non-human primates, and delay the onset of numerous age-related diseases including neurodegenerative disorders. Translation of the knowledge gained from CR research in animal models to disease prevention strategies in humans should provide therapeutic approaches for these diseases. Signaling pathways induced by CR are therefore potentially new therapeutic targets for neurodegenerative diseases. This review summarizes the evidence on key biological mechanisms underlying the beneficial effects of CR based on our current understanding, with particular emphasis on the recent impact of CR on neuroprotection, and on the emerging development of pharmacological agents that target signaling pathways induced by CR. We focus in particular on recent findings on sirtuins for skin care and prevention of neurodegenerative diseases.” Even outside the context of aging, there is potentially much to learn about human biochemistry by following the effects of calorie restriction.
MILD MEMORY LOSS WITH AGING AS A DISEASE (September 16 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4902
The process of declaring parts of aging as a disease is driven by regulation: the FDA does not permit treatments for aging, only for named diseases. Since there is little funding for research that cannot be legally commercialized, the incentive is to carve off chunks of the process of aging and go through the process of having government employees add it to the list of diseases – which can take years and millions of dollars. Sarcopenia, for example, is still not recognized by the FDA, meaning that no potential treatment can be commercially developed in the US. Here is an example of this process at work for memory loss: “Simply getting older is not the cause of mild memory lapses often called senior moments, according to a new study. Even the very early mild changes in memory that are much more common in old age than dementia are caused by the same brain lesions associated with Alzheimer’s disease and other dementias. The very early mild cognitive changes once thought to be normal aging are really the first signs of progressive dementia, in particular Alzheimer’s disease. The pathology in the brain related to Alzheimer’s and other dementias has a much greater impact on memory function in old age than we previously recognized. Dementias are the root cause of virtually all loss of cognition and memory in old age. They aren’t the only contributing factors; other factors affect how vulnerable we are to the pathology and to its effects. But the pathology does appear to be the main force that is driving cognitive decline in old age.”
CALORIE RESTRICTION CULLS SENESCENT CELLS (September 15 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4901
Calorie restriction has been shown to slow down almost every measure of degenerative aging examined to date. Here is another such open access study: “Dietary restriction (DR) extends the lifespan of a wide variety of species and reduces the incidence of major age-related diseases. Cell senescence has been proposed as one causal mechanism for tissue and organism ageing. We show for the first time that adult-onset, short-term DR reduced frequencies of senescent cells in the small intestinal epithelium and liver of mice, which are tissues known to accumulate increased numbers of senescent cells with advancing age. This reduction was associated with improved telomere maintenance without increased telomerase activity. We also found a decrease in cumulative oxidative stress markers in the same compartments despite absence of significant changes in steady-state oxidative stress markers at the whole tissue level. The data suggest the possibility that reduction of cell senescence may be a primary consequence of DR which in turn may explain known effects of DR such as improved mitochondrial function and reduced production of reactive oxygen species.” The telomere maintenance line item above might suggest that the shortest-telomere cells – i.e. senescent cells – are being destroyed and recycled, thus raising the average amongst remaining cells.
CREATING AN ARTIFICIAL OVARY (September 15 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4900
There are interesting intermediate destinations on the road to tissue engineered replacement organs. This is one of them: researchers have “invented the first artificial human ovary, an advance that provides a potentially powerful new means for conducting fertility research and could also yield infertility treatments for cancer patients. The team has already used the lab-grown organ to mature human eggs. An ovary is composed of three main cell types, and this is the first time that anyone has created a 3-D tissue structure with triple cell line. The ovary not only provides a living laboratory for investigating fundamental questions about how healthy ovaries work, but also can act as a testbed for seeing how problems, such as exposure to toxins or other chemicals, can disrupt egg maturation and health. To create the ovary, the researchers formed honeycombs of theca cells, one of two key types in the ovary, donated by reproductive-age (25-46) patients at the hospital. After the theca cells grew into the honeycomb shape, spherical clumps of donated granulosa cells were inserted into the holes of the honeycomb together with human egg cells, known as oocytes. In a couple days the theca cells enveloped the granulosa and eggs, mimicking a real ovary.”
