Aging Research - Science topic

Dear Dr. Omkar S. Kushwaha,

I consider that the first of all to have a great vocation for research work. Only in this way can we take responsibility for the content that we are going to offer to the research community in general. The research work must also be attractive and interesting with clear intentions of being able to contribute to advancing the knowledge of the disciplinary Sector to which we are dedicated. It is also important that we not only conceive theoretical works that would only find a physical location in a library, but that they be "living" research works, circulating and interacting in multidisciplinary environments.

It would depend on whether or not the Sirtuin1 causes the symptoms of your interest. Your best bet will be bypassing the Sirtuin 1 repression, activation mutations in another gene, etc. In general, you will need to design the experiments and screen what you want. Good luck.

Hi Anthony L, Yes: we often used the DNA-damaging drug etoposide to induce senescence. Soluble in DMSO. 10 uM was often ok, though the best concentration can vary with the cell type -- it gets toxic at higher concentrations (because extensive DNA damage is toxic). It was added to recently plated cells for 48 h, then removed, and the cells were left for 5 days to develop the senescent characteristics -- although this may also vary with cell type. So for a new cell type you might want to try lower and higher concentrations, and different timings. We published this method (used as a positive control) in Cairney CJ et al. 2017, PLoS Genetics. (See Supplementary File 2.)

Have a look at the following RG links.

Hello Pavel,

I was wondering if you ever analyzed TRF images; I have been struggling with the software I am currently using. Any recommendation regarding imaging the membrane and analyzing?

much appreciated and thank you in advance!

Cheers,

Amany

Editors are busy - they probably have two jobs! - so I think you should wait a while longer. They haven't forgotten you. :-)

Please go through our article "Aging induces a step-like change in the motor ability structure of athletes ". If you are interested in a change in motor performance.

It feels great to share it. Hope you find it useful P.J. White

OK great. Here are two our books that have case studies on NCDs

good luck

Mohamed

More scientific endeavors, constant updating, ability to supervise or train more PhD students etc...

No, I don't think so.

urbanization and industrialization are the end cause of urbanization and industrialization

I'm a qualitative, critical, community-engaged social work researcher in aging, a position from which I cannot necessarily answer your direct question but perhaps come at it from a different perspective, if that could be helpful. I am quite familiar with the issue of autonomy for older adults.

I wondered about your definition of "autonomy". Often this term is used to refer to a person's ability to age in place and perform their ADLs. It is located in a more medical model, with research dominated by nurses, physio/rehab, doctors, public health, and health policy researchers. Losing one’s autonomy has a wide range of consequences and this body of research provides many different tools for looking at the diverse concerns underlying loss of physical autonomy. In terms of social autonomy, there is also a great concern with social isolation, which is a risk factor for many negative outcomes, and study on the social networks of older adults. Both these are very broad fields of inquiry and it may be helpful to narrow down what you are hoping to “get at” with this question. Autonomy seems to be shaped by a wide variety of factors with varying impacts on different people.

I was also curious as to the purpose of your question. Is it to help reduce health-care costs, reduce chronic illness and disability, shape social and health policy? Or is it perhaps focused on the wellness and well-being of older adults?

While all of these purposes are important, my own interest is more in the latter area. I am currently conducting community-engaged with diverse groups of older rural men to learn from them what is most important to support them in navigating their later life changes (including changes in health and mobility). By conducting qualitative, photo voice research with the older men, we also hope to inform the work of policy makers. As social work researchers, we believe that starting with older men’s lived experiences is important to better understand their notions of wellness and well-being — social and otherwise — at this stage of their lives.

My apologies if this answer is not helpful. I know it is not directly answering your question, but sometimes it is helpful to have a different perspective on a question as well. Good luck with your research!

