Being language a paradigm of structural and functional asymmetry in cognitive processing, the left Inferior Frontal Gyrus has been consistently related to speech production. In fact, it has been considered a key node in cortical networks responsible for different components of naming. However, isolating these components (e.g., lexical, syntactic, and phonological retrieval) in neuroimaging studies is difficult due to the use of different baselines and tasks. In the present study, functional activation and connectivity of the left inferior frontal gyrus was explored using functional magnetic resonance imaging. Participants performed a covert naming task (pressing a button based on a phonological characteristic). Two conditions were compared: drawings of objects and single letters (baseline condition). Differences in activation and functional connectivity were obtained for objects and letters in different areas of the left Inferior Frontal Gyrus. The pars triangularis was involved in the retrieval of lexical-phonological information, showing a pattern of connectivity with temporal areas in the search for the name of objects and with perisylvanian areas for letters. Selection of phonological information seems to involve the pars opercularis both to letters and objects but recruiting supramarginal and superior temporal areas to letters, probably related to orthographic-phonological conversion. The results support the notion of the left Inferior Frontal Gyrus as a buffer forwarding neural information across cortical networks responsible for different components of speech production.

Functional connectivity studies to detect neurophysiological correlates of amnestic mild cognitive impairment (aMCI), a prodromal stage of Alzheimer’s disease, have generated contradictory results in terms of compensation and deterioration, as most of the studies did not distinguish between the different aMCI subtypes: single-domain aMCI (sd-aMCI) and multiple-domain aMCI (md-aMCI). The present study aimed to characterize the neurophysiological correlates of aMCI subtypes by using resting-state functional magnetic resonance imaging. The study included sd-aMCI (n = 29), md-aMCI (n = 26), and control (n = 30) participants. The data were subjected to independent component analysis (ICA) to explore the default mode network (DMN) and the fronto-parietal control network (FPCN). Additionally, seed-based and moderation analyses were conducted to investigate the connectivity of the medial temporal lobe and functional networks. aMCI subtypes presented differences in functional connectivity relative to the control group: sd-aMCI participants displayed increased FPCN connectivity and reduced connectivity between the posterior parahippocampal gyrus (PHG) and medial structures; md-aMCI participants exhibited lower FPCN connectivity, higher anterior PHG connectivity with frontal structures and lower posterior PHG connectivity with central-parietal and temporo-occipital areas. Additionally, md-aMCI participants showed higher posterior PHG connectivity with structures of the DMN than both control and sd-aMCI participants, potentially indicating more severe cognitive deficits. The results showed gradual and qualitative neurofunctional differences between the aMCI subgroups, suggesting the existence of compensatory (sd-aMCI) and deterioration (md-aMCI) mechanisms in functional networks, mainly originated in the DMN. The findings support consideration of the subgroups as different stages of MCI within the Alzheimer disease continuum.

The aim of this study was to determine whether individuals with Subjective Cognitive Decline (SCD), particularly those with a neurostructural marker of risk for AD (SCD+), exhibit differences in the functional connectivity of the Default-Mode Network (DMN) relative to controls, as this network is known to be altered in the AD continuum. Cross-sectional study. Galicia, Northwest Spain. The sample compromised 133 participants: 69 controls, 51 SCD and 13 SCD+. Seed-to-voxel analysis was conducted using four DMN ROIs. Dynamic independent component analysis of the DMN was also performed. The SCD and SCD+ groups exhibited DMN hyperconnectivity, which was more extensive in the SCD+ group. Increased anti-correlations between DMN and task-positive parietal regions were related to poorer executive scores in SCD+ and a tendency for higher DMN recurrence in SCD+. Hippocampal atrophy as a SCD+ biomarker is associated with extensive DMN hyperconnectivity and increased anti-correlations between DMN and task-positive network regions.

Several recent studies have utilized neuroimaging to delineate the localization and function of brain regions involved in language. However, many uncertainties persist regarding the organization of the linguistic system in the human brain. The aim of the present study was to characterize the structural changes produced in a sample of 9 patients with post-stroke aphasia (4 women; mean age = 60 years, SD = 14.86) and their relationship with performance in the entire Boston Diagnostic Aphasia Examination (BDAE). Magnetic Resonance Imaging was acquired from the brain of each patient and brain lesions were assessed. Disconnection’s severity of each white matter tract by embedding the lesion into the streamline tractography atlas of the Human Connectome Project was analyzed, and grey matter lesion load using a 7-Network Cortical parcellation template was estimated, with additional subcortical, cerebellar and brainstem parcels. Finally, all data obtained was correlated with performance in the BDAE. Somatomotor network correlated with repetition scale. The disconnection of the left acoustic radiation and inferior longitudinal fasciculus correlated with repetition sub-scale. Finally, the left U-fibers correlated with severity (a BDAE sub-scale that assesses the patient’s communicative skills), conversational speech and reading sub-scales. These findings emphasized that the disconnection of these fronto-parieto-temporal structures correlate with deficits in repetition, beyond the classical hypothesis attributing such deficits solely to the impairment of the arcuate fasciculus.