September 24th, Switzerland

Free Registration, Part of MipTec 2014, Congress Center Basel


MipTec is the largest drug discovery conference in Europe with over 3,000 delegates from pharmaceutical companies


Stem Sells, Translational Medicine, Protein Therapeutics, Medicinal Chemistry and others


New in silico approaches to evaluating the efficacy of and repurposing drugs for aging and age-related diseases


The forum will attract many young scientists in aging research providing the possibility to recruit scarse talent with unique skills and interests


Unlike other aging conferences, the forum is geared towards the pharmaceutical industry addressing the need for new markers and new drugs within the traditional regulatory frameworks

Tuesday, November 24, 2015

Label ageing as a disease and unleash the hunt for a cure:

Recent article on New Scientist by the talented Alex Zhavoronkov , chief science officer of the Biogerontology Research Foundation in the UK.

Friday, November 20, 2015


Beauty.AI is the first beauty contest judged entirely by robot jury, where humans and robots can participate. Every quarter this platform will open submissions for multiple developers of beauty-ranking algorithms to train and test their systems. The project is organized by the Youth Laboratories collective, which is dedicated to understanding of the human nature and effective ways to slow down aging and retain the youthful look for as long as possible.

The Beauty.AI contest will be conducted online at
It’s timeline is:
It starts as of November, 19, 2015,
All people of the world are welcome to submit their selfies up to January, 15, 2016 through the Beauty.AI App.
Data scientists teams are welcome to submit their algorithms up to January, 20, 2016 on,
Winners to be announced as of January, 28, 2016.

For further queries about the science of aging, bioinformatics, deep learning or Youth Laboratories collective’s plan for larger story, please email to team(at)beauty(dot)ai or visit:

Read the full story at

Thursday, November 19, 2015

Strategy for Reducing Side Effects of Anti Aging Drugs:

The development of anti-aging drugs to combat against both normal aging and age-related diseases is growing. Rapamycin, an FDA-approved drug  used to prevent organ rejection in transplant recipients, is known to extend lifespan in model organisms including mice, yeast and flies.  In mice, rapamycin is known to  inhibit a key metabolic protein called mTOR capable of slowing down both normal aging processes and the age-related diseases such as Alzheimer’s disease, cancer, and cardiovascular problems.

In humans, rapamycin is currently in several clinical trials for cancer. However, investigation of rapamycin as an anti-aging pill has shown undesirable metabolic side effects such as impaired glucose metabolism and infections.
A research team at the University of Wisconsin School of Medicine and Public Health showed in a mouse study that intermittent dosing every five days with rapamycin or daily dosing with the rapamycin reduces the undesirable side effects.

“Conventional rapamycin treatment has many side effects, including causing high blood sugar levels and diabetes. In this study, we have shown that we can get many of the same benefits of rapamycin at the molecular level with reduced side effects by changing the dosing regimen or by using a related FDA-approved analog,” says Dr. Dudley Lamming, assistant professor of medicine, University of Wisconsin School of Medicine and Public Health.

 “Daily treatment with rapamycin has a severe impact on the production of insulin by beta cells in response to glucose, and the altered dosing regimen decreases this effect,” says Kimple.
The results suggest that a carefully designed dosing strategy may enable the clinical use of rapamycin or related molecules for diseases of aging, but further research  is required. “Many important unanswered questions remain, including examination of other side effects of rapamycin and efficacy,” says Lamming.

The research was published in Aging Celland will be presented as scientific poster #340 at the Gerontological Society of America meeting.

KEYWORDS: Anti aging; Drugs;  Side effects

SOURCE: University of Wisconsin-Madison

Tuesday, November 17, 2015

New drug to block the proteins causing Alzheimer’s disease.

Recent research to combat against Alzheimer’s disease focuses on amyloid beta, a sticky proteins that forms plaques in the brain causing damaging the nerve cells and affecting the regular neural functions.
Scientists have claimed that they have discovered a compound that may be able to stop the body from making amyloid-beta proteins in the first place. Which means the need of cure for Alzheimer’s will not be needed in the first place.

Amyloid-beta is produced in the brain by enzymes that divide a larger protein. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells.
In the hope they might be able to prevent the creation of amyloid beta by affecting dimerisation process, researchers led by Carmela Abraham, a professor of biochemistry and medicine at Boston University in the US, screened some 77,000 molecules and struck upon one that could be relevant – a kinase inhibitor, which blocks the activity of kinase enzymes.
“This was the big eureka moment,” said Abraham. “Once we knew what the molecule was doing, we could search to see what kinase it inhibits and better understand the mechanism.”
Currently what the researchers understand about this compound is that it has an effect on a larger cell-signalling complex in the brain, but further research will be needed to find the specific, similar molecule or molecules that can act directly on APP.
If successful, this new discovery could be the basis of a medicine that will stop Alzheimer’s right in its tracks.

