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Related Experiment Videos

Cytosolic free calcium and cell spreading decrease in fibroblasts from aged and Alzheimer donors.

C Peterson, R R Ratan, M L Shelanski

    Proceedings of the National Academy of Sciences of the United States of America
    |October 1, 1986
    PubMed
    Summary

    Alzheimer disease and aging significantly reduce calcium levels in skin cells. This calcium deficit may be a key factor in Alzheimer disease pathology.

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    Area of Science:

    • Cell Biology
    • Neuroscience
    • Biochemistry

    Background:

    • Aging and Alzheimer disease are linked to disruptions in calcium homeostasis.
    • Cytosolic free calcium plays a critical role in cellular function.

    Purpose of the Study:

    • To investigate alterations in cytosolic free calcium concentration in skin fibroblasts from individuals with aging and Alzheimer disease.
    • To explore the functional consequences of altered calcium levels on fibroblast behavior.

    Main Methods:

    • Utilized calcium-sensitive fluorescent dyes quin-2 and fura-2 to measure cytosolic free calcium.
    • Employed cultured skin fibroblasts from aging, Alzheimer disease, and young adult donors.
    • Assessed fibroblast spreading behavior and response to calcium ionophore A23187.

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    Main Results:

    • Fibroblasts from Alzheimer disease donors exhibited a significant 70-81% reduction in cytosolic free calcium compared to controls.
    • This calcium reduction was not attributable to heavy metal quenching or altered intracellular pH.
    • Cells from aged and Alzheimer donors showed impaired spreading, partially reversible with calcium ionophore treatment.

    Conclusions:

    • Alzheimer disease is associated with profound alterations in cellular calcium homeostasis, extending beyond the brain.
    • Decreased cytosolic calcium in fibroblasts may be a significant pathophysiological factor in Alzheimer disease.
    • These findings support the view of Alzheimer disease as a systemic cellular disorder.