Effects of cleft lip on visual scanning and neural processing of infant faces.

Infant faces readily capture adult attention and elicit enhanced neural processing, likely due to their importance evolutionarily in facilitating bonds with caregivers. Facial malformations have been shown to impact early infant-caregiver interactions negatively. However, it remains unclear how such facial malformations may impact early visual processing. The current study used a combination of eye tracking and electroencephalography (EEG) to investigate adults' early visual processing of infant faces with cleft lip/palate as compared to normal infant faces, as well as the impact cleft palate has on perceived cuteness. The results demonstrated a significant decrease in early visual attention to the eye region for infants with cleft palate, while increased visual attention is registered on the mouth region. Increased neural processing of the cleft palate was evident at the N170 and LPP, suggesting differences in configural processing and affective responses to the faces. Infants with cleft palate were also rated significantly less cute than their healthy counterparts (mean difference = .73, p < .001). These results suggest that infants' faces with cleft lip/palate are processed differently at early visual perception. These processing differences may contribute to several important aspects of development (e.g., joint attention) and may play a vital role in the previously observed difficulties in mother-infant interactions.

A Review of Compartmentalised Inflammation and Tertiary Lymphoid Structures in the Pathophysiology of Multiple Sclerosis.

Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system (CNS). The most common form of MS is a relapsing-remitting disease characterised by acute episodes of demyelination associated with the breakdown of the blood-brain barrier (BBB). In the relapsing-remitting phase there is often relative recovery (remission) from relapses characterised clinically by complete or partial resolution of neurological symptoms. In the later and progressive stages of the disease process, accrual of neurological disability occurs in a pathological process independent of acute episodes of demyelination and is accompanied by a trapped or compartmentalised inflammatory response, most notable in the connective tissue spaces of the vasculature and leptomeninges occurring behind an intact BBB. This review focuses on compartmentalised inflammation in MS and in particular, what we know about meningeal tertiary lymphoid structures (TLS; also called B cell follicles) which are organised clusters of immune cells, associated with more severe and progressive forms of MS. Meningeal inflammation and TLS could represent an important fluid or imaging marker of disease activity, whose therapeutic abrogation might be necessary to stop the most severe outcomes of disease.

CCN3 is dynamically regulated by treatment and disease state in multiple sclerosis.

BACKGROUND: Multiple sclerosis (MS) is an immune-mediated disease that damages myelin in the central nervous system (CNS). We investigated the profile of CCN3, a known regulator of immune function and a potential mediator of myelin regeneration, in multiple sclerosis in the context of disease state and disease-modifying treatment. METHODS: CCN3 expression was analysed in plasma, immune cells, CSF and brain tissue of MS patient groups and control subjects by ELISA, western blot, qPCR, histology and in situ hybridization. RESULTS: Plasma CCN3 levels were comparable between collective MS cohorts and controls but were significantly higher in progressive versus relapsing-remitting MS and between patients on interferon-ß versus natalizumab. Higher body mass index was associated with higher CCN3 levels in controls as reported previously, but this correlation was absent in MS patients. A significant positive correlation was found between CCN3 levels in matched plasma and CSF of MS patients which was absent in a comparator group of idiopathic intracranial hypertension patients. PBMCs and CD4+ T cells significantly upregulated CCN3 mRNA in MS patients versus controls. In the CNS, CCN3 was detected in neurons, astrocytes and blood vessels. Although overall levels of area immunoreactivity were comparable between non-affected, demyelinated and remyelinated tissue, the profile of expression varied dramatically. CONCLUSIONS: This investigation provides the first comprehensive profile of CCN3 expression in MS and provides rationale to determine if CCN3 contributes to neuroimmunological functions in the CNS.