An LPS encounter in the severe stage of viral infection fallouts in an heightened pulmonary pro-inflammatory innate immune response. It shows an increase understanding towards viral-bacterial interaction. In one such case i.e., DENV infection can lead to seepage of LPS from the intestine into the blood of the affected individual and is an indicative of an increased permeability of the intestinal mucosal barrier. Reports have suggested an elevation in plasma LPS levels in DENV infected individual compared to healthy individuals. There is a strong correlation of plasma seepage severity score towards rate of infection with that of LPS level. With the outset of COVID 19 Coronavirus from China, the augmented plasma LPS might be parallel to predict its severity. Thus a decisive study is needed to draw a likely conclusion for the role of rising plasma LPS during COVID 19 infection. With the understanding of fundamental signalling cascades of COVID 19 infection and its pathophysiology, development of therapeutic/prophylactic strategies will be a plausible approach.

I had the same question years ago. I searched then and found an Apa article with adjustment of MMSE with age and level of education. I translated it in romanian for my supervised and attached it that way (“varsta“ = age). I’ll look for the paper and come back.

Please take a look at these useful RG links.

Autophagy, an evolutionaily conserved cytoplasmic degradation system, has been implicated as a convergent mechanism in various longevity pathways. Autophagic activity decreases with age in several organisms . Research has shown that the expression of Rubicon, a negative regulator of autophagy, increases in earth worm , fly and mouse tissues at transcript and/or protein levels, suggesting that an age - dependent increase Rubicon impairs over time, and therby curtails animal health-span.. Consistent with this idea, knockdown of Rubicon extends worm and fly lifespan and ameliorates several age - associated phenotype. For more information consult nature.com

i want to assess the attitude of my young university students attitude towards aging. that is why i am highly interested towards your standardized scale.

Maybe this: could be a good entry point for finding the most appropriate way to solve this.

Any form of disinhibition from drugs or dementia for example will release hitherto suppressed profanities. This is clearly seen nowadays with the phenomenon of the Midnight Tweeter. See my RG question Do drugs release racist comments?

How are you defining "health"?

IT is a beautiful question. I will myself be interested in the answer.

As far as I think, even if some therapy is curative by how can you regain the lost beta cell mass?

A question worth pondering upon!

Hi Sina,

There is the "DNA methylation clock", named "epigenetic clock": the degree of methylation of few CpG loci reflects the biological age. It keeps track of the "solar years", except for many diseased tissues which appear "epigenetically older" than healthy tissues, and has a different pace in different tissues.

Two reviews about this question: PMID: 25913071; PMID: 25341512. There are many recent papers about the epigenetic clock but not that many reviews. One founding paper: PMID: 24138928.

In zeolite synthesis, the term aging is related to a an aging period before the hydrothermal treatment. This aging is usually performed at room temperature. They are many reports of the positive impact of an aging period, but it does not mean that it is always necessary to add this step. It can help to orient the crystallisation toward the desired structure (favor the growth of the desired phase over an undesired one), decrease the crystallisation time or favor the formation of smaller particles (favor nucleation over growth).

See for example

or

Good point, Gulzar.  Thank you for the Q - all info available below.

@ Marianne Levon Shahsuvaryan: The link above leads to a paper about extra-virgin olive oil. Please give the correct link to the paper about medicinal mushrooms 

I agree wir Dr War response

Melatonin is a potent antioxidant through its scavenging effects of free radicals and its stimulative action on antioxidative enzymes e.g glutathione peroxidase, glutathion reductase, superoxide dismutase, and catalase. Another point is that melatonin plasma levels decline with age which suggests that all of its pharmacological properties disappear. Rhere is an abundant literature on the topic. Should you want papers please let me have more precision on what you want exactly

Good luck

Hi, Paul.

Please check whether this can be helpful

National Health and Morbidity Survey

Global Ageing Study (GLAS), 2007

Malaysian Population and Family Survey

National Medical Care Survey (NMCS) 2010

East Asia Retirement Survey

The Mental Health and Quality of Life of Older Malaysians Survey

Philippine Elderly Survey (PES)

Philippine Longitudinal Survey on Aging (PLSOA)

Best,

Mamta

Lucia, do you mean that your student will write thesis paper on this topic? Good luck for both of you. Merry Christmas!

