Therapeutic effect of tempo in Mozart's "Sonata for two pianos" (K. 448) in patients with epilepsy: An electroencephalographic study.

BACKGROUND: Mozart's "Sonata for two pianos" (Köchel listing 448) has proven effective as music therapy for patients with epilepsy, but little is understood about the mechanism of which feature in it impacted therapeutic effect. This study explored whether tempo in that piece is important for its therapeutic effect. METHODS: We measured the effects of tempo in Mozart's sonata on clinical and electroencephalographic parameters of 147 patients with epilepsy who listened to the music at slow, original, or accelerated speed. As a control, patients listened to Haydn's Symphony no. 94 at original speed. RESULTS: Listening to Mozart's piece at original speed significantly reduced the number of interictal epileptic discharges. It decreased beta power in the frontal, parietal, and occipital regions, suggesting increased auditory attention and reduced visual attention. It also decreased functional connectivity among frontal, parietal, temporal, and occipital brain regions, also suggesting increased auditory attention and reduced visual attention. No such effects were observed after patients listened to the slow or fast version of Mozart's piece, or to Haydn's symphony at normal speed. CONCLUSIONS: These results suggest that Mozart's "Sonata for two pianos" may exert therapeutic effects by regulating attention when played at its original tempo, but not slower or faster. These findings may help guide the design and optimization of music therapy against epilepsy.

The BigBrainWarp toolbox for integration of BigBrain 3D histology with multimodal neuroimaging.

Neuroimaging stands to benefit from emerging ultrahigh-resolution 3D histological atlases of the human brain; the first of which is 'BigBrain'. Here, we review recent methodological advances for the integration of BigBrain with multi-modal neuroimaging and introduce a toolbox, 'BigBrainWarp', that combines these developments. The aim of BigBrainWarp is to simplify workflows and support the adoption of best practices. This is accomplished with a simple wrapper function that allows users to easily map data between BigBrain and standard MRI spaces. The function automatically pulls specialised transformation procedures, based on ongoing research from a wide collaborative network of researchers. Additionally, the toolbox improves accessibility of histological information through dissemination of ready-to-use cytoarchitectural features. Finally, we demonstrate the utility of BigBrainWarp with three tutorials and discuss the potential of the toolbox to support multi-scale investigations of brain organisation.

Epidemic spreading model to characterize misfolded proteins propagation in aging and associated neurodegenerative disorders.

Misfolded proteins (MP) are a key component in aging and associated neurodegenerative disorders. For example, misfolded Amyloid-ß (Aß) and tau proteins are two neuropathogenic hallmarks of Alzheimer's disease. Mechanisms underlying intra-brain MP propagation/deposition remain essentially uncharacterized. Here, is introduced an epidemic spreading model (ESM) for MP dynamics that considers propagation-like interactions between MP agents and the brain's clearance response across the structural connectome. The ESM reproduces advanced Aß deposition patterns in the human brain (explaining 46∼56% of the variance in regional Aß loads, in 733 subjects from the ADNI database). Furthermore, this model strongly supports a) the leading role of Aß clearance deficiency and early Aß onset age during Alzheimer's disease progression, b) that effective anatomical distance from Aß outbreak region explains regional Aß arrival time and Aß deposition likelihood, c) the multi-factorial impact of APOE e4 genotype, gender and educational level on lifetime intra-brain Aß propagation, and d) the modulatory impact of Aß propagation history on tau proteins concentrations, supporting the hypothesis of an interrelated pathway between Aß pathophysiology and tauopathy. To our knowledge, the ESM is the first computational model highlighting the direct link between structural brain networks, production/clearance of pathogenic proteins and associated intercellular transfer mechanisms, individual genetic/demographic properties and clinical states in health and disease. In sum, the proposed ESM constitutes a promising framework to clarify intra-brain region to region transference mechanisms associated with aging and neurodegenerative disorders.