Astrocytes are the most numerous cell type in the human brain and are involved in many essential physiological functions that keep the brain homeostasis, among them the clearance of the Amyloid-β peptide that accumulates in brains with AD. In the case of AD, astrocyte senescence is claimed to be an important contributor to the development of the pathology. AD is an example of inflammaging disease, other cases are atherosclerosis, osteoporosis and diabetes. SASP contributes to ‘inflamm-aging’ (the development of a systemic proinflammatory status with normal aging) which involves an increase of blood plasma levels of inflammatory cytokines like interleukin 6 (IL-6). Experimental evidences support that senescent cells accumulate in aging mammal tissues and have an altered phenotype, called SASP (senescence-associated secretory phenotype), that apparently contributes to several aging diseases including Alzheimer’s disease (AD). Moreover, the model allows some predictions that remain to be tested experimentally.Ĭellular senescence is an anti-tumor program that is triggered by different insults like telomere shortening, oxidative stress and oncogene activation. Perturbations of the model were performed through gene gain or loss of functions and compared with results concerning cultures of normal and mutant astrocytes showing agreement in most cases. The model produces four alternative stable states: proliferation, transient cycle arrest, apoptosis and senescence (and SASP) computed from its inputs representing DNA damages.
In this work, we propose a discrete logical model for astrocyte senescence determined by the level of DNA damage (reparable or irreparable DNA strand breaks) where the kinase p38MAPK plays a central role in the regulation of senescence and SASP. These studies strongly involved the stress kinase p38MAPK in the regulation of the secretory phenotype of astrocytes, yet the molecular mechanisms underlying the onset of senescence and SASP activation remain unclear. Recent results have showed that markers of senescence in astrocytes from aged brains are increased in brains with Alzheimer’s disease. If you love ease and convenience, the best way to ensure you won't miss a Bed Bath & Beyond savings coupon is to sign up.Experimental evidence indicates that aging leads to accumulation of senescent cells in tissues and they develop a secretory phenotype (also known as SASP, for senescence-associated secretory phenotype) that can contribute to chronic inflammation and diseases. To access the offer when you're ready to use it, you can simply text "RESEND" any time before the offer expiration date, and then use it online or in any Bed Bath & Beyond store. Savvy shoppers appreciate the advantage of being a mobile offer subscriber: you'll always have deals at your fingertips, even when you don't have your postcard or email coupons handy.
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