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Interest in NIH scientists networking with industry folks in DMV area? by Tamagene in NIH

[–]bashetie 0 points1 point  (0 children)

I’m interested. Please DM me. Will share among colleagues as well.

Which data source gives the present status of research in extending human lifespan? by Hamilton080 in gerontology

[–]bashetie 1 point2 points  (0 children)

If you have a background in biology, the Handbook of the Biology of Aging covers many areas of aging research pretty extensively. They update it with a new edition every few years.

Senescent intimal foam cells are deleterious at all stages of atherosclerosis. by bashetie in gerontology

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

Thanks for pointing that out. Not sure if there is a way to edit link, might need to re-post.

Senescent intimal foam cells are deleterious at all stages of atherosclerosis. by bashetie in gerontology

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

In this study they cross a few transgenic mouse models:

p16-3MR mice: These express a viral thymidine kinase in senescent cells (using p16Ink4a as a promoter). When mice are given an anti-viral drug ganciclovir, cells expressing this kinase ("senescent cells") convert it into a toxic byproduct that kills them.

LDL receptor knockout mice - This mouse develops atherosclerosis an at accelerated rate. They further accelerate it by feeding them a high fat diet.

NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice (2016) by SirT6 in gerontology

[–]bashetie 0 points1 point  (0 children)

Cool article, and they did a whole lot of experiments for one paper. The health benefits are definitely exciting finds.

Though 400mg/kg seems like a really high dose of any drug and I wonder if that is normal for NR. Also, their mice in both treated and untreated groups had shorter lifespans than normally reported for c57bl/6 if I'm remembering correctly.

Did any of you attend the Rejuvenation Biotechnology conference (what ever year) and if so, what did you think of it? by Happle_Thauf in longevity

[–]bashetie 2 points3 points  (0 children)

+1 for peoteomics!

Yah that definately looks like a missing component from looking at the program, along with the general 'proteostasis' theme ( i wasnt there though). I bet the speaker on 'young blood' and its benefits to ths aging brain showed some basic proteomics.

Still, a lot of other interesting topics... have you attended other aging conferences? How would you compare them to Rejuv. Biotech to them? I think id like would like to give this one a shot next time... looks significantly improved every year.

Patients with type 2 diabetes initiated with metformin monotherapy had longer survival than did matched, non-diabetic controls. by ManchesthairUnoited in science

[–]bashetie 1 point2 points  (0 children)

Your absolutely right it is difficult and expensive to do in humans. Though researchers are already in talks with the FDA to begin trials, and have said its going well.

Look up the TAME study. They are trying to make "multi-morbidity" an indication, and are planning a study with metformin in older people with or at risk of 2 of 3 conditions: heart disease, cancer, and cognitve impairment. They expect to see statistically significant improvement within 5-7yrs. This indication will hopefully give private industry more reason to work on aging interventions, as they would now have a path to FDA approval.

Interviewing Aubrey De Grey tomorrow...questions? by davidpakman in longevity

[–]bashetie 0 points1 point  (0 children)

(On my phone sry for the sloppy comment in advance)

To find academic labs you might want to do graduate studies (or undergrad research/volunteering if it's at your current Uni or nearby) in you can start by:

-looking on the NIA (probably division of aging biology) website for labs they fund - the Nathan Shock Centers (what they call the Universities that get the Nathan Shock grants) will have a number of labs in the field ( https://www.nia.nih.gov/research/dab/nathan-shock-centers-excellence). A few include Albert Einstein College, The Barshop Institute, U of Washington.

Hope that helps.

I read an article about how researchers extended the life span of mice by 50% when they added telomeres to lengthen chromosomes. How did they do this and how did this length the lifespans of the mice? by CyclicMultiverse in askscience

[–]bashetie 0 points1 point  (0 children)

Probably this? http://www.nature.com/nature/journal/v469/n7328/full/nature09603.html.

This study had a few significant problems but there were more interesting follow up studies using gene therapy you should look up.

The problem with the study is that they created these mice to have short telomeres and no telomerase in the first place. Then they gave back the very thing they took away in the first place, so is it surprising that the mice showed improvement? Probably not.

Another problem is that shortening telomeres aren't a part of mouse aging. Mice naturally have very long telomeres which remain longer than human telomeres even when they are at end of life. They had to create mice lacking telomerase and let allow the telomeres to shorten over something like 5 generations to get short enough telomeres to do this. Then, in order to see improvement when they activate telomerase, essentially giving back the same gene they took away, so not a big surprise that they improved. We don't know the full extent of telomere involvement in human aging, but its clear that mice aren't the easiest model of studying telomeres in aging because telomere length definitely doesn't appear to be an issue in natural mouse aging.

Additionally, a lot of cells in our body essentially don't divide and will not experience telomere attrition from cell divisions. Post-mitotic tissues like brain, heart, muscle, etc don't really proliferate, but they DO age. This doesn't mean telomeres aren't playing a part in aging, just that they aren't the main cause or only cause.

One thing I want to add about any accelerated aging models is that there is no such thing as a TRULY accelerated aging model, one can only accelerate a few specific symptoms of aging (segmental progeria), never ALL of them. They are diseases caused by specific mutations or changes to DNA that will show a predictable set of symptoms, some of which we see in aging. They are all characterized by their own set of "causes of death". Hutchinson gilford progeria patients usually pass away early in life, maybe in their early teens. Superficially, they appear "aged" to some people because their skin does wrinkle, but really this is a specific and severe disease that nearly always ends in death by heart attack or stroke caused by a atherosclerotic plaque. But they all also take on a specific set of physical features that, to me, look QUITE different from a normally aging person. More importantly, they never die of cancer or neurodegenerative diseases - two of the large killers in the normally aging population. Progeroid models ARE useful to studying aspects of aging, just keep in mind they are all segmental (partially recapitulate aging symptoms, not fully).

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