Improving executive functioning and reducing the risk of Alzheimer's disease with music therapy: A narrative review of potential neural mechanisms

Abstract

The incidence of Alzheimer's disease (AD) and the concurrent cost of healthcare will increase as the population continues to age. Pharmaceutical interventions effectively manage symptoms of AD but carry side effects and ineffectively address underlying causes and disease prevention. Non-pharmaceutical interventions for AD, such as music training and therapy do not carry these side effects and can improve symptoms, and should therefore be explored as stand-alone or co-therapy for AD. In addition, music encapsulates modifiable lifestyle factors, such as cognitive stimulation, that have been shown to delay progression of and prevent AD. However, the neural mechanisms underpinning how music improves AD symptoms are not fully understood and whether music can target compensatory processes, activate neural networks, or even slow or prevent AD needs further research. Research suggests neural mechanism may involve stimulating brain areas to promote neurogenesis, dopaminergic rewards systems, and the default mode network (DMN). Alternatively, this review proposes that music improve symptoms of AD via the fronto-parietal control network (FPCN), the salience network (SN) and DMN, and neural compensation. This review will then present evidence for how music could activate the FPCN, SN, and DMN to improve their efficiency, organization, and cognitive functions they govern, protecting the brain from damage, slowing progression, and possibly preventing AD. Establishing how music improves symptoms of AD can lead to tailored music therapy protocols that target functional neural networks responsible for impaired executive functions common in AD.

Keywords: Alzheimer's disease; executive functioning; health intervention; music training and therapy; neural networks.

Figure 1.

(A) Typical activity of the increased FPCN and SN and decreased DMN during completion of executive functioning tasks. Fronto-Parietal Control Network (Green): DLPFC: dorsal lateral prefrontal cortex; MPC: medial prefrontal cortex; DMPFC: dorsal medial prefrontal cortex; Salience Network (Red): AC: anterior cingulate cortex; AI: anterior insula; VS: ventral striatum; AMYG: amygdala; MTL: medial temporal lobe; HYP: hypothalamus; LC: locus coeruleus; Default Mode Network (Purple): PCC: posterior cingulate cortex; TPJ: temporal parietal junction; IPL: inferior parietal lobule; P: precuneus. (B) Activity of the FPCN and SN and DMN during completion of executive functioning tasks in AD. The SN and FPCN do not increase activation, and DMN does not disengage, leading to impaired processing and performance of executive functioning tasks. (C) Proposed neural mechanisms of how music might improve executive functioning in AD. Increased SN activity occurs via the pre-supplementary motor area (SPMA), which may support FPCN function while DMN decreases, overall improving executive functioning.