WORKING TOWARDS REGENERATION OF THE ENTHESIS (September 14 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4899
An open access paper: “The enthesis, which attaches the tendon to the bone, naturally disappears with aging, thus limiting joint mobility. Tendons and ligaments are fibers made up of dense connective tissue and they are critical for physiological movement and the stability of joints because of their attachment to bone. Injury to these structures can significantly destabilize joints, resulting in the development of degenerative joint diseases, especially in the upper limbs. Surgery is frequently needed but the clinical outcome is often poor due to the decreased natural healing capacity of the elderly. This study explored the benefits of a treatment based on injecting chondrocyte and mesenchymal stem cells (MSC) [in rats] Damage was repaired by classical surgery without cell injection (group G1) and with chondrocyte (group G2) or MSC injection (group G3). The spontaneous healing rate in the G1 control group was 40%, close to those observed in humans. Cell injection significantly improved healing (69%). A new enthesis was clearly produced in cell-injected G2 and G3 rats, but not in the controls. Only the MSC-injected G3 rats had an organized enthesis with columnar chondrocytes as in a native enthesis 45 days after surgery. Cell therapy is an efficient procedure for reconstructing degenerative entheses. MSC treatment produced better organ regeneration than chondrocyte treatment. The morphological and biomechanical properties were similar to those of a native enthesis.”
INVESTIGATING THE ORIGIN OF AGGREGATES (September 13 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4897
Aggregates of unwanted proteins are important in aging, and researchers continue to investigate why it is that aggregates appear in the first place. Here, researchers “have solved a long-standing mystery of how cells conduct ‘quality control’ to eliminate the toxic effects of a certain kind of error in protein production. The new study suggests how cells in eukaryotic organisms, like humans, sense and destroy ‘non-stop’ proteins that remain stuck in the ribosome, the protein manufacturing plant of the cell. DNA is used to make RNA, which, in turn, is used to make proteins. In healthy cells, the ribosome translates the code carried by a messenger RNA (mRNA) to link together protein building blocks (amino acids) in a particular order to form specific proteins. But errors happen – which is why the body has a host of different quality control mechanisms to ensure that the proteins that emerge from this process are flawless. When aberrant proteins escape these surveillance mechanisms, they accumulate and form ‘aggregates’ that can be toxic to certain neuronal types, and disorders such as Alzheimer’s and Parkinson’s diseases can result. For some 15 years, scientists have understood the mechanism that identifies and destroys these problematic non-stop proteins in bacteria. In these organisms, non-stop proteins are tagged by a marker known as tmRNA or ssrA, which then leads to their destruction. In more complex eukaryotic organisms, which range from yeast to humans, though, the mechanism for identifying and eliminating such dangerous non-stop errors has remained a mystery – until now.”
TENGION WORKS ON KIDNEY REGENERATION (September 13 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4896
A press release from Tengion: “rodents with chronic kidney disease (CKD) were treated with healthy kidney cells to catalyze the regeneration of functional kidney tissue and delay disease progression, as evidenced by extended survival, improved kidney filtration, and reduced severity of kidney tissue pathology. The published data demonstrate that delivery of a selected population of kidney cells to the kidney significantly extended long-term survival and improved kidney function in rodents with chronic kidney disease during six months of follow-up. Further, the therapeutic effects reported in this study were more pronounced and more durable than have been previously reported with this animal model. Chronic kidney disease is a serious medical condition affecting millions of Americans and can lead to kidney failure requiring the need for transplant or lifelong dialysis. A treatment approach that can increase kidney tissue and improve function would be a significant advancement in the care of these patients. The scientific community has historically considered that CKD develops from an imbalance between tissue damage and the kidney’s ability to repair and regenerate itself. These preclinical data provide clear evidence that regeneration of functional renal tissue can delay progression of CKD.”
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DISCLAIMER: News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.longevitymeme.org/newsletter/.
David A. Kekich
Maximum Life Foundation
“Where Biotech, Infotech and Nanotech
Meet to Reverse Aging by 2029”