Diabetic Choroidopathy: a Review of the Current Literature

Diabetic retinopathy is an increasingly prevalent disease, and a leading contributor to the burden of all-cause blindness worldwide. In addition to retinal changes, choroidal abnormalities are common in patients with diabetes. The first studies concerning this vascular structure were based on histologic, indocyanine angiography and laser Doppler flowmetry techniques, but the development of new optical coherence tomography (OCT) technologies and imaging software for enhanced depth imaging (EDI)-OCT in recent years has made it possible to provide more detailed images of the choroidal anatomy and topography.In diabetic patients, several choroidal changes have been described in the literature throughout the years; the recent focus is choroidal thickness, which is significantly different from that in healthy patients. However, understanding choroidal manifestations of diabetic eye disease remains a real challenge, and this gap is hindering efforts towards better defining choroidal evaluation as a predictive factor for disease evolution and treatment response.This review aims to summarize the recent literature concerning changes in choroidal structure in diabetic patients, the relationship to diabetic retinal disease progression, and finally, the current and potential application of the measurement of variations in choroidal thickness for patient management.info:eu-repo/semantics/publishedVersio

Downbeat Nystagmus in Episodic Ataxia Type 1 Associated with a Novel KCNA1 Mutation

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Influence of Weather on Seizure Frequency - Clinical Experience in the Emergency Room of a Tertiary Hospital

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Automatic Choroid Layer Segmentation from Optical Coherence Tomography Images Using Deep Learning

The choroid layer is a vascular layer in human retina and its main function is to provide oxygen and support to the retina. Various studies have shown that the thickness of the choroid layer is correlated with the diagnosis of several ophthalmic diseases. For example, diabetic macular edema (DME) is a leading cause of vision loss in patients with diabetes. Despite contemporary advances, automatic segmentation of the choroid layer remains a challenging task due to low contrast, inhomogeneous intensity, inconsistent texture and ambiguous boundaries between the choroid and sclera in Optical Coherence Tomography (OCT) images. The majority of currently implemented methods manually or semi-automatically segment out the region of interest. While many fully automatic methods exist in the context of choroid layer segmentation, more effective and accurate automatic methods are required in order to employ these methods in the clinical sector. This paper proposed and implemented an automatic method for choroid layer segmentation in OCT images using deep learning and a series of morphological operations. The aim of this research was to segment out Bruch’s Membrane (BM) and choroid layer to calculate the thickness map. BM was segmented using a series of morphological operations, whereas the choroid layer was segmented using a deep learning approach as more image statistics were required to segment accurately. Several evaluation metrics were used to test and compare the proposed method against other existing methodologies. Experimental results showed that the proposed method greatly reduced the error rate when compared with the other state-of-the art methods

Reward-Related Behavioral, Neurochemical and Electrophysiological Changes in a Rat Model of Autism Based on Prenatal Exposure to Valproic Acid

Prenatal exposure to the antiepileptic drug valproic acid (VPA) induces autism spectrum disorder (ASD) in humans and autistic-like behaviors in rodents, which makes it a good model to study the neural underpinnings of ASD. Rats prenatally exposed to VPA show profound deficits in the social domain. The altered social behavior displayed by VPA-exposed rats may be due to either a deficit in social reward processing or to a more general inability to properly understand and respond to social signals. To address this issue, we performed behavioral, electrophysiological and neurochemical experiments and tested the involvement of the brain reward system in the social dysfunctions displayed by rats prenatally exposed to VPA (500 mg/kg). We found that, compared to control animals, VPA-exposed rats showed reduced play responsiveness together with impaired sociability in the three-chamber test and altered social discrimination abilities. In addition, VPA-exposed rats showed altered expression of dopamine receptors together with inherent hyperexcitability of medium spiny neurons (MSNs) in the nucleus accumbens (NAc). However, when tested for socially-induced conditioned place preference, locomotor response to amphetamine and sucrose preference, control and VPA-exposed rats performed similarly, indicating normal responses to social, drug and food rewards. On the basis of the results obtained, we hypothesize that social dysfunctions displayed by VPA-exposed rats are more likely caused by alterations in cognitive aspects of the social interaction, such as the interpretation and reciprocation of social stimuli and/or the ability to adjust the social behavior of the individual to the changing circumstances in the social and physical environment, rather than to inability to enjoy the pleasurable aspects of the social interaction. The observed neurochemical and electrophysiological alterations in the NAc may contribute to the inability of VPA-exposed rats to process and respond to social cues, or, alternatively, represent a compensatory mechanism towards VPA-induced neurodevelopmental insults

Involvement of phosphodiesterase 2A activity in the pathophysiology of fragile X syndrome

The fragile X mental retardation protein (FMRP) is an RNA-binding protein involved in translational regulation of mRNAs that play key roles in synaptic morphology and plasticity. The functional absence of FMRP causes the fragile X syndrome (FXS), the most common form of inherited intellectual disability and the most common monogenic cause of autism. No effective treatment is available for FXS. We recently identified the Phosphodiesterase 2A (Pde2a) mRNA as a prominent target of FMRP. PDE2A enzymatic activity is increased in the brain of Fmr1-KO mice, a recognized model of FXS, leading to decreased levels of cAMP and cGMP. Here, we pharmacologically inhibited PDE2A in Fmr1-KO mice and observed a rescue both of the maturity of dendritic spines and of the exaggerated hippocampal mGluR-dependent long-term depression. Remarkably, PDE2A blockade rescued the social and communicative deficits of both mouse and rat Fmr1-KO animals. Importantly, chronic inhibition of PDE2A in newborn Fmr1-KO mice followed by a washout interval, resulted in the rescue of the altered social behavior observed in adolescent mice. Altogether, these results reveal the key role of PDE2A in the physiopathology of FXS and suggest that its pharmacological inhibition represents a novel therapeutic approach for FXS