Neurodegeneration has multiscalar impacts, including behavioral, neuroanatomical, and neurofunctional disruptions. Can disease-differential alterations be captured across such dimensions using naturalistic stimuli? To address this question, we assessed comprehension of four naturalistic stories, highlighting action, nonaction, social, and nonsocial events, in Parkinson’s disease (PD) and behavioral variant frontotemporal dementia (bvFTD) relative to Alzheimer’s disease patients and healthy controls. Text-specific correlates were evaluated via voxel-based morphometry, spatial (fMRI), and temporal (hd-EEG) functional connectivity. PD patients presented action–text deficits related to the volume of action–observation regions, connectivity across motor-related and multimodal-semantic hubs, and frontal hd-EEG hypoconnectivity. BvFTD patients exhibited social–text deficits, associated with atrophy and spatial connectivity patterns along social-network hubs, alongside right frontotemporal hd-EEG hypoconnectivity. Alzheimer’s disease patients showed impairments in all stories, widespread atrophy and spatial connectivity patterns, and heightened occipitotemporal hd-EEG connectivity. Our framework revealed disease-specific signatures across behavioral, neuroanatomical, and neurofunctional dimensions, highlighting the sensitivity and specificity of a single naturalistic task. This investigation opens a translational agenda combining ecological approaches and multimodal cognitive neuroscience for the study of neurodegeneration.
Introduction: Visual manifestations are the most prominent non-painful features of migraine. During the last decades, visual area V3a has gathered attention of headache scientists because of its apparent implication on aura initiation, photophobia and cortical hyper-responsiveness related to visual motion perception. In this hypothesis-generating study, we performed an in silico analysis of gene expression in left V3a and the cerebral gyrus that harbours it (left superior occipital gyrus (lSOG)) searching for transcriptomic patterns that could be linked with migraine’s pathophysiology. Materials and methods: Neurotransmitter receptor gene expression levels in left V3a were extracted from validated brain mRNA expression models using a probabilistic volumetric mask of this region. The primary visual cortex and other sensory cortices (auditory, olfactory and somatosensory) were used as comparators. Genome-wide transcriptomic differences between the gyrus harbouring left V3a (lSOG) and the rest of the cerebral cortex were assessed using the Allen Brain Institute Human RNA micro array atlas/database. Results: Adrenergic receptor β1, dopaminergic receptor D3 and serotoninergic receptors 1B, 1F and 2A, which have been previously implicated in migraine’s pathophysiology and/or treatment, showed significantly higher expression levels on left V3a. Transcriptomic differences between the lSOG harbouring V3a and the rest of the cortex comprise genes whose products are involved in neuronal excitability (SLC17A6, KCNS1, KCNG1 and GABRQ), activation of multiple signal transduction pathways (MET) and cell metabolism (SPHKAP via its interaction with cAMP-dependent protein kinase). Conclusions: Focal gene expression analysis of V3a suggests some clues about its implication in migraine. Further studies are warranted.
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