Metabolic Syndrome,Cognitive Impairment and the Role of Diet: A Narrative Review

Background: This narrative review presents the association between metabolic syndrome (MetS), along with its components, and cognition-related disorders, as well as the potential reversal role of diet against cognitive impairment by modulating MetS. Methods: An electronic research in Medline (Pubmed) and Scopus was conducted. Results: MetS and cognitive decline share common cardiometabolic pathways as MetS components can trigger cognitive impairment. On the other side, the risk factors for both MetS and cognitive impairment can be reduced by optimizing the nutritional intake. Clinical manifestations such as dyslipidemia, hypertension, diabetes and increased central body adiposity are nutrition-related risk factors present during the prodromal period before cognitive impairment. The Mediterranean dietary pattern stands among the most discussed predominantly plant-based diets in relation to cardiometabolic disorders that may prevent dementia, Alzheimer’s disease and other cognition-related disorders. In addition, accumulating evidence suggests that the consumption of specific dietary food groups as a part of the overall diet can improve cognitive outcomes, maybe due to their involvement in cardiometabolic paths. Conclusions: Early MetS detection may be helpful to prevent or delay cognitive decline. Moreover, this review highlights the importance of healthy nutritional habits to reverse such conditions and the urgency of early lifestyle interventions.     

Polygenic analysis suggests the involvement of calcium signaling in executive function in schizophrenia patients

European Archives of Psychiatry and Clinical Neuroscience - Cognitive deficits are increasingly recognized as a core dimension rather than a consequence of schizophrenia (SCZ). The previous...     

Baseline MRI atrophy predicts 2-year cognitive outcomes in early-onset Alzheimer’s disease

Journal of Neurology - MRI atrophy predicts cognitive status in AD. However, this relationship has not been investigated in early-onset AD (EOAD, < 65 years) patients...     

Ultrastructural changes in prostate cells during hormone-induced canine prostatic hyperplasia

Benign prostatic hyperplasia is a prevalent disease that has received relatively little attention in spite of its morbidity and remarkable social impact. There are few animal models of prostatic hyperplasia. The dog is the only species, along with humans, in which prostatic hyperplasia develops spontaneously and almost universally with age. The aim of the present study has been to compare the ultrastructural findings in a model of experimentally induced canine prostatic hyperplasia with those of the spontaneously developed changes in untreated dogs. An experimental group of 5 male beagle dogs were castrated and treated with combined steroids (3 weekly doses for over 30 weeks). Prostate samples were surgically obtained every 42 days (experimental stages 0 through 6). The control group consisted of 3 noncastrated dogs that were treated with vehicle and in which samples were taken only at stages 0, 1, 4, and 6. Changes in the control groups were similar but of lower intensity compared to those of the experimental groups. In luminal cells, crowding with papillary projections, prominent, branching microvilli, and abundant, often compartmentalized granules were observed. The most striking change was the previously unreported finding of caveolae in basal cells. They were mostly located in the basal aspect of basal cells and were more prominent in the experimental group and in advanced stages of treatment. These ultrastructural findings have not been previously reported in canine or human prostatic hyperplasia and merit further research. The model of experimentally induced canine prostatic hyperplasia provides an adequate setting for the understanding of this disease.     

Detection of abnormalities of PRV-1, TPO, and c-MPL genes detected by fluorescence in situ hybridization in essential thrombocythemia

No specific diagnostic markers have been described in essential thrombocythemia (ET). PRV-1 (polycythemia rubra vera-1), TPO (thrombopoietin), and c-MPL (myeloproliferative leukemia virus oncogene) genes are candidate ET molecular markers because of their implication in the pathogenesis of ET. We have studied the status of PRV-1, TPO, and c-MPL genes in 30 ET patients by a fluorescence in situ hybridization (FISH) technique using three noncommercial, locus-specific probes for PRV-1 (BAC RP11-160A19, located at 19q13.2), TPO (BAC RP11-45NP16, located at 3q27), and c-MPL (BAC RP11-297L5, located at 1p34). FISH study showed no PRV-1, TPO, and c-MPL cytogenetic abnormalities in any of the analyzed cases. Our results suggest a lack of structural and numerical rearrangements (deletions, translocations, or amplifications) of PRV-1, TPO, and c-MPL genes in ET patients.     

