Although literature evidence suggests deficits in social and non-social cognition in patients with autistic spectrum disorder (ASD) and schizophrenia (SCZ), the difference in neural correlates of the impairments between the two disorders has not been elucidated. We examined brain function in response to a non-social cognition and a social cognition task using functional near-infrared spectroscopy (fNIRS) in 13 patients with ASD, 15 patients with SCZ, and 18 healthy subjects. We assessed the brain function of participants using a verbal fluency task and an emotional facial recognition task. The patients with ASD showed significantly reduced brain activation in the left frontotemporal area during both tasks compared to healthy subjects. The patients with ASD with larger score in ‘attention to detail’ in the autism spectrum quotient showed lower activation of the left frontotemporal area during the two tasks. The patients with SCZ showed significantly reduced activation, compared to healthy subjects, and greater activation, compared to patients with ASD, in the area during the verbal fluency task. The patients with SCZ with more severe symptoms had lower brain activation during the task in this area. Our results suggest that two distinct areas are involved in the distinctive brain pathophysiology relevant to cognitive processing in patients with ASD and SCZ.
Mutations in the gene encoding the microtubule-associated protein tau (MAPT) cause frontotemporal dementia and parkinsonism linked to chromosome 17. Clinical variability is seen not only among families with different mutations, but also among family members with the same mutation. We investigated a newly identified familial frontotemporal dementia and parkinsonism family. The disease was of early onset and was inherited as an autosomal dominant trait. Clinically, parkinsonism was the prominent and often early feature, and it preceded dementia. Three autopsied cases shared involvement predominantly in the frontal and temporal lobes and also in the subcortical nuclei, including substantia nigra, globus pallidus, and subthalamic nucleus, that microscopically consisted of neuronal loss, microvacuolation, and astrocytic fibrosis. Immunohistochemistry demonstrated neuropil threads, ballooned cells, and glial fibrillary tangles. Sequencing analysis of the MAPT gene showed an alteration in one allele, resulting in a P301S substitution. These findings suggest that the MAPT P301S mutation can cause pathologically subcortical-predominant, neuropil thread-rich, tau-containing lesions, which could result in consistent parkinsonism. Our study confirms the notion that the phenotype observed in affected individuals from P301S MAPT mutation families is heterogeneous and is broader than the phenotypes seen to date in affected family members carrying other MAPT mutations.
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