Calcium and the aging nervous system |
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| Authors: | G E Gibson C Peterson |
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| Affiliation: | 1. Programa de Pós-Graduação em Ciências Médicas, Universidade Federal do Rio Grande do Sul, Brazil;2. Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul, Brazil;3. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Brazil;4. Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul, Brazil;5. Departamento de Medicina Interna, Universidade Federal do Rio Grande do Sul, Brazil;6. Serviço de Neurologia, Hospital de Clínicas de Porto Alegre, Rio Grande do Sul, Brazil;7. Serviço de Genética Médica, Hospital de Clínicas de Porto Alegre, Rio Grande do Sul, Brazil;8. Laboratório de Identificação Genética, Hospital de Clínicas de Porto Alegre, Rio Grande do Sul, Brazil;9. Rede Neurogenética, Hospital de Clínicas de Porto Alegre, Rio Grande do Sul, Brazil;10. Setor de Neurologia Geral e Ataxias, Disciplina de Neurologia Clínica da UNIFESP - Escola Paulista de Medicina, Universidade Federal de São Paulo, Brazil;11. Departamento de Genética e Biologia Molecular, Universidade Federal do Estado do Rio de Janeiro, Brazil;12. Instituto Nacional de Genética Médica Populacional, Brazil;1. Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases and the Second Affiliated Hospital of Soochow University, Soochow University, Suzhou City, Jiangsu Province, China;2. The Institute of Neuroscience, Soochow University, Suzhou City, Jiangsu Province, China;3. Department of Neurology, Suzhou Kowloon Hospital, 118 Wansheng Street, Suzhou City, China;4. Department of Pharmacology, Emory University School of Medicine, Atlanta, GA, USA;1. Department of Physiology, Emory University, Atlanta, GA 30322, United States;2. Department of Psychiatry & Behavioral Sciences, Emory University, Atlanta, GA 30322, United States;1. Department of Biomedical Engineering, Sapporo Medical University School of Medicine, Sapporo, Japan;2. Department of Orthopaedic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan;3. Division of Orthopaedic Surgery, Saiseikai Otaru Hospital, Otaru, Japan;4. Department of Educational Development, Sapporo Medical University Center for Medical Education, Sapporo, Japan;1. Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA;2. Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA 92093, USA;3. Department of Neurosciences, University of California San Diego, La Jolla, CA 92093, USA;4. National Center for Microscopy and Imaging Research, University of California San Diego, La Jolla, CA, USA;5. Laboratorios de Investigación y Desarrollo, Universidad Peruana Cayetano Heredia, Lima 36, Peru;6. New Mexico Health Enhancement and Marathon Clinics Research Foundation, Albuquerque, NM 87122, USA;7. The Rady Children’s Hospital, San Diego, CA 92123, USA |
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| Abstract: | ![]()
Many aspects of calcium homeostasis change with aging. Numerous calcium compartments complicate studies of altered calcium regulation. However, age-related decreases in calcium permeation across membranes and mobilization from organelles may be a common fundamental change. Deficits in ion movements appear to lead to altered coupling of calcium-dependent biochemical and neurophysiological processes and may lead to pathological and behavioral changes. The calcium-associated changes during aging probably do not occur with equal intensity in all cell types or in different parts of the same cell. Thus, cells or compartments with a high proportion of calcium activated processes would be more sensitive to diminished calcium availability. These age-related changes may predispose the brain to the development of age-related neurological disorders. The effects of decreased ion movement may be further aggravated by an age-related decline in other calcium-dependent processes. Depression of some of these calcium-dependent functions appears physiologically significant, since increasing calcium availability ameliorates age-related deficits in neurotransmission and behavior. A better understanding of the interactions between calcium homeostasis and calcium-dependent processes during aging will likely help in the design of more effective therapeutic strategies. |
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