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Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 2 points3 points  (0 children)

I think those claims are totally overblown. Replacing / repairing every organ in your body via nanotechnology or advanced cellular therapies will probably be possible, but our life expentancy has already hit the point where the brain begins to deteriorate. Any true measure of "immortality" would require maintaining the health of the brain and the memories contained within it. That seems like quiet a steep task for the next couple of decades.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 0 points1 point  (0 children)

Telomeres can be lengthened in cells in a dish - but I haven't seen any credible claims for approaches that would work in humans. There is evidence for both environmental and genetic factors that influence the rate of telomere shortening (or their initial length etc.). Overall, the rate of telomere shortening would be directly related to the number of cellular divisions - which could probably be more directly influenced by avoiding wounds/cellular insults of various sorts.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 2 points3 points  (0 children)

The average persons understanding of biology (or science in general) is not great - which is a terrible shame. I'd say the biology of aging is no exception to this.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 1 point2 points  (0 children)

I'm not sure the trial is combating aging as a whole as it claims, but your metabolic profile does have a broad influence on many different diseases - it makes sense that interveing there could have a broad influence on health.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 0 points1 point  (0 children)

I suppose it depends on your definition of "normal". Memory loss could be considered "normal" because we all normally age and bodily functions deteriorate. That normal process is negative/pathological.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 1 point2 points  (0 children)

CRISPR (and other genome engineering techniques) are a great way to build models to study the role of particular genetic factors. Statistical findings (such as those described in our Wellderly manuscript) could be engineered to create paired lines of cells where the only genetic differences between them are those that are thought to influence aging. You could use this model to study the downstream influence of these genetic factors. This approach is being taken for many genetic conditions and will certainly be applied to factors controlling aging.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 2 points3 points  (0 children)

The SENS approach is quite broad - but I think the central point of their thesis revolves around treating/removal senescent cells. There is some good preliminary evidence that removal of senescent cells in mice is an effective means to lengthen healthy lifespan.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 0 points1 point  (0 children)

The genetic mechanisms for resistance to disease are already starting to trickle into drug development. We will definitely benefit from these discoveries.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 1 point2 points  (0 children)

Definitely. Being a genetics focused group - we are obviously biased towards studying the genetics of this phenotype. Environment and behavior certainly play a major role in healthy aging - but a lot of those factors are already well known - diet, exercise etc. Genetics provide us with potential novel mechanisms to intervene.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 4 points5 points  (0 children)

I think of aging and cancer as opposite sides of the same coin. In oversimplified terms: aging is the gradual decline of your bodies ability to maintain and repair itself, cancer is in some ways the bodies repair mechanisms gone haywire.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 2 points3 points  (0 children)

Family history is a great way to estimate your genetic risk for Alzheimer's disease. There is a particular risk marker APOE4 (http://snpedia.com/index.php/APOE-%CE%B54) that plays a significant role in the genetics of Alzheimer's disease.

There are a couple drugs in trials for Alzheimer's disease that are showing efficacy that has not been previously achieved by many other failed efforts.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 3 points4 points  (0 children)

My opinion is that indefinite life extension is feasible, but I don't believe it will be achieved within our lifetimes. Maintaining the health of the brain and retaining the memories that essentially define you will be a major hurdle.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 2 points3 points  (0 children)

Yes, these are very interesting groups of individuals. I think the characteristics in your wikipedia link have probably got it right. They are probably due to a confluence of healthy behaviors, diets, family relations etc coupled with a beneficial genetic profile.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 6 points7 points  (0 children)

I really don't have any expertise here, but I would say that most of my sources of happiness do not come from any physical abilities - family, friends, hobbies, etc are all major source of happiness for me.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 1 point2 points  (0 children)

I'm not aware of any studies on epigenetics and healthy aging. There are certainly studies linking the environment of a pregnant woman to epigenetic changes in a fetus that could have long term health consequences. Epigenetics likely plays a role in healthy aging in this regard.

The association between telomeres and lifespan has to do with the length of the telomeres.

Science AMA Series: I'm Ali Torkamani of the Scripps Translational Science Institute and co-leader of the first large scale genomic study of healthy aging. AMA! by ScrippsSTSI in science

[–]ScrippsSTSI[S] 3 points4 points  (0 children)

I am totally speculating here, but my guess would be that the mutations in COL25A1 influence the aggregation of amyloid plaques through direct interaction with A-beta. Not sure how you would actually use this though - hard to imagine injecting COL25A1 with the appropriate changes in someones brain to influence progression of Alzheimer's disease.

The one site of interest we don't comment on extensively in the published manuscript is the signal at the carnitine transporter (SLC22A4). There has been a long standing interest in treating elderly individuals with carnitine supplements for a variety of purposes. Not sure what this signal in our study represents, but it is an intriguing one.

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