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The science of ageing
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
The various theories of ageing mentioned earlier in this chapter are all examples of intrinsic ageing. These are factors that an individual can do little about as they are dictated by their underlying genetics and physiological parameters. Despite the power of genetics, intrinsic ageing is actually a lesser determinant of ageing than extrinsic factors and is supposed to contribute to only 10% of the overall appearances of ageing demonstrated in the skin.
The aging body
Published in Jennifer R. Sasser, Harry R. Moody, Gerontology, 2018
Jennifer R. Sasser, Harry R. Moody
One in four of you reading this book has a specific genetic time bomb that makes you three to ten times more susceptible to developing late-onset Alzheimer’s. The gene is known as the apolipoprotein E4 (ApoE4). If you inherit a single variant of ApoE4 from one parent, your Alzheimer’s risk triples. If you inherit a double dose from both parents, your risk rises by ten times. Since we don’t know the cause of Alzheimer’s Disease, and there is no cure, it’s understandable that many people don’t want to know if they are carrying the ApoE4 gene. But the genetic link raises important questions and has implications for biological research on genetics and aging.
Free Radicals Damage Cells
Published in Robert Fried, Lynn Nezin, Evidence-Based Proactive Nutrition to Slow Cellular Aging, 2017
The genetics of aging has made substantial strides, but it has been confined primarily to the study of animals. There really are differences in individual longevity. There are longevity genes but, as luck would have it, that knowledge does not help us to predict anything. A researcher from the Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, New Orleans, reports that these longevity genes (about 35 or so) encode a wide array of cellular functions, leading to the conclusion that there are also multiple mechanisms of aging.
Neuromodulators: an essential part of survival
Published in Journal of Neurogenetics, 2020
ILP signaling has long been associated with survival (see Kenyon, 2010; and references therein). The worm ILP receptor DAF-2, which is a receptor tyrosine kinase (Kimura, Tissenbaum, Liu, & Ruvkun, 1997), promotes reproductive growth and inhibits dauer arrest (Riddle, Swanson, & Albert, 1981). The downregulation of DAF-2 activity doubles C. elegans lifespan (Kenyon, Chang, Gensch, Rudner, & Tabtiang, 1993), a discovery that ushered the birth of a field—the genetics of aging. Like DAF-2 (Gems et al., 1998), at least some of the worm ILPs (Hobert, 2013; Li & Kim, 2008) have pleiotropic functions (Fernandes de Abreu et al., 2014), which might be a consequence of their ILP-to-ILP network organization, where one ILP regulates multiple ILPs (Fernandes de Abreu et al., 2014). Many of the ILP functions typify neuromodulator functions. For example, there are ILPs that sometimes behave like the DAF-2 receptor in one context and opposite from DAF-2 in another context (Fernandes de Abreu et al., 2014). The articles in this collection discuss the roles of ILPs in temperature-sensing (see Takeishi, Takagaki, & Kuhara, 2020), in context-dependent avoidance behaviors (see Cheon, Hwang, & Kim, 2020; Kim & Flavell, 2020), in neuroprotection (see Liang, McKinnon, & Rankin, 2020), the dauer program (see Yang et al., 2020), and longevity (see Kim et al., 2020).