Brain Stimulation (Nov 2020)

Age-related differences of motor cortex plasticity in adults: A transcranial direct current stimulation study

  • Ensiyeh Ghasemian-Shirvan,
  • Leila Farnad,
  • Mohsen Mosayebi-Samani,
  • Stefanie Verstraelen,
  • Raf L.J. Meesen,
  • Min-Fang Kuo,
  • Michael A. Nitsche

Journal volume & issue
Vol. 13, no. 6
pp. 1588 – 1599

Abstract

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Background: Cognitive, and motor performance are reduced in aging, especially with respect to acquisition of new knowledge, which is associated with a neural plasticity decline. Animal models show a reduction of long-term potentiation, but not long-term depression, in higher age. Findings in humans are more heterogeneous, with some studies showing respective deficits, but others not, or mixed results, for plasticity induced by non-invasive brain stimulation. One reason for these heterogeneous results might be the inclusion of different age ranges in these studies. In addition, a systematic detailed comparison of the age-dependency of neural plasticity in humans is lacking so far. Objective: We aimed to explore age-dependent plasticity alterations in adults systematically by discerning between younger and older participants in our study. Methods: We recruited three different age groups (Young: 18–30, Pre-Elderly: 50–65, and Elderly: 66–80 years). Anodal, cathodal, or sham transcranial direct current stimulation (tDCS) was applied over the primary motor cortex with 1 mA for 15 min to induce neuroplasticity. Cortical excitability was monitored by single-pulse transcranial magnetic stimulation as an index of plasticity. Results: For anodal tDCS, the results show a significant excitability enhancement, as compared to sham stimulation, for both, Young and the Pre-Elderly groups, while no LTP-like plasticity was obtained in the Elderly group by the applied stimulation protocol. Cathodal tDCS induced significant excitability-diminishing plasticity in all age groups. Conclusion: Our study provides further insight in age-related differences of plasticity in healthy humans, which are similar to those obtained in animal models. The decline of LTP-like plasticity in higher age could contribute to cognitive deficits observed in aging.

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