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Phenoptosis Concept Essay

1060 words - 5 pages

In particular: a) species which show no aging (“animals with negligible senescence”) show the same telomerase activity at any age and have no cancer problem, as demonstrated by their constant mortality rate at any age; b) in our species, studied in wild conditions, the increase in age-related mortality is precedent to cancer-related deaths cases and it is impossible that defenses against cancer kill before cancer can develop; c) shortened telomeres, as a result of telomerase inactivity, cause dysfunctional telomere-induced instability and so the likelihood of cancer increases; d) in normal mice, telomerase expression delays aging but does not increase cancer risk.

Telomerase activation is ...view middle of the document...

For the photoreceptor cells (cones and rods), these cells are retina pigmented cells (RPC). Each day, every RPC, by phagocytosis, removes from roughly 50 photoreceptor cells, approximately 10% of the membranes having photopsin or rodhopsin molecules on them. These cells, which have a very high metabolic activity, show cell turnover and, when this turnover slows down, damaging substances such as A2E (a vitamin A-derived breakdown product) accumulates, cells of RPC layer rarefy and leave holes in the RPC layer. This results in the death of the photoreceptors served and the onset of symptoms of ARMD, beginning from the macula, which is the part of the retina with the greatest density of photoreceptors.
Just like photoreceptor cells (particular neurons without turnover) are dependent on other cells (particular gliocytes showing cell turnover), other neurons - as those of the Central Nervous System - depend on another type of gliocytes (microglia cells). As explanation for Alzheimer Disease (AD), the decline of turnover and functionality of microglia cells has been hypothesized. Microglia cells remove β-amyloid protein and it is proved that, in AD, there is inadequate removal and harmful accumulation of this protein. Patients likely affected by AD show telomeres that are significantly shorter than in apparently normal subjects. An age-related dysfunction of endothelial cells could be, at least in part, an explanation for AD, but “a cell senescence model might explain Alzheimer dementia without primary vascular involvement”. There is an association between Alzheimer disease or ARMD and unhealthy lifestyle, which reduces the number of endothelial progenitor cells as a likely consequence of a quicker cell turnover of endothelial cells. "Protective drugs" like statins, ACE-inhibitors and sartans, which contrast excessive cell turnover, are effective against AD.

Cures in accordance with the view that ARMD and AD are caused by the accumulation of damaging substances have been a big very expensive failure for pharmaceutical companies [83]. Although "the retina, with its high oxygen content and constant exposure to light, is particularly susceptible to oxidative damage", the meta-analysis of 12 studies “did not show that antioxidant supplements prevented early [ARMD]”. Drugs or vaccines against the formation of β-amyloid peptide have proven unsuccessful against AD. “Post-mortem...

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