Best regards, Yuri

Brain Longevity

Dear

I hope to find what you need and im sorry I cant help you because it is not my field. Regards 

I think it may be helpful, although a level of disabilty is needed for people to be agreeable to using any of the wearable tehnologies any way this is a review article I hope it helps

A review of wearable sensors and systems with application in rehabilitation

Shyamal Patel,Hyung Park,Paolo Bonato,Leighton Chan andMary Rodgers

Journal of NeuroEngineering and Rehabilitation 20 129:21

DOI: 10.1186/1743-0003-9-21

are we talking about ADs to older consumer or the use of ancient ads, repeated ad nauseum through diverse TV channels? For example, Mars via its Galaxy (Dove) chocolate ad delights in repeating the same old AD over years now. For me, the outcome is a complete turn-off for Galaxy itself, and an annoyance with Mars who do not seem to understand too frequent repetition of the same AD drives customers away from - not toward the brand.

sir,

By the littile knowledge i m trying to explain......

First I would like to explain that not only androgen but several hormones are also involved in telomerase regulation/activation. The current studies revealed (2016) fact only for androgen, that androgen can increase Telomere length and indirect measure for lifespan, making previous studies more stronger which were conducted in 2000 i.e., (telomerase activity is reduced by androgen deprivation, while treatment with testosterone/androgen restores high levels of telomerase activity (Soda et al., 2000).

Besides this Estrogen is also playing a strong role in telomerase activity and  directly or indirectly activates telomerase (Kyo et al., 1999).

Which one is playing more role in telomerase activity not studied well (lacking comprehensive studies). So it is very difficult to understand the contradiction of life span of women and men that whose role are better in longer life span.

plz share more information of telomere......

Thanks, Darlene! I just saw this, finally! Best wishes,

Matt

I can't see the relevance of this study. If the client has the motivation to eat and the skills involved - what is the significance of grip strength after meals? How will your study provide information that is meaningful to clients healthcare outcomes? What are the assumptions/hypotheses underpinning your study?

Rudi G Westendorp has published several studies on this subject - for instance:

von Faber M, Bootsma-van der Wiel A, van Exel E, Gussekloo J, Lagaay AM, van Dongen E, et al. Successful aging in the oldest old: Who can be characterized as successfully aged? Arch Intern Med. 2001;161(22):2694-700.

Dear Krzysztof Ksiazek, 

The following article was last publication on alagebrium (Jan 2014):

Further Confirmation that AGE-Breaker Alagebrium Has No Significant Effect in Human

Alagebrium (or ALT-711) was an early and ultimately unsuccessful foray into the development of an AGE-breaker drug: a treatment intended to safely break down the build up of advanced glycation end-products (AGEs) that characterize aged tissue. These are chemical cross-links that form as a byproduct of the normal operation of metabolism, and which glue together proteins to cause various forms of harm, such as destroying the elasticity of skin and blood vessels. Eventually this process contributes significantly to age-related disease and death, meaning that any attempt to treat and reverse aging by attacking the causes must include proficient AGE-breakers.

The attempted clinical development of alagebrium followed initially promising studies in rats, but as it turns out the types of AGE important in human tissue are not the same at all, and as a consequence alagebrium had no meaningful effect in human trials. This was sufficiently well determined that you can color me surprised to see that anyone is continuing with the thankless but important work of confirming past negative results for this line of research. But here we have it:

Present work on AGE-breaker development is very limited indeed. At the present time it is known that one type of AGE - glucosepane - makes up the overwhelming majority of AGEs present in human tissue, so in theory finding ways to treat and reverse AGE build up in our species is in fact a comparatively simple research and development undertaking. Unfortunately the drug development community has little infrastructure in place for working with this sort of compound, and little interest in building that infrastructure: groups with funding tend to find other things to work on, where there is a shorter and more certain path to producing a useful end result.

