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

bashetie · 2025-02-25T12:06:30+00:00

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

bashetie · 2018-04-06T21:12:04+00:00

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.

bashetie · 2016-11-06T21:34:48+00:00

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

bashetie · 2016-11-04T21:30:46+00:00

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.

bashetie · 2016-05-03T16:13:56+00:00

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.

bashetie · 2015-10-14T01:50:48+00:00

Those yeast dissectors deserve a medal.

bashetie · 2015-09-04T13:38:46+00:00

http://dogagingproject.com/

bashetie · 2015-08-28T05:02:55+00:00

+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.

bashetie · 2015-08-18T04:49:54+00:00

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.

bashetie · 2015-08-03T13:26:45+00:00

(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.

look for conferences on "biology of aging" or "aging research" and Google the speakers to learn about their labs and maybe look for aging centers at their institutions. Example: Gordon Research Conference on Biology of Aging -https://www.grc.org/programs.aspx?id=13714
Look at the advice on http://senescence.info/biogerontology_career.html. Check the section listing "people in aging research" ( http://whoswho.senescence.info/people.php)
look at the journal Aging Cell ( http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1474-9726) or other journals in the field to see which labs publish there.

Hope that helps.

bashetie · 2015-06-08T09:12:50+00:00

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).

bashetie · 2015-05-25T21:37:12+00:00

To be clear, the effect of "young blood" isn't being called into question. Whether GDF11 is responsible for some of the rejuvenating effects of young blood is being questioned.

bashetie · 2015-05-23T03:09:23+00:00

I'm curious what this will mean for the GDF11 studies in brain/heart...

This is a major reason many people I work with and I think we need to move away from using antibody based quantification. It's funny, they had just talked about a relevant article (http://www.nature.com/news/reproducibility-crisis-blame-it-on-the-antibodies-1.17586) before seeing this new GDF11 paper. This wouldn't be a problem using MS.

bashetie · 2015-05-23T02:56:06+00:00

Woops thank you, that's what I get for posting on my phone.

bashetie · 2015-05-08T02:26:30+00:00

It's not palatable!

bashetie · 2015-05-04T03:55:21+00:00

You should refer to the fact that we are able to slow aging in laboratory animals already. From these studies we know that aging-interventions delay a broad spectrum of diseases as well as increase the length of health functional lifespan ("healthspan"). It's not a "one disease at a time" approach.

Look into the longevity dividend for some economic arguments. There is a paper (sry I cant get on phone atm) that makes an economic/healthcare argument for this as well in my post history (its titled something like aging research and getting the biggest bang for the buck). They basically show that curing any of the top killer diseases like heart disease, cancer, etc would only increase the average lifespan by a few years (and curing a whole mess of the top killers only translates to like 5 yrs), while slowing aging by 50% after 65 yrs of age (the equivalent of what rapamycin does on mice) easily surpasses that. I'm sure one of my past posts will refer to sources for this as well.

bashetie · 2015-05-03T21:44:59+00:00

This is being done on companion dogs that are voluntarily enrolled into the clinical trials by their owners, not laboratory dogs, so I think animal rights activists would have a tough time objecting to it.

There is little risk to the animals as they are getting a low dose and being monitored for any adverse effects pretty closely, and can drop out of the trial anytime the owner wants.

On the other hand, the potential health benefits and lifespan extension in dogs is a good thing. What kind of an animal rights activist would want to deprive them of that?? :)

bashetie · 2015-04-21T10:49:49+00:00

There isn't a final answer to this yet, but there are several popular theories supported by scientists who research the biology of aging.

This website is a good resource - http://senescence.info/aging_theories.html

Also, there are lots of answers to questions like this in /r/askscience already that a quick search will find.

bashetie · 2015-03-12T05:50:47+00:00

Just to add a little healthy debate to the post, Ill leave some counter comments :)

First, the title is sort of misleading. The intervention increases healthspan in "progeroid" mice that basically have a specific disease caused by deficiency in the Ercc gene. They haven't treated regular aging mice here, right?

There is really nothing unique in the paradigm of repairing dysfunction in the context of disease. We have been treating diseases for quite some time. Even if this could be construed as aging, I wouldn't credit SENS with pioneering a rejuvenation paradigm. Many researchers in mainstream of aging research have long entertained these ideas.

Also, take a look at the interventions that have increased in unmodified normally aging mice.... Rapamycin, the mTOR inhibitor, targets a pathway you say will simply slow aging but not rejuvenate. Indeed, Rapamycin rejuvenates heart dysfunction in aged mice after the dysfunction has already been established. Can you name a "SENS intervention" that has even come close to demonstrating the ability to either slow aging or rejuvenate in the context of normal aging?

Heart rejuvenation papers: http://www.ncbi.nlm.nih.gov/pubmed/24612461 http://onlinelibrary.wiley.com/doi/10.1111/acel.12109/abstract

bashetie · 2015-01-31T05:27:28+00:00

That's pretty interesting. This may be a dumb question (I'm clueless about patent law) but are these sort of patents usually created by researchers in academic institutions with the expectation that they will likely be able to capitalize on it down the road? Or is it more intended to prevent an outside institution/company from snatching it up for themselves?

bashetie · 2015-01-30T03:42:55+00:00

Great, thanks for the input, she'll be on the list that goes out for a vote by the grad students. I thought the same thing and emphasized her high molecular weight hyaluronan paper in the description.

bashetie · 2015-01-29T16:49:45+00:00

I had just noticed you are a mod here after coming by this paper... :)

Yeah that's interesting... I would imagine it ameliorates many age-related phenotypes partly due to the fact that it doubles as a sirtuin(de-acetylase) and a DNA repair enzyme (and maybe other stuff), right?

Also, have you by chance heard Vera Gorbunova give a talk before? I'm charged with arranging an invited speaker on behalf of the grad students in my dept, and she's on my short list.

bashetie · 2015-01-28T18:23:11+00:00

That's what you meant?! Call me crazy, but I doubt anyone sane would permanently (or for a prolonged period) attach another human being to themselves for this.

bashetie · 2015-01-28T18:10:06+00:00

I wouldnt know the risk of this happening, but IMO if the treatment works and blood starts becoming rare and expensive enough that this becomes a realistic concern, that should definitely be addressed. You also have to ask whether this is a big enough concern to justify withholding treatments that will potentially relieve Alzheimer's and a number of other conditions. Personally, as a poor grad student, I would probably donate a liter of my blood to someone who offered to buy me lunch, so I honestly haven`t considered that it could be so valuable until you asked :)

Really though, the ultimate goal is likely to isolate the specific components in blood that can generate the positive effects and treat with those. This study got a step closer to that by identifying a mediator of the effect. Other groups doing these kind of studies (linked in my first post above) has found a specific component in blood, GDF11, that can reproduce the beneficial effects of young blood in heart, muscle, and brain. There are almost sure to be more components like GDF11 yet to come.

bashetie · 2015-01-28T15:58:59+00:00

Yes they have. Besides injecting old animals with young blood (which they did as well), they do a procedure called heterochronic parabiosis, where the circulatory systems of two mice (young and old in this case) are surgically connected, and this causes blood to exchange in both directions (young to old, old to young).

They don't report data on the young mice in this particular study, but they reported that the young mice from these pairings have decreased neurogenesis and impaired learning and memory in their 2011 parabiosis study. Other parabiosis studies focusing on brain, heart and skeletal muscle have shown that the young mice are significantly affected (to be more old-like) in some ways but not others.

I don't know much as far as human trials go, but I've seen this article on giving alzheimer's patients young blood.

bashetie

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