Free intracellular calcium in aging and Alzheimer's disease
| Autor: | Henrike Hartmann, H. Forstl, Anne Eckert, K. Velbinger, Walter E. Müller |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Aging
chemistry.chemical_element Degeneration (medical) Disease Calcium Biology General Biochemistry Genetics and Molecular Biology Calcium in biology Mice History and Philosophy of Science Alzheimer Disease medicine Dementia Animals Humans Brain aging Calcium metabolism General Neuroscience Age Factors Brain medicine.disease Rats chemistry Intracellular calcium homeostasis Potassium Neuroscience |
| Zdroj: | Annals of the New York Academy of Sciences. 786 |
| ISSN: | 0077-8923 |
| Popis: | Brain cells of aged mice exhibit distinct alterations of [Ca2+]i regulation resulting in lower levels of [Ca2+]i after stimulation. These alterations are probably more related to disturbances of mechanisms regulating transmembraneous Ca2+ fluxes than to mechanisms of intracellular Ca2+ release and storage. Comparable although not identical disturbances of [Ca2+]i regulation are present in mouse, rat, and human lymphocytes. Accordingly, one is tempted to speculate that in the human brain similar alterations of [Ca2+]i regulation might be present in aging as found in the aged mouse and rat brain. Since the downregulation of [Ca2+]i levels in aged brain cells seems to be accompanied by an enhanced intracellular sensitivity for changes of [Ca2+]i, both divergent alterations might compensate each other under normal conditions. However, it seems quite conceivable that the ability of the Ca2+ signal transduction pathway to adopt to periods of over-or understimulation (e.g., hypoxia, stress) might be disturbed in the aging brain. One of those conditions of additional alterations of [Ca2+]i regulation might be AD. Although we did not see AD-specific changes of [Ca2+]i regulation per se, the effect of beta A4 on cellular [Ca2+]i regulation was significantly and specifically disturbed in AD. It is not unlikely that a small, but long lasting (years or even decades) alterations of cellular [Ca2+]i regulation by beta A4, which is a product of normal brain metabolism, might finally contribute to the severe neuronal damage seen during the disease. |
| Databáze: | OpenAIRE |
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