Association of Micro RNA and Postoperative Cognitive Dysfunction: A Review

2020 ◽  
Vol 20 (17) ◽  
pp. 1781-1790
Author(s):  
Noor Anisah Abu Yazit ◽  
Norsham Juliana ◽  
Srijit Das ◽  
Nur Islami Mohd Fahmi Teng ◽  
Nadia Mohd Fahmy ◽  
...  
Keyword(s):  
Cognitive Dysfunction ◽  
Chromosomal Abnormalities ◽  
Current Knowledge ◽  
System Development ◽  
Genetic Disorder ◽  
Postoperative Cognitive Dysfunction ◽  
Clinical Importance ◽  
Nervous System Development ◽  
Micro Rna ◽  
A Genome

Postoperative Cognitive Dysfunction (POCD) refers to the condition of neurocognitive decline following surgery in a cognitive and sensory manner. There are several risk factors, which may be life-threatening for this condition. Neuropsychological assessment of this condition is very important. In the present review, we discuss the association of apolipoprotein epsilon 4 (APOE ε4) and few miRNAs with POCD, and highlight the clinical importance for prognosis, diagnosis and treatment of POCD. Microarray is a genome analysis that can be used to determine DNA abnormalities. This current technique is rapid, efficient and high-throughout. Microarray techniques are widely used to diagnose diseases, particularly in genetic disorder, chromosomal abnormalities, mutations, infectious diseases and disease-relevant biomarkers. MicroRNAs (miRNAs) are a class of non-coding RNAs that are widely found distributed in eukaryotes. Few miRNAs influence the nervous system development, and nerve damage repair. Microarray approach can be utilized to understand the miRNAs involved and their pathways in POCD development, unleashing their potential to be considered as a diagnostic marker for POCD. This paper summarizes and identifies the studies that use microarray based approaches for POCD analysis. Since the application of microarray in POCD is expanding, there is a need to review the current knowledge of this approach.

scholarly journals Neurons interact with the microbiome: an evolutionary-informed perspective

Neuroforum ◽  
2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Christoph Giez ◽  
Alexander Klimovich ◽  
Thomas C. G. Bosch
Keyword(s):  
Nervous System ◽  
Neural Circuits ◽  
Current Knowledge ◽  
System Development ◽  
Nervous System Development ◽  
Comprehensive Understanding ◽  
Strategic Model ◽  
Microbe Interactions ◽  
Host Microbe Interactions ◽  
And Function

Abstract Animals have evolved within the framework of microbes and are constantly exposed to diverse microbiota. Microbes colonize most, if not all, animal epithelia and influence the activity of many organs, including the nervous system. Therefore, any consideration on nervous system development and function in the absence of the recognition of microbes will be incomplete. Here, we review the current knowledge on the nervous systems of Hydra and its role in the host–microbiome communication. We show that recent advances in molecular and imaging methods are allowing a comprehensive understanding of the capacity of such a seemingly simple nervous system in the context of the metaorganism. We propose that the development, function and evolution of neural circuits must be considered in the context of host–microbe interactions and present Hydra as a strategic model system with great basic and translational relevance for neuroscience.

scholarly journals Genome-Wide Association Study of Postoperative Cognitive Dysfunction in Older Surgical Patients

2020 ◽  
Author(s):  
Marc Rickenbacher ◽  
Céline S Reinbold ◽  
Stefan Herms ◽  
Per Hoffmann ◽  
Sven Cichon ◽  
...  
Keyword(s):  
Association Study ◽  
Candidate Genes ◽  
Cognitive Dysfunction ◽  
Genome Wide Association Study ◽  
Postoperative Cognitive Dysfunction ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Genome Wide Association ◽  
Genome Wide ◽  
A Genome

