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Lipidomic Insight into Membrane Remodeling in Aging and Neurodegenerative Diseases
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
As given in Figure 7.1, the hallmarks of aging involve genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, deregulated nutrient sensing, loss of proteostasis, cellular senescence, stem cell exhaustion, and altered intercellular communication. These alterations are also identified as the main factors leading to neurodegenerative diseases.
Mitochondrial Dysfunction in the Pathophysiology of Alzheimer’s Disease
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Mitochondrial dysfunction and impairment of the ubiquitin proteasome system (UPS) are two hallmarks of aging and both are implicated in AD [151,152]. Mitochondrial proteins are a substantial part of proteins that are tagged with ubiquitin. Initial studies of ubiquitin-conjugated proteomes identified several mitochondrial proteins in yeast and mammals as ubiquitination substrates and constituting up to 38% of all cellular ubiquitin conjugates [153,154]. Aβ accumulation induces both the UPRmt and mitophagy in a strikingly conserved manner from C. elegans to humans. It has been shown that boosting mitochondrial function and proteostasis may decrease the formation of detrimental protein aggregates suggesting that enhancing mitochondrial proteostasis may abrogate the Aβ proteotoxicity in AD [155].
Aging Epigenetics
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Vasily V. Ashapkin, Lyudmila I. Kutueva, Boris F. Vanyushin
Why we age has been a question of heated debate for a very long time. Now, it is quite clear that aging has multiple causes [1]. Nine hallmarks of aging proposed in a recent review are genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication [2]. Epigenetic systems control gene activity and thus, directly or indirectly, affect all other hallmarks. Once differentiated, every cell in metazoan organisms must “remember” its appropriate pattern of gene expression for the organism to survive and function normally. Studies of developmental biology have established a role for epigenetic systems in establishing and maintaining these differentiated states of cells. For quite a long time, the epigenome was thought of as a static entity; once a cell becomes differentiated and its genome is appropriately methylated and chromatin configured, no further changes in the epigenome are supposed to occur. Unexpectedly, multiple studies in the past few years have shown that, in fact, an epigenome is a dynamically regulated system involved in aging, or at least affected by it, and responsive to various external and internal factors.
Impact of occupational categories on the incidence of amyotrophic lateral sclerosis in Sardinia Island, Italy
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2023
Vincenzo Pierri, Giuseppe Borghero, Francesca Pili, Tommaso Ercoli, Angelo Fabio Gigante, Luigi Isaia Lecca, Rosario Vasta, Marcello Campagna, Adriano Chiò, Giovanni Defazio
The significant additive interaction between agricultural/breeding and older age raised the possibility that variation in the age of study populations have contributed to the variable results of previous controlled studies on agriculture in ALS. More importantly, the additive interaction between the two exposures may provide insights into the mechanism through which these exposures operate. Positive interaction indicates that the joint presence of the two exposures enhances their independent effect. This may reflect a causal relationship between the two factors or shared pathophysiological mechanisms. Indeed, several hallmarks of aging correlate with susceptibility to neurodegenerative disease (including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, deregulated nutrient sensing, stem cell exhaustion, and altered intercellular communication) and pesticides may contribute to some of these mechanisms.
Emerging therapeutic targets for osteoporosis
Published in Expert Opinion on Therapeutic Targets, 2020
Luigi Gennari, Daniela Merlotti, Alberto Falchetti, Cristina Eller Vainicher, Roberta Cosso, Iacopo Chiodini
Being osteoporosis an age-related disorder and because of the increase in life expectancy, the potential development of compounds that are able to slow-down the cellular and molecular mechanisms of aging has become imperative for bone research (revised by [155]). A relevant article proposed the following major mechanisms as the hallmarks of aging in most, if not all tissues: 1) genomic instability, 2) telomere attrition, 3) epigenetic alterations, 4) loss of proteostasis, 5) deregulated nutrient sensing, 6) mitochondrial dysfunction, 7) cellular senescence, 8) stem cell exhaustion, and 9) altered intercellular communication [156]. Indeed, advances in the bone field have strongly suggested that most, if not all those hallmarks, are also manifested in aged bone [157–159]. Thus, a major challenge in the coming years will be to dissect the interconnectedness between these hallmarks and their relative contribution to skeletal aging, with the final goal of identifying pharmaceutical targets to improve skeletal and possibly general health, with minimal side effects.
Is anti-ageing drug discovery becoming a reality?
Published in Expert Opinion on Drug Discovery, 2020
Aging is also the gradual accumulation of cellular and tissue damage. There are several universal hallmarks of aging including [16]: DNA damage, ROS-induced lesions, mitochondrial dysfunction, epigenetic changes, proteostasis impairment, stem cell exhaustion and immunosenescence. The cell and the body delay damage accumulation in several ways: a) by preventing lesions, b) by repairing it or c) by removing and replacin unrepairable structures. Aging is primarily the dysregulation of these systems aimed at preventing, repairing and regenerating. Therefore, potential geroprotectors can be divided into subclasses according to these aging-preserving mechanisms. The same compound can affect several mechanisms. Potential anti-aging therapies may be based on completely different approaches that could be combined. Many of the approaches mentioned above are unattainable in the state of the art, but some of them are potentially available.