This is where the SENS Research Foundation comes into the picture. The Foundation is presently funding research to produce the tools needed to work with glucosepane and thereafter produce technology demonstrations to show that it can be cleared from tissues. Hopefully work on AGE-breakers will pick up again over the next few years as a result of this intervention. This whole situation might not be the best candidate for an example of clearly useful near-term medical research and development that should yield enormous benefits, but yet just isn't happening - but it is certainly up there in the charts. From a distance we might see constant progress, but down in the weeds every field is beset with this sort of problem.

Hoping this will be helpful,

Rafik

Dear Taratorn,

regarding re-testing of the same animal in various repetition of the test, it is possible however, you have to take that into accound when you do your statistical analysis as well as your results interpretations.

In particular in a learning task like the Morris Water Maze, where some procedural learning is present as well as spatial learning.

In particular some "training" effect might shadow your age-induced deficit.

If you keep that in mind there is no reason you should not re-use the same animals, especially considering that you seem to plan to test them every 4 months, which should be enough to reduce the impact of each repetition of the test.

In an attempt to reduce the transfert of learning from one iteration to the next, you could consider testing them in different room (if feasible) or changing the distal and local cues used during the visual learning and spatial learning phase of the task.

I hope it helps

best 

thank you Mr.Gurmohan Singh

i wish to communicate

with my respect

here follows a paper that could fit the question

best regards, Mauro Colombo

Dear all,

thx for answers.

Yes, we done everything acording to procedure reported in McFarlane et al. (2002) but it seems that vertebrae are not calcified at all (:-)! I will pas through all proposed literature. I will inform you about eventual sucess.

Thx once again,

Sanja

DNA methylation age and telomere length have only a weak negative correlation after you correct for chronological age. As an aside I mention that it is important to correct for chronological age before one relates DNAm age to telomere length because chronological age confounds the relationship between the two variables.

We correlated DNAm Age with telomere length in *adipose* tissue (Horvath et al 2014, PNAS, Title: Obesity accelerates epigenetic aging of human liver") and only found a weak and insignificant negative correlation between the two variables after correcting for chronological age (e.g., r = −0.28, P = 0.22). We and others have seen similar correlation coefficients in blood tissue but these appear to be unpublished.

Bottom line: the epigenetic clock relates to a biological process that is largely independent of telomere attrition and cellular senescence. 

In the language of multivariate linear models:

if you fit the following regression model:

lm(DNAmAge~AgeAtBloodDraw+TelomereLength)  then TelomereLength will only have a marginally significant p value.

Conversely, if you fit

lm(TelomereLength~AgeAtBloodDraw+DNAmAge) then DNAmAge will only have a marginally significant p-value. Caveat: bmulti-collinearities between the 2 covariates will make the coefficient estimates unstable.

Best,

Steve

Cycloastragenol through the buccal delivery method

Hi Paul,

Like Alan, I think it's a monumental task to come up with a figure - even a range on the impact of demographic change on healthcare spending not least because of the comparability of data even as the OECD try to rectify this matter. There is even debate as to the direction of the impact. Consequently, such an endeavor would be courageous as it would be riveting.

That being said, two references that might be helpful are:

Payne G, Laporte A, Deber R, Coyte PC. Counting backward to health care's future: using time-to-death modeling to identify changes in end-of-life morbidity and the impact of aging on health care expenditures. Milbank Q. 2007 Jun;85(2):213-57.

Reinhardt UE.Does the aging of the population really drive the demand for health care? Health Aff (Millwood). 2003 Nov-Dec;22(6):27-39.

Cheers,

Human beings (all mammals) can be seen as complex systems composed of interconnected sub-systems and sub-parts at several levels (DNA, ...proteins, ... cells, ...organs, ... neural-, immune-, ...systems, ...). As the complex system is continuously subject to stressors – this is inherent to life - it ages. Not only the parts and sub-systems, but also the efficiency of the interconnections do age. Parts/ sub-systems and interconnections age at different paces in function of the stressors they have to adapt to and of their (innate or acquired) skills to do so. Moreover, the internal stresses which result from the stressors vary from individual to individual. So the efficiency of the adaptation processes depends on the intensity and steadiness of the stressors, of the resulting stresses and of the quality of the innate and acquired body "internal organization". There is also a kinetic aspect as the adaptations must be done in due time. With time going, the adaptation abilities may decrease in appropriateness and reaction speed. At the end, local or global exhaustion is reached. 