Abstract Background: Postoperative cognitive dysfunction (POCD) is a common neurocognitive complication after surgery and anesthesia, particularly in elderly patients. Various studies have suggested genetic risk factors for POCD. The study aimed to detect genome-wide associations of POCD in older patients.Methods: In this prospective observational cohort study, participants aged ≥65 years completed a set of neuropsychological tests before, at 1 week, and 3 months after major noncardiac surgery. Test variables were converted into standard scores (z-scores) based on demographic characteristics. POCD was diagnosed if the decline was >1 standard deviation in ≥2 of the 15 variables in the assessment battery. A genome-wide association study (GWAS) was performed to determine potential alleles that are linked to the POCD phenotype. In addition, candidate genes for POCD were identified in a literature search for further analysis.Results: Sixty-three patients with blood samples were included in the study. POCD was diagnosed in 47.6% of patients at 1 week and in 34.2% of patients at 3 months after surgery. Insufficient sample quality led to exclusion of 26 patients. In the remaining 37 patients, a GWAS was performed, but no association (P < 5*10-8) with POCD was found. The subsequent gene set enrichment analysis of 34 candidate genes did not reveal any significant associations.Conclusion: In this patient cohort, a GWAS did not reveal an association between specific genetic alleles and POCD at 1 week and 3 months after surgery. Future genetic analysis should focus on specific candidate genes for POCD.Trial registration: ClinicalTrials.gov (NCT02864173)

scholarly journals Population-specific adaptation in malaria-endemic regions of asia

2021 ◽  
Author(s):  
Elena S. Gusareva ◽  
Paolo Alberto Lorenzini ◽  
Nurul Adilah Binte Ramli ◽  
Amit Gourav Ghosh ◽  
Hie Lim Kim
Keyword(s):  
System Development ◽  
Asian Population ◽  
Population Group ◽  
Nervous System Development ◽  
Evolutionary Mechanisms ◽  
Population Groups ◽  
Genome Wide ◽  
A Genome ◽  
Endemic Population ◽  
Mechanisms Of Adaptation

Evolutionary mechanisms of adaptation to malaria are understudied in Asian endemic regions despite a high prevalence of malaria in the region. In our research, we performed a genome-wide screening for footprints of natural selection against malaria by comparing eight Asian population groups from malaria-endemic regions with two non-endemic population groups from Europe and Mongolia. We identified 285 adaptive genes showing robust selection signals across three statistical methods, iHS, XP-EHH, and PBS. Interestingly, most of the identified genes (82%) were found to be under selection in a single population group, while adaptive genes shared across populations were rare. This is likely due to the independent adaptation history in different endemic populations. The gene ontology (GO) analysis for the 285 adaptive genes highlighted their functional processes linked to neuronal organizations or nervous system development. These genes could be related to cerebral malaria and may reduce the inflammatory response and the severity of malaria symptoms. Remarkably, our novel population genomic approach identified population-specific adaptive genes potentially against malaria infection without the need for patient samples or individual medical records.

scholarly journals TET1-DNA Hydroxymethylation Mediated Oligodendrocyte Homeostasis is Required for CNS Myelination and Remyelination

2019 ◽  
Author(s):  
Ming Zhang ◽  
Jian Wang ◽  
Kaixiang Zhang ◽  
Guozhen Lu ◽  
Keke Ren ◽  
...  
Keyword(s):  
Target Genes ◽  
Calcium Release ◽  
System Development ◽  
Nervous System Development ◽  
Oligodendrocyte Differentiation ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Dna Hydroxymethylation ◽  
Adult Mice ◽  
A Genome

