Contribution of TMS and TMS-EEG to the Understanding of Mechanisms Underlying Physiological Brain Aging

Abstract

In the human brain, aging is characterized by progressive neuronal loss, leading to disruption of synapses and to a degree of failure in neurotransmission. However, there is increasing evidence to support the notion that the aged brain has a remarkable ability to reorganize itself, with the aim of preserving its physiological activity. It is important to develop objective markers able to characterize the biological processes underlying brain aging in the intact human, and to distinguish them from brain degeneration associated with many neurological diseases. Transcranial magnetic stimulation (TMS), coupled with electromyography or electroencephalography (EEG), is particularly suited to this aim, due to the functional nature of the information provided, and thanks to the ease with which it can be integrated with behavioral manipulation. In this review, we aimed to provide up to date information about the role of TMS and TMS-EEG in the investigation of brain aging. In particular, we focused on data about cortical excitability, connectivity and plasticity, obtained by using readouts such as motor evoked potentials and transcranial evoked potentials. Overall, findings in the literature support an important potential contribution of TMS to the understanding of the mechanisms underlying normal brain aging. Further studies are needed to expand the current body of information and to assess the applicability of TMS findings in the clinical setting.

Keywords: EEG; aging; connectivity; excitability; plasticity; transcranial magnetic stimulation.

Figure 1

Age-related changes in local motor circuits, wide-range networks and plasticity processes RMT: resting motor threshold; I/O curve: input-output curve; SICI: short-interval intracortical inhibition; ICF: intracortical facilitation; LICI: long-interval intracortical inhibition; SICF: short-interval intracortical facilitation; SAI: short-latency afferent inhibition; M1: primary motor cortex; TEP: transcranial evoked potential; SIHI: short-latency interhemispheric inhibition; LIHI: long-latency interhemispheric inhibition; cM1: contralateral M1; iM1: ipsilateral M1; ISP: ipsilateral silent period; PMd: dorsal premotor cortex; DLPFC: dorsolateral prefrontal cortex; PAS: paired-associative stimulation; iTBS: intermittent theta burst stimulation; cTBS: continuous theta burst stimulation; tACS: transcranial alternating current stimulation.