Global aging at one same pace is the best case: the case of the mankind seniors of 110 - 120 years we all have heard of (the maximum estimated lifespan would rather be of 136 - 140 years).

However, more commonly, one or a few parts/ sub-systems (and their interconnections) would sooner fail to adapt to their specific stressors and a macroscopic (irreversible) disease would develop up to the end of life (long) before the maximum lifespan would have been reached.

Referring to the article of Lipsitz & Goldberger (1992), there might be connexions with chaos theory but probably less with fractals.

I've written two articles on the subject of the aging of biological complex systems :

Also, a chapter of my book "Quantitative general adaptation" is devoted to it (chapter 6). And there are some thoughts on the possible links with chaos theory in chapter 8.3. 

Kind regards     

Thank you Jose and Barbara for adding the information.

Hi Hannah

I agree with Jennifer and would advocate for the CASP-19 or its shorter variant the CASP-12. It is a lot better at assessing older adult QOL than a number of current indicators because (1) it was designed specifically for older adults, and (2) it actually measure self-perceived QoL instead of proxy measure that focus on health or functioning. It is excellent. We've used it in our New Zealand longitudinal study for 4 waves now and it has been used widely in the European longitudinal ageing studies (i.e., ELSA, TILDA, SHARE) as well as some of the occupational cohort studies. There is a growing body of work attesting to its stability across countries. Please let me know if you need any links or related articles.

Andy

In terms of cognitive-communication variables would want to consider: sensory loss (both hearing & vision); any pseudodementias (confused responses due to another condition such as delirium or depression); medications that can induce a cognitive or communication loss; undiagnosed mental health issues (e.g., depression, anxiety, bipolar, etc.), and second language considerations.  Regarding impact on 'study design' these would impact any cognitive-communication assessment including screenings (e.g., Montreal Cognitive Assessment) or full-battery psychological assessments as well as follow-through on given directions for tasks given.

Well spotted Adrea,

thank you for the additioanl infomation.

Best wishes

Catrin

This question is partly triggered in my memory when I read the abstract of Helena's paper.  She has just uploaded the full text for me.  Thanks Helena!

Thank you Liliana, this will be a great resource for scholars working within this area!

I think that there isn't a specific test for assessment all cognitive functions but the neuropsychologist's battery. The Mini Mental Test (Moca, etc..) is an instrument of general screening. I use many tests for evaluate a cognitive domain:

ATTENTION AND EXECUTIVE FUNCTION:

Visual Search

Symbol Digit

Trail Making

Stroop

FAB......etc....

LANGUAGE:

Semantic Fluency

Phonemic Fluency

Denomination of figures (ENPA, BADA; CaGi, etc...)

Comprension of phrases or word (ENPA, CaGi, BADA)....etc

MEMORY:

Digit Span

15 Rey's Words

Rey's figure A or B

303P

FCSRT.....

VISUOSPATIAL:

CD

Complex figure A or B....

For each test that I use I have generally the italian validation.

Dear Mauro,

Both sex and sex x Age interaction are not significant (p > .6).

Well ! Don’t guess the age od a person from the FACE. Face can be deceptive. Facial age and biological / chronological age do not go togather in most cases. Facial age / biological age are dependent on genetics and environment. Some people may look younger than their chronological age and vice versa. This is due to their genetic endowment. Extreme case is of Progeria in which gene(s) alone make a person of 6 years look like a person of 60. This is early aging  in which biological clock is running faster than chronological clock

People who cares about their looks and take care of their face through crèmes, etc.,  may look younger. They feel happy but they cannot cheat the chronological age. Their body is aging slowly or fastly according to their genetic makeup. This is our genetic fate.  