“Alzheimer’s is now the number six killer of adults in the United States. Deaths from breast cancer and heart disease keep dropping, but Alzheimer’s increases every year,” said Abraham. “Caring for Alzheimer’s patients costs over US$200 billion per year. The estimate for 2050 is US$1.1 trillion, which means it will completely break the health care system. We have to find a drug.”

This research was presented at Neuroscience 2015.

Keywords: Alzheimer’s; Amyloid-beta; Neuroscience; 

Monday, November 16, 2015


Many strategies that can be pursued to test the efficacy of geroprotectors in humans, including large scale publicly-funded supplement studies and studies designed to address a specific set of biomarkers of aging (Hefti and Bales, 2006; Le Couteur et al., 2012; Scott and DeFrancesco, 2015).

Even though major advances have been made since the final ICD-10 meeting in tracking aging at all levels of organization (Sprott, 2010; Le Couteur et al., 2012; Hatse et al., 2014; Wu et al., 2015), there is no universal set of biomarkers and guidelines for measuring aging as a system. Gerontologists have previously struggled to extrapolate biomarkers from animal models to humans (Butler et al., 2004). But with the advent of Big Data, it is now possible to track aging on the epigenetic level and measure accelerated aging in many diseases (Horvath et al., 2014; Horvath and Levine, 2015). There are also promising studies of transcriptomic (Nakamura et al., 2012; Dhahbi, 2014), telomere-length (Zhang et al., 2014; Shamir, 2015) and multi-variate (Sanders et al., 2014) blood-based biomarkers that may lead to minimally invasive diagnostic tests. It is now also possible to use system-wide biomarkers like heart rate variability (HRV) as biomarkers of aging (Corino et al., 2007). There is a rapidly growing body of evidence that biomarkers of aging contribute to and are very similar to the many age-related diseases on all levels of organization, and it is possible to multiplex epigenetic, transcriptomic, proteomic, signalomic, metabolomic, metagenomic, and phenotypic biomarkers to track the progression of aging as a disease.

The paper is available via the Frontiers open access system:
Paper Citation: Zhavoronkov A and Bhullar B (2015) Classifying aging as a disease in the context of ICD-11.Front. Genet. 6:326. doi: 10.3389/fgene.2015.00326

Friday, November 13, 2015

Aging is a complex and continuous deterioration of the physiological function of the body leading to the vulnerability of different organs along with many age-related diseases.
 The recent arguments for classifying aging as a disease in the context of the upcoming World Health Organization’s 11th International Statistical Classification of Diseases and Related Health Problems (ICD-11), expected to be finalized in 2018. It is hypothesized that classifying aging as a disease will result in new approaches for addressing aging as a treatable condition, which will lead to both economic and healthcare benefits for all stakeholders.
Also proposed forming a Task Force to interface the WHO in order to develop a multidisciplinary framework for classifying aging as a disease with multiple disease codes facilitating for therapeutic interventions and preventative strategies.

Keywords: Aging; ICD; Disease classification; WHO; gerontology.
 Citation: Zhavoronkov A and Bhullar B (2015) Classifying aging as a disease in the context of ICD-11. Front. Genet. 6:326. doi: 10.3389/fgene.2015.00326

Wednesday, November 4, 2015

Effects of physical exercise in telomere length:

Evidence suggests there is a probable effect of exercise on the telomere length. Hence a very detailed statistical review was conducted which was aimed to assess the effects of exercise on telomere length. The following databases were closely observed: MEDLINE, EMBASE, Scopus, Cochrane Central Register of Controlled Trials, LILACS and Web of Science. All the articles that assessed the effects of exercise in telomere length were included in this review. Thirty-seven original studies were included in this review, comprising of almost 41,000 participants. Twenty articles did not show any valid association and  only 15 described a positive relation. It was shown that there is a tendency toward demonstrating the effects of exercise on the length of telomeres. Few studies were found, many studies did not reach statistical importance and there was diversity in the final result. Hence, a possible significant association between physical activity and telomere length is still questionable.
Keywords: TelomerePhysical exerciseAging

Corresponding author at: Pontifícia Universidade Católica do Rio Grande do Sul, Instituto de Pesquisas Biomédicas (IPB).