Neuroscience
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Dyslexia is an impairment of reading and spelling that affects both children and adults even after many years of schooling. Dyslexic readers have deficits in the integration of auditory and visual inputs but the neural mechanisms of the deficits are still unclear. This fMRI study examined the neural processing of auditorily presented German numbers 0-9 and videos of lip movements of a German native speaker voicing numbers 0-9 in unimodal (auditory or visual) and bimodal (always congruent) conditions in dyslexic readers and their matched fluent readers. ⋯ Importantly, such an enhancement effect was absent in dyslexic readers. Moreover, the auditory network (bilateral superior temporal regions plus medial PFC) was dynamically modulated during audiovisual integration in fluent, but not in dyslexic readers. These results suggest that superior temporal dysfunction may underly poor audiovisual speech integration in readers with dyslexia.
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G-protein-coupled receptors (GPCRs) are shown to be involved in Alzheimer's disease (AD) pathogenesis. However, because GPCRs include a large family of membrane receptors, it is unclear which specific GPCR or pathway with rational ligands can become effective therapeutic targets for AD. ⋯ Because amylin shares a similar secondary structure with amyloid-β peptide (Aβ), I propose that the AmR/GPCR pathway is disturbed by a large amount of Aβ in the AD brain, leading to tau phosphorylation, neuroinflammation and neuronal death in the pathological cascade. Amylin-type peptides, readily crossing the blood-brain barrier (BBB), are the rational ligands to enhance this GPCR pathway and may exhibit utility as novel therapeutic agents for treating AD.