Just saw this impressive publication:

J Prev Alz Dis 2015;2(2):142-152

Within the last 20 years, several standardized cognitive trainings have been developed aiming at the delay of cognitive decline in older people who are at risk of Alzheimer’s Disease (AD) or in mild stages of dementia. The transfer of cognitive training effects into activities of daily living was very limited in most previous studies. Therefore, multimodal Cognitive Rehabilitation approaches have been designed that aim to improve the activities of daily living. These approaches also attempt to integrate the patient’s psychopathological and behavioral status as well as social relationships into the treatment plan. Contrary to other approaches, CR mainly focuses on compensation rather than restoration of impaired functionality. In this review, we define CR conceptually, and derive specific criteria to evaluate current CR approaches for individuals with mild cognitive impairment (MCI) and AD dementia. In addition, we perform a critical, methodical analysis of available CR studies, reviewing their short- and long-term treatment effects. Findings suggest that CR approaches improve memory performance and competence of activity of daily living (ADL) in mildly cognitively impaired subjects (MCI), when compensatory, integrative, as well as interactive elements and domain specificity are taken into account. Interactive and individual aspects also appear to be relevant to sustain long-term effects. In AD dementia, similar results emerged, although with smaller effect sizes. The efficacy of individualized CR approaches was comparable with theory-based, manual-guided concepts as long as promoting interaction was part of the treatment. So far, only few randomized controlled studies of sufficient sample size are available. Future systematic efficacy studies need to consider precisely defined outcome variables. This is necessary before one can draw conclusions of how CR can be used for secondary prevention of AD dementia as well as AD treatment.

CITATION:

E. Kasper ; S. Ochmann ; W. Hoffmann ; W. Schneider ; E. Cavedo ; H. Hampel ; S. Teipel (2015): Cognitive Rehabilitation in Alzheimer’s Disease – A Conceptual and Methodological Review. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2015.58

Dear Michael,

I think you could look at these articles/reviews.

- Lenze, E. J. et al. Mindfulness-based stress reduction for older adults with worry symptoms and co-occurring cognitive dysfunction. Int. J. Geriatr. Psychiatry 29, 991-1000 (2014).

- Gard, T., Hölzel, B. K. & Lazar, S. W. The potential effects of meditation on age-related cognitive decline: a systematic review. Ann. N. Y. Acad. Sci. 1307, 89–103 (2014).

- Marciniak, R. et al. Effect of meditation on cognitive functions in context of aging and neurodegenerative diseases. Front. Behav. Neurosci. 8, 17 (2014).

Enjoy reading these, it's a great topic!

Renaud

Dear Wasana:

I recommend a study of skulls where you can compare various methods. If the skulls are less than 70 years old (with evidence of root translucency), and are individuals who had more than 20 years after his death, it is viable method Lamendin and its variants as Prince & Ubelaker, Gonzalez Colmenares and Schmitt.

Regards.

You should read an excellent new paper about important factors for quantitative immunoblot analysis. It recommends use of multiple internal loading controls, for maximum precision and reproducibility. Also suggests diagnostic experiments you can run to look for sources of variability.

Migration is a particularly interesting example where dissection of the genetic and environmental contributions should be possible. In my field, rates of schizophrenia and other psychotic disorders are known to be raised amongst certain migrant groups and their descendants living in Western Europe (and elsewhere). In the UK, the largest relative risks are found amongst people of black Caribbean and black African origin, beginning in first generation migrants, largely from the Caribbean and sub-Saharan Africa in the 1960s. Elevated risk persists amongst UK-born children and grandchildren. We know this is not explained entirely by socio-economic status [1]. Further, rates of these psychotic disorder are not elevated amongst the Caribbean population in the Caribbean (they are in fact similar to the background incidence rate in the UK) [2-4] and rates do not appear to be elevated in these groups as a result of selection issues [5] (i.e. a tendency for people with genetic vulnerability to schizophrenia to be more likely to migrate). Therefore the experiences of migration and minority status suggest a particularly social origin to elevated risk, which might co-participate with genetic vulnerability. The findings on ethnic density (where neighbhourhood ethnic composition modify individual risk of schizophrenia amongst different ethnic groups i.e. [6] cannot readily be explained by genetic selection effects either. 

