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September 04, 2009

SENS4 : Antiaging conference coverage

Ouroboros has coverage of the SENS4: Antiaging conference.

The SENS site has all of the conference abstracts

UPDATE: SENS4, Session 6: Eliminating recalcitrant intracellular molecules: other

Claude Wischik spoke about preventing aggregation of tau protein, which is implicated in Alzheimer’s disease. Clinical trials of their aggregation-inhibiting drug Rember are promising.

Andrei Seluanov talked about naked mole rats, those odd-looking miracle rodents that live for 30 years and don’t seem to ever get cancer. Mole rat contact inhibition/cancer resistance was controlled by p53 and pRB, both known tumour suppressors.

Alex Whitworth spoke about the relationship between mitochondrial degradation and Parkinson’s disease genes [Parkin and PINK1 genes].


SENS4, Sessions 9 and 10: Rejuvenating extracellular material

Mark Pepys talked about treating amyloidosis by targeting serum amyloid P component (SAP), which is present in all amyloid deposits and plays a role in stabilizing them. Several years ago, Pepys discovered a compound (CPHPC) that quickly removes SAP from the bloodstream and from most amyloid plaques; however, clinical trials showed that CPHPC alone does not help people with advanced disease. Today, Pepys reported on some very promising results from combining CPHPC with an antibody, effectively targeting the antibody to amyloid: in mouse studies, plaques completely disappear. Clinical testing of this combination approach will begin in 2011.

Kendall Houk gave a very interesting talk on computationally designing enzymes from scratch. They plan to apply their recently published protocol to develop enzymes that can reverse the formation of Advanced Glycation End-products (AGEs) – sugar-modified proteins that accumulate with age and are implicated in several age-related diseases.


END UPDATE


Session 5: Eliminating recalcitrant intracellular molecules: the lysosome

Jeffrey Grubb spoke about new methods for delivering missing enzymes to the lysozomes of patients suffering from lysosomal storage diseases. Several of these should be able to deliver any protein to the lysozome, including novel ones capable of degrading undesirable intracellular molecules that accumulate with age and that normal lysosomes can’t handle. Central goal of the LysoSENS project

Ana Maria Cuervo spoke about the relationship between autophagy and aging. Artifically maintaining autophagy shows improved liver function in mice.

John Schloendorn discussed ongoing work at the SENS Foundation Research Center to develop new enzymes that can degrade harmful intracellular junk that accumulates with age. So far, they have discovered enzymes that can degrade A2E and 7-ketocholesterol, which are implicated in macular degeneration and osteoporosis, respectively. Their next step will be to construct a drug delivery system to get these enzymes to lysozomes, possibly using methods similar to those of Jeffrey Grub.


SENS4, Session 4: Adult regenerative capacity

Brandon Reines presented a counterintuitive result on regeneration: sometimes old animals have a higher regenerative capacity than young animals. In particular, if you punch a hole in the ear of a young mouse, then it won’t heal; but in a middle-aged mouse it will heal completely. He argued that this happens because mouse ear connective tissues never fully differentiate, and suggested that other neural-crest-derived connective tissues might show similar properties.

Kaisa Selesniemi talked about possible methods for sustaining fertility in older women. They found that an infusion of bone marrow from younger females keeps older mice fertile longer. They hope that these treatments might not only prolong fertility, but also female health: mice with longer “ovarian lifespan” show reduced disease incidence.

Alexandra Stolzing presented a new method for generating induced pluripotent stem cells (i.e., for reprogramming adult somatic cells to become pluripotent) that doesn’t use viral compounds or plasmids. Viruses can cause abnormalities in the reprogrammed cells, so much recent work has focused on developing alternate methods for deriving iPS cells
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SENS4, Session 3: Optimising metabolism against aging

Stephen Spindler described his (ongoing) project to screen a large number of potential lifespan-affecting compounds in mice – so far, several candidates look promising. Interestingly, he also argued that the majority of previous studies measuring the effects of various compounds on rodent life expectancy suffer from serious flaws. In particular, he argued that many of them were confounded by a possible calorie restriction effect.

Manuel Serrano talked about his recent experiments with sirtuins in mice. Overexpression of sirtuins in yeast, worms, and flies delays aging, but their role in mammalian aging is still highly controversial. He found that mice overexpressing Sirt1 had improved health, according to several metrics – but no difference in lifespan.

David Melzer talked about his analyses of human genetic association studies. A large number of single nucleotide polymorphisms (SNPs) have been associated with age-related diseases in humans; Melzer showed that many of these are near genes that play a role in pathways relevant to aging, and also identified three genes associated with two or more age-related diseases: p16/p15, MYC, and TERT.


SENS4, Session 1: Combating oxidation

Vladimir Skulachev spoke about his extensive work with SkQ1, an antioxidant targeted to mitochondria. He reported that SkQ1 supplementation extends median lifespan in several species (including mammals), and slows the development of multiple age-related diseases and conditions.

Holly Brown-Borg talked about the connections between stress resistance and longevity in Ames dwarf mice, which live around 50% longer than normal mice and show elevated levels of some antioxidants.

Cathy Clarke tested an original and interesting approach to avoiding free radical damage to poly-unsaturated fatty acids, or PUFAs: isotope reinforcement. The basic idea here, explained in an earlier paper, is very simple: heavier isotopes make stronger bonds, so isotope-reinforced PUFAs will be more resistant to free radical attack. Will these results transfer to higher organisms? Is there any chance that the deuterium could get incorporated into other molecules, stabilizing proteins that we want to degrade? The authors plan to follow up this study in worms and mice.


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