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      Role of Helicobacter pylori infection in the manifestation of old age‐related diseases

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          Abstract

          Helicobacter pylori is one of the most prevalent infection worldwide. It affects individuals of different age groups. Elderly people tend to resist eradication treatment and worsening of infection can lead to several gastric and non‐gastric pathologies. Aging‐associated cellular and molecular alteration can increase the risk of other pathologies such as osteoporosis, Alzheimer's disease, Parkinson's disease, respiratory and renal dysfunction, and cancer in geriatric patients, more than other age groups. This review article highlights some of the most common old age diseases and the role of H. pylori infection as a risk factor to worsen the conditions, presented by the molecular evidences of these associations. These studies can help clinicians to understand the underlying pathogenesis of the disease and identify high‐risk patients, aiding clearer diagnosis and treatment.

          Abstract

          Helicobacter pylori is one of the most prevalent infection worldwide. It affects individuals of different age groups. Aging‐associated risk factors should be considered. Future studies, related to aging and H. pylori infection with extragastric disease can help to provide vivid evidences.

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          Most cited references103

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          The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates

          Geroscience, the new interdisciplinary field that aims to understand the relationship between aging and chronic age-related diseases (ARDs) and geriatric syndromes (GSs), is based on epidemiological evidence and experimental data that aging is the major risk factor for such pathologies and assumes that aging and ARDs/GSs share a common set of basic biological mechanisms. A consequence is that the primary target of medicine is to combat aging instead of any single ARD/GSs one by one, as favored by the fragmentation into hundreds of specialties and sub-specialties. If the same molecular and cellular mechanisms underpin both aging and ARDs/GSs, a major question emerges: which is the difference, if any, between aging and ARDs/GSs? The hypothesis that ARDs and GSs such as frailty can be conceptualized as accelerated aging will be discussed by analyzing in particular frailty, sarcopenia, chronic obstructive pulmonary disease, cancer, neurodegenerative diseases such as Alzheimer and Parkinson as well as Down syndrome as an example of progeroid syndrome. According to this integrated view, aging and ARDs/GSs become part of a continuum where precise boundaries do not exist and the two extremes are represented by centenarians, who largely avoided or postponed most ARDs/GSs and are characterized by decelerated aging, and patients who suffered one or more severe ARDs in their 60s, 70s, and 80s and show signs of accelerated aging, respectively. In between these two extremes, there is a continuum of intermediate trajectories representing a sort of gray area. Thus, clinically different, classical ARDs/GSs are, indeed, the result of peculiar combinations of alterations regarding the same, limited set of basic mechanisms shared with the aging process. Whether an individual will follow a trajectory of accelerated or decelerated aging will depend on his/her genetic background interacting lifelong with environmental and lifestyle factors. If ARDs and GSs are manifestations of accelerated aging, it is urgent to identify markers capable of distinguishing between biological and chronological age to identify subjects at higher risk of developing ARDs and GSs. To this aim, we propose the use of DNA methylation, N-glycans profiling, and gut microbiota composition to complement the available disease-specific markers.
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            Structural and Functional Changes With the Aging Kidney.

            Senescence or normal physiologic aging portrays the expected age-related changes in the kidney as compared to a disease that occurs in some but not all individuals. The microanatomical structural changes of the kidney with older age include a decreased number of functional glomeruli from an increased prevalence of nephrosclerosis (arteriosclerosis, glomerulosclerosis, and tubular atrophy with interstitial fibrosis), and to some extent, compensatory hypertrophy of remaining nephrons. Among the macroanatomical structural changes, older age associates with smaller cortical volume, larger medullary volume until middle age, and larger and more numerous kidney cysts. Among carefully screened healthy kidney donors, glomerular filtration rate (GFR) declines at a rate of 6.3 mL/min/1.73 m(2) per decade. There is reason to be concerned that the elderly are being misdiagnosed with CKD. Besides this expected kidney function decline, the lowest risk of mortality is at a GFR of ≥75 mL/min/1.73 m(2) for age <55 years but at a lower GFR of 45 to 104 mL/min/1.73 m(2) for age ≥65 years. Changes with normal aging are still of clinical significance. The elderly have less kidney functional reserve when they do actually develop CKD, and they are at higher risk for acute kidney injury.
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              Pathogenesis and Management of Sarcopenia.

              Sarcopenia represents a loss of muscle strength and mass in older individuals. Sarcopenia in the elderly has now become a major focus of research and public policy debate due to its impact on morbidity, mortality, and health care expenditure. Despite its clinical importance, sarcopenia remains under-recognized and poorly managed in routine clinical practice. This is, in part, due to a lack of available diagnostic testing and uniform diagnostic criteria. The management of sarcopenia is primarily focused on physical therapy for muscle strengthening and gait training. There are no pharmacologic agents for the treatment of sarcopenia.
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                Author and article information

                Contributors
                roham.m@iums.ac.ir
                Journal
                Mol Genet Genomic Med
                Mol Genet Genomic Med
                10.1002/(ISSN)2324-9269
                MGG3
                Molecular Genetics & Genomic Medicine
                John Wiley and Sons Inc. (Hoboken )
                2324-9269
                17 February 2020
                April 2020
                : 8
                : 4 ( doiID: 10.1002/mgg3.v8.4 )
                : e1157
                Affiliations
                [ 1 ] Department of Geriatric Medicine Ziaeian Hospital Tehran University of Medical Sciences Tehran Iran
                [ 2 ] Iran University of Medical Sciences Tehran Iran
                Author notes
                [*] [* ] Correspondence

                Maryam Roham, Infectious disease specialist, Antimicrobial‐Resistant Research Center, Iran University of Medical Sciences, Tehran, Iran.

                Email: roham.m@ 123456iums.ac.ir

                Author information
                https://orcid.org/0000-0003-2243-1912
                https://orcid.org/0000-0001-5406-709X
                Article
                MGG31157
                10.1002/mgg3.1157
                7196471
                32067423
                f4f22e75-c30a-44d5-b03c-3289c8f20d22
                © 2020 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 06 June 2019
                : 10 November 2019
                : 11 January 2020
                Page count
                Figures: 1, Tables: 0, Pages: 11, Words: 8467
                Categories
                Review Article
                Review Article
                Custom metadata
                2.0
                April 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.1 mode:remove_FC converted:03.05.2020

                aging-associated disease,elderly population,helicobacter pylori

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