Senescence longevity

C. Finch. Longevity, senescence and the genome. University of Chicago Press, Chicago, 1990. 

Anti-glycating effects. It was shown in 1990 that camosine (50-100 mg/kg body weight) increases survival of rodents when it was administered to animals before sub-lethal dose of y-irradiation [5]. Kurella et al. [58] have found that under these conditions viability of haemopoietic stem cells is significantly increased and their colony forming activity is activated as well. These phenomena can be addressed to anti-radical protection of biomacromolecules by camosine, however camosine was additionally found to protect nuclear DNA from oxidative modification induced by hyperoxia, to preserve its native stmcture and to synchronize cell cycle in vitro [59]. Its addition to the medium where fibroblasts were cultivated increased the longevity of cell life and reversed the senescence features of the cells [60]. Moreover, camosine was demonstrated to increase stability of... 

Moriguchi T, Saito H, Nishiyama N. Aged garlic extract prolongs longevity and improves spatial memory deficit in senescence-accelerated mouse. Biol Pharm Bull 1996 19 305-307. 

Mountz JD, Wu J, Zhou T, Hsu H-C. Cell death and longevity implications of Pas-mediated apoptosis in T-cell senescence. Immunol Rev 1997 160 19-30. 

Finch, C. E. (1990). Longevity, Senescence and the Genome. Chicago, IL University of Chicago Press. 

Garlic extract used in many indigenous traditions to treat age-related memory loss, c ertain preparations documented to have anti-oxidative activity, controlled animal study showed immunomodulatory effect that may positively impact age-related changes in anti-body production and prolonged longevity. controlled animal study showed enhanced spatial learning and reduced age-related memory deficits in senescence-accelerated mice. 

Moriguchi, T. e( al Aged garlic exiraci prolongs longevity and Improves Spatial Memory Deficit in Senescence-accelerated Mouse, Biol. Pham Bulletin, 1996 /9(2), pp. 305- 307. 

SIRTl belongs to the mammalian sirtuin family of NAD -dependent histone deacetylases (HDAGs) [198, 199]. Targets known to be deacetylated by SIRTl include histone 4 (H4), NFkB, and p53 [198, 199]. Through its deacetylase activity, SIRTl is considered to control cellular metabolic homeostasis, and to play important roles in the regulation of gene expression, cell proliferation, differentiation, survival, and senescence [198, 199]. SERTl activation has been considered to play a crucial role in calorie-restriction-induced longevity in several species [200]. 

The number of diseases that affect the colon is much higher than those that affect other organs. Moreover, colonic diseases are not comparable to diseases that affect other organs, because they are caused by intestinal bacteria that damage colonic tissue directly. Intestinal barrier function also declines as a consequence of aging (Ma et al. 1992). This phenomenon means that induction of inflammation is caused by the invasion of inflammatory factors derived from food and intestinal bacteria. Therefore, 1 believe that inhibition of colonic senescence may promote longevity. 

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