Startseite Defective actin dynamics in dendritic spines: cause or consequence of age-induced cognitive decline?
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Defective actin dynamics in dendritic spines: cause or consequence of age-induced cognitive decline?

  • Till Georg Alexander Mack , Patricia Kreis und Britta Johanna Eickholt EMAIL logo
Veröffentlicht/Copyright: 8. Oktober 2015

Abstract

Ageing is a complex deteriorating process that coincides with changes in metabolism, replicative senescence, increased resistance to apoptosis, as well as progressive mitochondria dysfunction that lead to an increase production and accumulation of reactive oxygen species (ROS). Although controversy on the paradigm of the oxidative damage theory of ageing exists, persuasive studies in Caenorhabditis elegans and yeast have demonstrated that manipulation of ROS can modify the process of ageing and influences the damage of proteins, lipids and DNA. In neurons, ageing impacts on the intrinsic neuronal excitability, it decreases the size of neuronal soma and induces the loss of dendrites and dendritic spines. The actin cytoskeleton is an abundant and broadly expressed system that plays critical functions in many cellular processes ranging from cell motility to controlling cell shape and polarity. It is thus hardly surprising that the expression and the function of actin in neurons is crucial for the morphological changes that occur in the brain throughout life. We propose that alterations in actin filament dynamics in dendritic spines may be one of the key events contributing to the initial phases of ageing in the brain.


Corresponding author: Britta Johanna Eickholt, Institute of Biochemistry and Cluster of Excellence NeuroCure, Charité – Universitätsmedizin Berlin, Charitéplatz 1, D-10115 Berlin, Germany, e-mail:
aTill Georg Alexander Mack and Patricia Kreis: These authors contributed equally to this article.

Acknowledgments

We would like to thank Pirta Hotulainen for commenting on the review.

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Received: 2015-6-2
Accepted: 2015-9-27
Published Online: 2015-10-8
Published in Print: 2016-3-1

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