AbstractTen-eleven translocation (TET) proteins, encoding dioxygenase for DNA hydroxymethylation, are important players in nervous system development and diseases. However, their role in oligodendrocyte homeostasis, myelination and remyelination remains elusive. Here, we detected a genome-wide and locus-specific DNA hydroxymethylation landscape shift during oligodendrocyte-progenitor (OPC) differentiation. Ablation of Tet1, but not Tet3, results in stage-dependent defects in oligodendrocyte development and myelination in the brain. The mice lacking Tet1 in the oligodendrocyte lineage develop schizophrenia-like behaviors. We further show that TET1 is also required for proper remyelination after demyelination injury in the adult mice. Transcriptomic and DNA hydroxymethylation profiling revealed a critical TET1-regulated epigenetic program for oligodendrocyte differentiation and identified a set of TET1-5hmC target genes associated with myelination, cell division, and calcium transport. Tet1-deficient OPCs exhibited reduced calcium activity in response to stimulus in culture. Moreover, deletion of a TET1-5hmC target gene, Itpr2, an oligodendrocyte-enriched intracellular calcium-release channel, significantly impaired the onset of oligodendrocyte differentiation. Together, our results suggest that stage-specific TET1-mediated epigenetic programming and oligodendrocyte homeostasis is required for proper myelination and repair.

scholarly journals Ten-eleven translocation 1 mediated-DNA hydroxymethylation is required for myelination and remyelination in the mouse brain

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ming Zhang ◽  
Jian Wang ◽  
Kaixiang Zhang ◽  
Guozhen Lu ◽  
Yuming Liu ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Intracellular Signaling ◽  
System Development ◽  
Nervous System Development ◽  
Oligodendrocyte Progenitor Cells ◽  
Calcium Activity ◽  
Dna Hydroxymethylation ◽  
Tet Proteins ◽  
A Genome

AbstractTen-eleven translocation (TET) proteins, the dioxygenase for DNA hydroxymethylation, are important players in nervous system development and diseases. However, their role in myelination and remyelination after injury remains elusive. Here, we identify a genome-wide and locus-specific DNA hydroxymethylation landscape shift during differentiation of oligodendrocyte-progenitor cells (OPC). Ablation of Tet1 results in stage-dependent defects in oligodendrocyte (OL) development and myelination in the mouse brain. The mice lacking Tet1 in the oligodendrocyte lineage develop behavioral deficiency. We also show that TET1 is required for remyelination in adulthood. Transcriptomic, genomic occupancy, and 5-hydroxymethylcytosine (5hmC) profiling reveal a critical TET1-regulated epigenetic program for oligodendrocyte differentiation that includes genes associated with myelination, cell division, and calcium transport. Tet1-deficient OPCs exhibit reduced calcium activity, increasing calcium activity rescues the differentiation defects in vitro. Deletion of a TET1-5hmC target gene, Itpr2, impairs the onset of OPC differentiation. Together, our results suggest that stage-specific TET1-mediated epigenetic programming and intracellular signaling are important for proper myelination and remyelination in mice.

scholarly journals SOX Transcription Factors as Important Regulators of Neuronal and Glial Differentiation During Nervous System Development and Adult Neurogenesis

2021 ◽  
Vol 14 ◽  
Author(s):  
Milena Stevanovic ◽  
Danijela Drakulic ◽  
Andrijana Lazic ◽  
Danijela Stanisavljevic Ninkovic ◽  
Marija Schwirtlich ◽  
...  
Keyword(s):  
Nervous System ◽  
Transcription Factors ◽  
Adult Neurogenesis ◽  
Current Knowledge ◽  
System Development ◽  
Nervous System Development ◽  
Glial Differentiation ◽  
Neural Lineage ◽  
Stage Of Development ◽  
Sox Proteins

