Journal of anti-aging medicine最新文献

Telomeres, located at the ends of eukaryotic chromosomes, are synthesized by the enzyme telomerase and are responsible for maintaining chromosome length. The absence of telomerase in most somatic cells has been associated with telomere shortening and aging of these cells. In contrast, high levels of telomerase activity are observed in over 90% of human cancer cells. The absence of telomerase in normal and aging cells is considered a natural defense against development of cancer. However, we do not know what triggers the reappearance of telomerase in cancer cells. Telomerase activity is directly correlated with the expression of its active catalytic component, the human telomerase reverse transcriptase (hTERT), which is believed to be controlled primarily at the level of transcription. Elucidation of the control of telomerase in aging and in cancer as an age-related disease has considerable potential in leading to novel approaches in anti-aging medicine.

It is supposed that longevity might be programmed by early life exposures. We had carried out demographic and experimental researches for the examination of the possibility of longevity programming. In demographic study, the recorded deaths in Kiev (Ukraine) between 1990 and 2000 (51,503 men and 50,131 women) were used. Age at death was strongly associated with month of birth. Subjects born in the middle of year (April-July) had the lowest longevity. Increasing longevity was observed with each successive birth-month in the second half of the year, with a peak longevity for births in December. To research of the mechanisms responsible for longevity programming, study of adult D. melanogaster DNA repair capacity after irradiation at the egg stage was carried out, using marker such as DNA strand breaks. Insects irradiated in low doses (0.50 and 0.75 Gy) had extended life span and increased stability to S1 nuclease treatment. The probable explanation of observed postponed effects might be the long-term modulation of certain (possibly repair) genes activity. We hypothesize that life-extending effects of different anti-aging treatments might be a consequence of their unspecific (hormetic) action, rather then specific (geroprotector) action on the some aging-related processes, and induction an "transcriptional reprogramming" may be a key mechanism of the longevity programming and artificial life extension.

The concepts of "anti-aging" and "anti-aging medicine" in particular are hotly debated now, both in the mass media and among some researchers. This paper represents an open discussion of anti-aging terms and related ideas by nine leading experts in the field of aging studies, and it describes in detail the arguments presented by both supporters and opponents of these concepts. Candid exchange of opinions makes it clear that more efforts are required before a consensus on these issues can be reached. The paper also presents evidence that the term "anti-aging" is routinely used now in scientific literature as a legitimate scientific term, including even the titles of publications in reputable scientific journals, written by established researchers.

Normal somatic cells have a finite replicative capacity. With each cell division, telomeres, the ends of linear chromosomes, progressively shorten until they reach a critical length, at which point the cells enter replicative senescence. Some cells maintain their telomeres by the action of the telomerase enzyme. Glia, particularly microglia, are the only adult cell type in the central nervous system (CNS) that exhibit a significant mitotic potential, and are thus susceptible to telomere shortening. Previous research in our laboratory has found that telomeres shorten in rat microglia with increasing time in vitro. Our current hypothesis is that telomeres shorten in rat brain in vivo with increasing age. Tissue samples of cerebellum and cortex were obtained from Sprague-Dawley rats of various ages. Genomic DNA and total protein was isolated from each sample for telomere length measurement via Southern blot analysis (up to 5 months) and telomerase activity measurement via TRAP analysis (up to 6 months), respectively. Telomere shortening occurs in vivo in both rat cerebellum and cortex from day 21 to approximately 5 months of age. Cortex samples possessed shorter telomeres than did cerebellum samples. The longest telomeres undergo the most dramatic shortening, while the shortest telomeres exhibit only slight attrition. Telomerase activity slowly increases from day 21 to approximately 6 months of age, with the cerebellum exhibiting higher activity than cortex in all instances. These results indicate that telomere shortening occurs in rat brain in vivo with increasing age, and that the low levels of telomerase activity present may be preferentially recruited to maintain the shortest telomeres while allowing the longer ones to shorten more rapidly. Since microglia are thought to be the only mature cells of the postnatal CNS undergoing appreciable cell division, we propose that the telomere shortening occurring in the adult rat brain with age can be largely attributed to microglial cell division. Our findings provide an impetus to further investigate the pattern of telomere length and telomerase activity that emerges with further aging in the rat brain.