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      The relationship between stress and Alzheimer's disease

      review-article
      Neurobiology of Stress
      Elsevier
      Alzheimer's disease, Stress, Cortisol, Corticosteroids, CRF, CRH

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          Abstract

          Stress is critically involved in the development and progression of disease. From the stress of undergoing treatments to facing your own mortality, the physiological processes that stress drives have a serious detrimental effect on the ability to heal, cope and maintain a positive quality of life. This is becoming increasingly clear in the case of neurodegenerative diseases. Neurodegenerative diseases involve the devastating loss of cognitive and motor function which is stressful in itself, but can also disrupt neural circuits that mediate stress responses. Disrupting these circuits produces aberrant emotional and aggressive behavior that causes long-term care to be especially difficult. In addition, added stress drives progression of the disease and can exacerbate symptoms. In this review, I describe how neural and endocrine pathways activated by stress interact with ongoing neurodegenerative disease from both a clinical and experimental perspective.

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          Most cited references130

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          Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice.

          Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer beta-amyloid (Abeta) precursor protein containing a Lys670 --> Asn, Met671 --> Leu mutation had normal learning and memory in spatial reference and alternation tasks at 3 months of age but showed impairment by 9 to 10 months of age. A fivefold increase in Abeta(1-40) and a 14-fold increase in Abeta(1-42/43) accompanied the appearance of these behavioral deficits. Numerous Abeta plaques that stained with Congo red dye were present in cortical and limbic structures of mice with elevated amounts of Abeta. The correlative appearance of behavioral, biochemical, and pathological abnormalities reminiscent of Alzheimer's disease in these transgenic mice suggests new opportunities for exploring the pathophysiology and neurobiology of this disease.
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            Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases.

            A range of human degenerative conditions, including Alzheimer's disease, light-chain amyloidosis and the spongiform encephalopathies, is associated with the deposition in tissue of proteinaceous aggregates known as amyloid fibrils or plaques. It has been shown previously that fibrillar aggregates that are closely similar to those associated with clinical amyloidoses can be formed in vitro from proteins not connected with these diseases, including the SH3 domain from bovine phosphatidyl-inositol-3'-kinase and the amino-terminal domain of the Escherichia coli HypF protein. Here we show that species formed early in the aggregation of these non-disease-associated proteins can be inherently highly cytotoxic. This finding provides added evidence that avoidance of protein aggregation is crucial for the preservation of biological function and suggests common features in the origins of this family of protein deposition diseases.
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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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                Author and article information

                Contributors
                Journal
                Neurobiol Stress
                Neurobiol Stress
                Neurobiology of Stress
                Elsevier
                2352-2895
                21 April 2018
                February 2018
                21 April 2018
                : 8
                : 127-133
                Affiliations
                [1]Institute of Molecular Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA
                Author notes
                []Institute of Molecular Medicine, University of Texas Health Sciences Center, 1825 Pressler Street, Houston, TX, 77030. USA. Nicholas.J.Justice@ 123456uth.tmc.edu
                Article
                S2352-2895(18)30003-1
                10.1016/j.ynstr.2018.04.002
                5991350
                29888308
                d37ec637-fa73-4b31-8965-cfb4174de168
                © 2018 The Author

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 11 January 2018
                : 3 April 2018
                : 19 April 2018
                Categories
                Article from the Special Issue on "Stress and the Pathogenesis of Alzheimer’s Disease"; Edited by Hongxin Dong, John Csernansky

                alzheimer's disease,stress,cortisol,corticosteroids,crf,crh
                alzheimer's disease, stress, cortisol, corticosteroids, crf, crh

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