Hope this helps. 

References (B J Psych heavy - sorry! - just a coincidence)

1. Kirkbride et al. 2008. Br J Psych. http://www.ncbi.nlm.nih.gov/pubmed/18700213

2. Mahy et al. 1999. Br J Psych. http://www.ncbi.nlm.nih.gov/pubmed/?term=10621765

3. Bhugra et al. 1996. Br J Psych. http://www.ncbi.nlm.nih.gov/pubmed/8932887

4. Hickling et al. 1995. Br J Psych. http://www.ncbi.nlm.nih.gov/pubmed/7582668

5. Selten et al. 2002. Am J Psychiatry. http://www.ncbi.nlm.nih.gov/pubmed/11925311

6. Kirkbride et al. Schiz Bull. http://www.ncbi.nlm.nih.gov/pubmed/23236081

Hi Matt,

The NTC Ct values for both telomere and 36B4 are way behind the (8-10 Ct) the Ct value of the last standard curve points. So in that sense it is ok. But when I see the melt curve, it is coming at the same temp of the product, i.e, 80oC. We have changed the primers (re ordered), water and master mix but not much success. 

Dear Jose-Ignacio and Sandra,

Do appreciate your responses. What I am looking for is recent published or unpublished literature/data on health systems responses to population ageing, the determinants and drivers in LMICs. The NCD burden will certainly be one component of health system expenditures unless we can change the trajectory of ageing at an earlier stage in life.

Sincerely, Paul

The symptom are quite common and epidemiological studies support a conversion rate between 15% to 30 %.  Review the following papers by Morris and Petersen:

I think the answer mainly depends of your objectives and goals. For example, if you want to screen patients for frailty, the 6 meters walking test is one of the most useful. If it is for waking disorders in general, the seat test is very interesting. For screening fallers, I use the one leg balance test.

Hi,

Regarding dietary factors paying attention to amount of protein intake received recently increasing attention. Further anti inflammatory factors such as fatty acids and anit-oxidants may plan an important role in prevention and treatment of sarcopenia of ageing.

BR

Dear Shahrukh,

I am interested in this too. I work as a freelance statistician, from Argentina, although I have worked also in intenational projects in Chile, Uruguay, Spain and Paraguay. I have worked in several large scala projects and I have a very solid experience in programming for Data Analysis and in using the Statistical Data Analysis Procedures but most of it is in SAS. I have worked with cohorts in education matters (IRT (for UIS-Unesco), Flow Model). For these projects I have worked both in Statistical Data Analysis and in the Sampling Design..

Let me know ...

Guillermo E. Ramos

Hi Amy

Our GP practice is using their own version of the MMSE and screening people over the age of 60 years. They are using a Phlebotomist who has received specific training to record the test and then the GP will review the results particularly if their is evidence of memory problems. They have chosen to do this because of the copyright issue. I am not aware of other GP practices that have done this. Good luck in your research.

Thank you very much for your answer Alexander. Your field of work is very interesting. If we find a group that wants to coordinate the proposal, I will contact you again. Best regards, Elena.

I am not unbiased, as you can imagine. The answer also depends on your objectives. I am skeptical about the distinction about aging and age-related diseases and also try to avoid going to semantics. There are many biomarkers of aging but all they are "weak", in a sense. Using the frailty index approach we can find a summary measure that is much superior to any single biomarker.  Aging is a systemic property of the organism therefore any assessment should also be systemic, i.e. to combine available information.  Such information can be based on clinical assessment  or even self-reports but also can be more "objective". Take a look at the recent paper Howlett et al. BMC Medicine, 2014 where the lab tests were combined together in a FI-Lab. To go in this direction you should not hate math, although math is very basic.

