“…As a consequence, a series of “neural markers,” typical of DS, may be extrapolated (e.g., Brown et al, 2005 ; Neef et al, 2015 ). They can be summarized as (1) the hypoactivation of speech and the motor structures of the left hemisphere (e.g., Watkins et al, 2008 ; Chang et al, 2009 ; Desai et al, 2017 ; compare with Neef et al, 2015 ); (2) a larger hyperactivation of the homologous regions of the right hemisphere (e.g., Brown et al, 2005 ; Chang et al, 2009 ; compare with Neef et al, 2015 ); (3) the impaired/abnormal structure of a cortical gray matter and white matter , thus resulting in altered connectivity patterns, which are responsible for an unsuccessful neural communication (e.g., Sommer et al, 2002 ; Beal et al, 2007 ; Watkins et al, 2008 ; Chang et al, 2011 ); (4) an altered neural activity in cortico-basal-thalamo-cortical circuits (e.g., Wu et al, 1995 ; Giraud et al, 2008 ; Watkins et al, 2008 ; Chang and Guenther, 2020 ), also in relation to a “defective” dopaminergic regulation (e.g., Wu et al, 1997 ; Alm, 2004 ; compare with Alm, 2021 ; Turk et al, 2021 ); and (5) altered sensorimotor interactions in a neural level (e.g., audio–motor interactions, “sensory-to-motor” feedback/transformation, or “motor-to-sensory” projections) (e.g., Beal et al, 2010 , 2011 ; Cai et al, 2012 , 2014a ; Daliri and Max, 2015 ; Saltuklaroglu et al, 2017 ; Jenson et al, 2020 ), which may easily result in the alterations of the functional communication among the brain regions (e.g., Busan et al, 2019 ).…”