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      Theories of Aging and the Prevalence of Alzheimer's Disease

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          Abstract

          Objective

          Aging and AD are associated in some way, then it is reasonable to ask whether or not it is possible to age without AD inexorably appearing at any moment, depending on the period of life. Therefore, the goal of this review is to verify, in light of some aging theories, the prevalence of AD.

          Methods

          For the purpose of this manuscript, the indexers Alzheimer, aging, Alzheimer, and aging were considered; theories of aging were researched. The research was conducted using PubMed, Medline, Scopus, Elsevier, and Google Scholar.

          Results

          The most common subjects in the papers analyzed for this manuscript were aging and Alzheimer's disease. The association between Alzheimer and theories of aging seems inconclusive.

          Conclusions

          Accordingly, the general idea is that AD is associated with aging in such a way that almost all people will present this disease; however, it is plausible to consider that the increase in life expectancy will generate a high prevalence of AD. In a general sense, it seems that the theories of aging explain the origin of AD under superlative and catastrophic considerations and use more biomolecular data than social or behavioral data as the bases of analysis, which may be the problem.

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          Most cited references90

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          Primary age-related tauopathy (PART): a common pathology associated with human aging.

          We recommend a new term, "primary age-related tauopathy" (PART), to describe a pathology that is commonly observed in the brains of aged individuals. Many autopsy studies have reported brains with neurofibrillary tangles (NFTs) that are indistinguishable from those of Alzheimer's disease (AD), in the absence of amyloid (Aβ) plaques. For these "NFT+/Aβ-" brains, for which formal criteria for AD neuropathologic changes are not met, the NFTs are mostly restricted to structures in the medial temporal lobe, basal forebrain, brainstem, and olfactory areas (bulb and cortex). Symptoms in persons with PART usually range from normal to amnestic cognitive changes, with only a minority exhibiting profound impairment. Because cognitive impairment is often mild, existing clinicopathologic designations, such as "tangle-only dementia" and "tangle-predominant senile dementia", are imprecise and not appropriate for most subjects. PART is almost universally detectable at autopsy among elderly individuals, yet this pathological process cannot be specifically identified pre-mortem at the present time. Improved biomarkers and tau imaging may enable diagnosis of PART in clinical settings in the future. Indeed, recent studies have identified a common biomarker profile consisting of temporal lobe atrophy and tauopathy without evidence of Aβ accumulation. For both researchers and clinicians, a revised nomenclature will raise awareness of this extremely common pathologic change while providing a conceptual foundation for future studies. Prior reports that have elucidated features of the pathologic entity we refer to as PART are discussed, and working neuropathological diagnostic criteria are proposed.
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            Risk factors for Alzheimer's disease: a prospective analysis from the Canadian Study of Health and Aging.

            J. Lindsay (2002)
            A prospective analysis of risk factors for Alzheimer's disease was a major objective of the Canadian Study of Health and Aging, a nationwide, population-based study. Of 6,434 eligible subjects aged 65 years or older in 1991, 4,615 were alive in 1996 and participated in the follow-up study. All participants were cognitively normal in 1991 when they completed a risk factor questionnaire. Their cognitive status was reassessed 5 years later by using a similar two-phase procedure, including a screening interview, followed by a clinical examination when indicated. The analysis included 194 Alzheimer's disease cases and 3,894 cognitively normal controls. Increasing age, fewer years of education, and the apolipoprotein E epsilon4 allele were significantly associated with increased risk of Alzheimer's disease. Use of nonsteroidal anti-inflammatory drugs, wine consumption, coffee consumption, and regular physical activity were associated with a reduced risk of Alzheimer's disease. No statistically significant association was found for family history of dementia, sex, history of depression, estrogen replacement therapy, head trauma, antiperspirant or antacid use, smoking, high blood pressure, heart disease, or stroke. The protective associations warrant further study. In particular, regular physical activity could be an important component of a preventive strategy against Alzheimer's disease and many other conditions.
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              Working Memory and Executive Function Decline across Normal Aging, Mild Cognitive Impairment, and Alzheimer's Disease

              Alzheimer's disease (AD) is a progressive neurodegenerative disease marked by deficits in episodic memory, working memory (WM), and executive function. Examples of executive dysfunction in AD include poor selective and divided attention, failed inhibition of interfering stimuli, and poor manipulation skills. Although episodic deficits during disease progression have been widely studied and are the benchmark of a probable AD diagnosis, more recent research has investigated WM and executive function decline during mild cognitive impairment (MCI), also referred to as the preclinical stage of AD. MCI is a critical period during which cognitive restructuring and neuroplasticity such as compensation still occur; therefore, cognitive therapies could have a beneficial effect on decreasing the likelihood of AD progression during MCI. Monitoring performance on working memory and executive function tasks to track cognitive function may signal progression from normal cognition to MCI to AD. The present review tracks WM decline through normal aging, MCI, and AD to highlight the behavioral and neurological differences that distinguish these three stages in an effort to guide future research on MCI diagnosis, cognitive therapy, and AD prevention.
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                Author and article information

                Contributors
                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi
                2314-6133
                2314-6141
                2019
                16 June 2019
                : 2019
                : 9171424
                Affiliations
                1Laboratory of Physical Anthropology and Biomathematics, Department of Anatomy, Institute of Biomedical Science, Federal University of Alfenas, Alfenas, Brazil
                2Department of Physiology, School of Medicine and Pharmaceutical Sciences, System Emotional Science, University of Toyama, Toyama, Japan
                Author notes

                Academic Editor: Stavros Baloyannis

                Author information
                https://orcid.org/0000-0002-4417-7209
                Article
                10.1155/2019/9171424
                6601487
                31317043
                d6c27e1d-7106-4f71-ae4b-8766c9984764
                Copyright © 2019 Kaynara Trevisan et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 8 January 2019
                : 22 April 2019
                : 14 May 2019
                Categories
                Review Article

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