The SOX proteins belong to the superfamily of transcription factors (TFs) that display properties of both classical TFs and architectural components of chromatin. Since the cloning of the Sox/SOX genes, remarkable progress has been made in illuminating their roles as key players in the regulation of multiple developmental and physiological processes. SOX TFs govern diverse cellular processes during development, such as maintaining the pluripotency of stem cells, cell proliferation, cell fate decisions/germ layer formation as well as terminal cell differentiation into tissues and organs. However, their roles are not limited to development since SOX proteins influence survival, regeneration, cell death and control homeostasis in adult tissues. This review summarized current knowledge of the roles of SOX proteins in control of central nervous system development. Some SOX TFs suspend neural progenitors in proliferative, stem-like state and prevent their differentiation. SOX proteins function as pioneer factors that occupy silenced target genes and keep them in a poised state for activation at subsequent stages of differentiation. At appropriate stage of development, SOX members that maintain stemness are down-regulated in cells that are competent to differentiate, while other SOX members take over their functions and govern the process of differentiation. Distinct SOX members determine down-stream processes of neuronal and glial differentiation. Thus, sequentially acting SOX TFs orchestrate neural lineage development defining neuronal and glial phenotypes. In line with their crucial roles in the nervous system development, deregulation of specific SOX proteins activities is associated with neurodevelopmental disorders (NDDs). The overview of the current knowledge about the link between SOX gene variants and NDDs is presented. We outline the roles of SOX TFs in adult neurogenesis and brain homeostasis and discuss whether impaired adult neurogenesis, detected in neurodegenerative diseases, could be associated with deregulation of SOX proteins activities. We present the current data regarding the interaction between SOX proteins and signaling pathways and microRNAs that play roles in nervous system development. Finally, future research directions that will improve the knowledge about distinct and various roles of SOX TFs in health and diseases are presented and discussed.

scholarly journals Conservation and Innovation: Versatile Roles for LRP4 in Nervous System Development

2021 ◽  
Vol 9 (1) ◽  
pp. 9
Author(s):  
Alison T. DePew ◽  
Timothy J. Mosca
Keyword(s):  
Nervous System ◽  
Cell Surface ◽  
Current Knowledge ◽  
System Development ◽  
Critical Role ◽  
Surface Protein ◽  
Nervous System Development ◽  
Cell Surface Receptor ◽  
Synaptic Development ◽  
Disease Etiology

As the nervous system develops, connections between neurons must form to enable efficient communication. This complex process of synaptic development requires the coordination of a series of intricate mechanisms between partner neurons to ensure pre- and postsynaptic differentiation. Many of these mechanisms employ transsynaptic signaling via essential secreted factors and cell surface receptors to promote each step of synaptic development. One such cell surface receptor, LRP4, has emerged as a synaptic organizer, playing a critical role in conveying extracellular signals to initiate diverse intracellular events during development. To date, LRP4 is largely known for its role in development of the mammalian neuromuscular junction, where it functions as a receptor for the synaptogenic signal Agrin to regulate synapse development. Recently however, LRP4 has emerged as a synapse organizer in the brain, where new functions for the protein continue to arise, adding further complexity to its already versatile roles. Additional findings indicate that LRP4 plays a role in disorders of the nervous system, including myasthenia gravis, amyotrophic lateral sclerosis, and Alzheimer’s disease, demonstrating the need for further study to understand disease etiology. This review will highlight our current knowledge of how LRP4 functions in the nervous system, focusing on the diverse developmental roles and different modes this essential cell surface protein uses to ensure the formation of robust synaptic connections.

scholarly journals The Role of Chondroitin Sulfate Proteoglycans in Nervous System Development

2020 ◽  
Vol 69 (1) ◽  
pp. 61-80 ◽  
Author(s):  
Caitlin P. Mencio ◽  
Rowan K. Hussein ◽  
Panpan Yu ◽  
Herbert M. Geller
Keyword(s):  
Nervous System ◽  
Chondroitin Sulfate ◽  
Neural Development ◽  
Synapse Formation ◽  
Current Knowledge ◽  
System Development ◽  
Nervous System Development ◽  
Chondroitin Sulfate Proteoglycans ◽  
Cell Proliferation And Differentiation

