Saturday, 26 January 2013

Lectures of my academic leaders

During surfing the Internet for useful scientific information I came across three videos:

There my highly respected academic leaders talk about their research. I am so proud to learn from such people! Thank you, Anton and Alexander!

P.S. Lectures are in Russian, but they are so cool that it is worth to learn language to listen them! 

Friday, 25 January 2013

Caloric Restriction Has a Protective Effect On Chromosomes

     According to a study carried out by a team led by MarĂ­a Blasco, the director of the Spanish National Cancer Research Centre (CNIO), a sustained lowering of food intake over time results in an increase of telomere length -- the ends of chromosomes -- in adult mice, which has a protective effect on the DNA and genetic material.
     These beneficial effects on the youth of the chromosomes translate to a lower incidence of cancer and other age-related illnesses. 

     To carry out the study, researchers used young mice -- just three months old -- and reduced their caloric intake by 40% before observing them until the end of their life cycle.Mice that undergo caloric restriction show a lower telomere shortening rate than those fed with a normal diet. These mice therefore have longer telomeres as adults, as well as lower rates of chromosome anomalies. 
     To study the effects of this phenomenon on the health of the mammals, researchers observed the incidence of age-related illnesses like cancer. The mice that had been fed a lower calorie intake showed a reduction in the incidence of cancer. Furthermore, these mice also showed a lower incidence of other age-related illnesses such as osteoporosis, greater glucose uptake or improvements in motor coordination.
     When the researchers carried out these same experiments with a variety of mice that produce more telomerase - a protein that lengthens telomeres and protects chromosomes --they observed that these mice not only enjoyed better health but also lived up to 20% longer.
     Such significant increase in longevity is due to the protective effect against cancer produced by caloric restriction - incidents fall by 40% if  compare them with the mice that produce more telomerase and have a normal diet -- and, added to the presence of longer telomeres, this makes the mice live longer and better.
     Despite the effects of caloric restriction depending on the genetic characteristics of each organism, this study opens the way to studying the effect other factors and lifestyle habits, such as smoking or exercise, might have on aging.
      Furthermore, it is calculated that there are currently more than 10,000 people in the world on some form of controlled caloric restriction, so the observation of these individuals will be decisive in discovering the effects of this type of diet on humans.

Souse: Science Daily

Wednesday, 23 January 2013

My first published article

     In recent years researchers have focused on the identification of genes that play a role in the aging process and age-related diseases.  One such illnesses is Hutchinson-Gisford Progeria Syndrome, also known as progeria. The cause of progeria is single-nucleotide polymorphism in 1824 position in gene LMNA, that codes nuclear protein lamin A.

Hutchinson-Gilford Progeria Syndrome

     The nuclear lamina is the structural support of the nucleus and it serves as the scaffold for DNA-protein interactions. Given that the nuclear lamina is involved in a wide array of biological processes, including DNA replication, transcription, cell cycle progression, and chromatin organization, it is not surprising that alterations in the proteins that make up this structure would have significant deleterious effects and give rise to diseases. The diseases that are associated with defects in the lamin proteins that compose the nuclear lamina are referred to as laminopathies. Lamin A is one of the lamin proteins that has been shown to be highly mutated; to date, over 400 point mutations have been identified in lamin A. Genetic alterations of the lamin A gene contributes to laminopathies and aging-related diseases, which makes lamin A a viable target for the treatment these diseases.     
The biological effects of genetic alterations in lamin A are not only related to the mutations in the lamin A gene, but also to the balance of normal lamin A proteins to mutated lamin A proteins within the cell. 

Functions of nuclear lamina (Travis A Dittme and Tom Misteli, 2011).

     So the optimal therapeutic strategy for laminopathies and aging-related diseases that are linked to lamin A  should be a multifaceted approach that targets lamin A at a genetic level in combination with downstream cell signaling and cellular processes approaches. Our computation analysis project identified signaling pathways that regulated lamin A expression as well as lamin A - protein interactions that mediated diseases. To date, this is the first study of its kind to identify these 12 potential treatment strategies for laminopathies and diseases related to aging: (1) IGF-1/GH balance restorers, (2) Notch inhibitors, (3) reactive oxygen species scavengers, (4) telomerase activators, (5) Rb inhibitors, (6) apoptosis inhibitors, (7) translation- and autophagy-activator inhibitors, (8) cAMP activators, (9) thyroid hormone supplements, (10) PI3K inhibitors, (11) epigenetics marks reversal, and (12) farnesylation inhibitors. 

Signaling pathways in which LMNA gene is involved

However,  further trials are needed to validate these treatments and to determine their efficacy in a clinical setting. 

You can read full article on the link:

Tuesday, 8 January 2013

Hello World (and I never want to say Goodbye World!)

My first post... Where do I start?

My life's goal is continuous improvement and the main impediment to this goal is aging.

Presently, we are the slaves to aging and inevitable age-related decline and death, but in the near future we have a chance to change the history-long paradigm and intelligently evolve our bodies and society to live longer and healthier lives in peace and prosperity. I decided to dedicate my life to helping humanity achieve freedom from aging, age-related diseases and decline by doing good science in several directions of aging research. And in this blog I would like to document my quest.