Considering multiple etiological triggers, the age associated changes start up with Initiator trigger mechanisms subsequently followed by damaging the protective reactionary shielding mechanism, both the initiator and the reactionary set of molecular mechanisms regulate multiple pathways, leading to the terminal molecular mechanisms - the two most significant molecular pathways involved are – the final gateways which when lethally affected send the cell to the grave yard. The terminal End point mechanisms involve, Flawed intercellular crosstalks and Stem cell fatigue and resulting in phenotypic changes in the cell/tissue and organism.
FLAWED INTERCELLULAR CROSSTALKS:
As age advances in any organism, cell’s own capacity to divide, rejuvenate and repair tends to slow down resulting in gradual oxidative damage, in addition to the obvious decline in telomerase activity and the dysfunctioning of the nutrient sensing pathways. However beyond these changes which occur within the cell’s own internal …show more content…
Since NF-kB seems to have a major influence over the the inflammatory response in an organism, plenty of researches have shown that NF-kB to has a consistent and an active role with multiple inflammatory diseases such as Inflammatory bowel disease, Arthritis, Gastritis, Asthma, Atherosclerosis. Various researches clearly point towards the hyper functioning of NFkB in aged mice there by promoting excess of undesired inflammation on the tissue and organ systems. The role of NFkB inhibitors definitely influence aging as seen in experiments on mice skin, resulting in cell and tissue regeneration. The Genetic modulation, or drug based inhibition of NFkB has shown delay and reversal of age related changes in animal experiments.NF-κB recently has shown varied role in many central nervous system disorders specially were there is involvement of plasticity, learning, and
FLAWED INTERCELLULAR CROSSTALKS:
As age advances in any organism, cell’s own capacity to divide, rejuvenate and repair tends to slow down resulting in gradual oxidative damage, in addition to the obvious decline in telomerase activity and the dysfunctioning of the nutrient sensing pathways. However beyond these changes which occur within the cell’s own internal …show more content…
Since NF-kB seems to have a major influence over the the inflammatory response in an organism, plenty of researches have shown that NF-kB to has a consistent and an active role with multiple inflammatory diseases such as Inflammatory bowel disease, Arthritis, Gastritis, Asthma, Atherosclerosis. Various researches clearly point towards the hyper functioning of NFkB in aged mice there by promoting excess of undesired inflammation on the tissue and organ systems. The role of NFkB inhibitors definitely influence aging as seen in experiments on mice skin, resulting in cell and tissue regeneration. The Genetic modulation, or drug based inhibition of NFkB has shown delay and reversal of age related changes in animal experiments.NF-κB recently has shown varied role in many central nervous system disorders specially were there is involvement of plasticity, learning, and