The orderly development of the nervous system is characterized by phases of cell proliferation and differentiation, neural migration, axonal outgrowth and synapse formation, and stabilization. Each of these processes is a result of the modulation of genetic programs by extracellular cues. In particular, chondroitin sulfate proteoglycans (CSPGs) have been found to be involved in almost every aspect of this well-orchestrated yet delicate process. The evidence of their involvement is complex, often contradictory, and lacking in mechanistic clarity; however, it remains obvious that CSPGs are key cogs in building a functional brain. This review focuses on current knowledge of the role of CSPGs in each of the major stages of neural development with emphasis on areas requiring further investigation:

scholarly journals Natural variation in the regulation of neurodevelopmental genes modifies flight performance in Drosophila

PLoS Genetics ◽  
2021 ◽  
Vol 17 (3) ◽  
pp. e1008887
Author(s):  
Adam N. Spierer ◽  
Jim A. Mossman ◽  
Samuel Pattillo Smith ◽  
Lorin Crawford ◽  
Sohini Ramachandran ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
System Development ◽  
Nervous System Development ◽  
Bmp Signaling ◽  
Flight Performance ◽  
Genetic Modifiers ◽  
Epistatic Interactions ◽  
Novel Approach ◽  
A Genome ◽  
And Function

The winged insects of the order Diptera are colloquially named for their most recognizable phenotype: flight. These insects rely on flight for a number of important life history traits, such as dispersal, foraging, and courtship. Despite the importance of flight, relatively little is known about the genetic architecture of flight performance. Accordingly, we sought to uncover the genetic modifiers of flight using a measure of flies’ reaction and response to an abrupt drop in a vertical flight column. We conducted a genome wide association study (GWAS) using 197 of the Drosophila Genetic Reference Panel (DGRP) lines, and identified a combination of additive and marginal variants, epistatic interactions, whole genes, and enrichment across interaction networks. Egfr, a highly pleiotropic developmental gene, was among the most significant additive variants identified. We functionally validated 13 of the additive candidate genes’ (Adgf-A/Adgf-A2/CG32181, bru1, CadN, flapper (CG11073), CG15236, flippy (CG9766), CREG, Dscam4, form3, fry, Lasp/CG9692, Pde6, Snoo), and introduce a novel approach to whole gene significance screens: PEGASUS_flies. Additionally, we identified ppk23, an Acid Sensing Ion Channel (ASIC) homolog, as an important hub for epistatic interactions. We propose a model that suggests genetic modifiers of wing and muscle morphology, nervous system development and function, BMP signaling, sexually dimorphic neural wiring, and gene regulation are all important for the observed differences flight performance in a natural population. Additionally, these results represent a snapshot of the genetic modifiers affecting drop-response flight performance in Drosophila, with implications for other insects.

scholarly journals Role of Semaphorins in Immunopathologies and Rheumatic Diseases

2019 ◽  
Vol 20 (2) ◽  
pp. 374 ◽  
Author(s):  
Samuel Garcia
Keyword(s):  
Rheumatic Diseases ◽  
Lupus Erythematosus ◽  
Current Knowledge ◽  
System Development ◽  
Joint Inflammation ◽  
Nervous System Development ◽  
Migration And Invasion ◽  
Potential Applications ◽  
Fibrotic Diseases

Rheumatic diseases are disorders characterized by joint inflammation, in which other organs are also affected. There are more than two hundred rheumatic diseases, the most studied so far are rheumatoid arthritis, osteoarthritis, spondyloarthritis, systemic lupus erythematosus, and systemic sclerosis. The semaphorin family is a large group of proteins initially described as axon guidance molecules involved in nervous system development. Studies have demonstrated that semaphorins play a role in other processes such as the regulation of immunity, angiogenesis, bone remodeling, apoptosis, and cell migration and invasion. Moreover, semaphorins have been related to the pathogenesis of multiple sclerosis, asthma, Alzheimer, myocarditis, atherosclerosis, fibrotic diseases, osteopetrosis, and cancer. The aim of this review is to summarize current knowledge regarding the role of semaphorins in rheumatic diseases, and discuss their potential applications as therapeutic targets to treat these disorders.

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