Fast in silico assessment of physical stress for peripheral nerves

The level of physical stress rules the adaptative response of peripheral nerves, which is crucial to assess their physiological and pathological states. To this aim, in this work, different computational approaches were presented to model the stress response of in vitro peripheral nerves undergoing longitudinal stretch. More specifically, the effects of geometrical simplifications were studied with respect to the amount of computational time needed to obtain relevant information. Similarly, the variation of compressibility of the peripheral nervous tissue was investigated with respect to the variation of longitudinal stress and transversal stretch variations, and with reference to the computational time needed for simulations. Finally, the effect of small dimensional changes was investigated to better understand whether the variation of time was only due to the amount of nodes or elements. In conclusion, since fast in silico models, able to assess the nerve stress, could be a strategic advantage in case of time constraints or on-line evaluation (e.g., surgical interventions), a synergistic use of these approaches was proposed as a possible strategy to decrease the computational time needed for simulations from minutes to seconds.

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Graphical Abstract A synergistic approach involving both symmetry and tuning ofcompressibility allows the computational time to be considerably decreased

     

Characterization of new arylsulfatase A gene mutations reinforces genotype‐phenotype correlation in metachromatic leukodystrophy

Metachromatic Leukodystrophy (MLD) is a rare inherited lysosomal storage disorder caused by the deficiency of Arylsulfatase A (ARSA). The disease manifests itself with a broad spectrum of clinical variants, all characterized by progressive neurodegeneration in the central and peripheral nervous systems. The correlation between mutations in the ARSA gene, residual enzymatic activity associated with the mutated alleles and patients' phenotype, which has been extensively drawn for common ARSA mutations, has recently been expanded to rare ones. In this context, functional studies on the rare allelic variances acquire particular relevance for patients' prognostic evaluation. Here we have characterized eight newly identified ARSA mutations, through lentiviral vector‐based expression studies on cell lines and ARSA defective murine fibroblasts. In each case, the residual activity associated with the new mutant allele correlates well with the patient's phenotype. Therefore, our results confirm the importance of functional characterization of mutant alleles for a precise genotype‐based classification and definition of prognosis in MLD patients, which is particularly relevant for pre‐symptomatic diagnosis. © 2009 Wiley‐Liss, Inc.     

Morbidity and mortality of very low birth weight multiples compared with singletons

Background: Previous studies comparing the neonatal outcome of very low birth weight (VLBW) multiples and singletons have suggested a worse outcome for multiples at gestational ages on the limits of viability.

Objectives: The objective of this study is to determine the neonatal mortality and morbidity of VLBW multiples compared to singletons.

Methods: This is a retrospective study including all infants registered in the Spanish network for infants under 1500?g (SEN1500), over a 12-year period (from 2002 to 2013). Mortality and major morbidities were compared between singletons and multiples.

Results: About 32,770 infants were included: 21,123 singletons (64.5%) and 11,647 multiples (35.5%), with a mean gestational age of 29.5 weeks (22–38), and mean birth weight of 1115?g (340–1500). When adjusted by other perinatal factors, multiple pregnancy has a significantly higher risk of mortality than singleton pregnancy (odds ratio (OR) 1.15; IC 95% 1.05–1.26, p?=?.002), but not a higher risk of major morbidity or composite adverse outcome. In the subgroup of infants born before 26 weeks, multiples showed a higher risk of mortality (63.9% versus 51%, OR 1.7; 95% CI 1.47–1.96) and a higher risk of composite adverse outcome (88.9% versus 81.5%, OR 1.82, 95% CI 1.28–2.24).

Conclusions: In preterm infants born with less than 1500?g, multiple pregnancy is a prognostic factor that can slightly increase mortality. Extremely preterm infants born before 26 weeks have a greater risk of mortality and major morbidity if they come from a multiple pregnancy.