Arnold

Most of the developing countries do not have significant aging populations (let's not consider China a developing country as they already surpassed the developed world in many areas). But most likely, extending productive longevity in these countries will boost economic growth. And in poor countries it may be easier to motivate people to work and study longer. And there should be at least some attempts to improve their level of well being while providing additional incentives to establish a life long learning and life long career planning mindset. This would be a very neat experiment to perform on a small population group. 

Here is one of my papers on the subject concerning developed countries:

http://www.mdpi.com/1660-4601/10/11/5936 

Are you looking for cell-free sirtuins or sirtuin levels in specific cells? 

For plasma you may check out this recent paper by a group in Italy. They used good old ELISA to mesure SIRT-1:

http://link.springer.com/article/10.1007/s12020-014-0465-x 

and here is a paper evaluating the levels of SIRT-1 in Alzheimer's. They have controls:

I'm engaging on a research about Frailty Syndrome and brazilians oldest-old. This group was chosen because it's the most growing group of Brazil and world. We're looking for related factors (sociodemographics and clinicals) and trying to make a model of clinical management to frail elderly.

Hi Paul, I don't know if this will help you, but my company was looking at using saliva to measure diabetic markers found in plasma.

There is diffusion of proteins from plasma to saliva.

Anyway, we found that most saliva samples are contaminated by bacterial proteins and bacterial DNA.   

Former colleague of mine at the University of British Columbia is just writing a up her dissertation and she conducted walking interviews with older adults - I don't think she has publications out on it yet but has published extensive on older adults and mobility devices. http://scholar.google.co.uk/citations?user=bj5M46IAAAAJ&hl=en

The correct term is “sarcopenia” and means cellular atrophy of muscle cells.

For question1: Sarcopenia must be seen in the context of aging phenomenon. Please, see: Libertini G., Programmed aging paradigm: how we get old. Biochem (Mosc) 2014, 79(10):1004-16. (If you want a free copy, ask me giacinto.libertini@tin.it)

In this paper, about cardiac sarcopenia: “An old and deep-rooted belief is that the heart is an organ incapable of regeneration and without cell turnover. On the contrary, “The Heart is a Self-Renewing Organ” [13]: in a normal heart, every day about 3 million myocytes die by apoptosis and are replaced by cardiac stem cells: “the entire cell population of the heart is replaced approximatively every 4.5 years … The human heart replaces completely its myocyte population about 18 time during the course of life, independently from cardiac diseases.” [13].

Cardiac stem cells duplicate and differentiate, allowing myocyte turnover, and show age-related telomeric shortening and cell senescence [36-38]. In the old heart there is a global loss of myocytes, with a progressive increase in myocyte cell volume per nucleus [39]. The decreasing number of myocytes is due the progressive decline in the ability to duplication of cardiac stem cells [13].

The decline of cardiac contractile capacities causes an enlargement of the heart that conceals the underlying atrophy of the contractile cells. So, in apparent contradiction, the heart chambers are dilated and the senile heart, although atrophic as number of cells, is morphologically hypertrophic [40].

“With aging, there is also a progressive reduction in the number of pacemaker cells in the sinus node, with 10 percent of the number of cells present at age 20 remaining at age 75. ... Age-associated left ventricular hypertrophy is caused by an increase in the volume but not in the number of cardiac myocytes. Fibroblasts undergo hyperplasia, and collagen is deposited in the myocardial interstitium.” [40]

The heart shows “... some increase in the amount of fibrous tissue and fat in the atrial myocardium with a decrease in the number of muscle fibres, and loss of fibres in the bifurcating main bundle of His and at the junction of the main bundle and its left fascicles, with lesser degrees of loss in the distal bundle branches.” [41].

Drugs effective in “organ protection”, as ACE-inhibitors, sartans and statins, are effective in the prevention of atrial fibrillation [42, 43].”

"How old is the Web? Characterizing the age and the currency of the European scientific Web" this paper studies the age of a sample of webpages