scholarly journals Advances in the Relationship between Tau Protein and Morphine De-pendence in Cognitive Dysfunction

2021 ◽  
Vol 9 (4) ◽  
pp. 96
Author(s):  
Qing Ji ◽  
Xin Li
Keyword(s):  
Oxidative Stress ◽  
Cognitive Dysfunction ◽  
Tau Protein ◽  
Hippocampal Neurons ◽  
System Development ◽  
Cognitive Disorders ◽  
Nervous System Development ◽  
Tau Proteins ◽  
Morphine Dependence ◽  
The Relationship

<span lang="EN-US">Morphine is an opioid drug. Long-term use can cause morphine dependence or addiction, and there are cognitive dysfunction such as abnormal mental behavior, decline in learning and memory, and decline in executive ability. The occurrence of this disease is related to many factors, such as oxidative stress, hippocampal neuronal injury, mitochondrial function injury, etc. Tau protein is a microtubule-associated protein involved in nervous system development. Studies have found that hyperphosphorylation of tau proteins can cause apoptosis of hippocampal neurons<sup>[1]</sup>, and tau proteins can cause oxidative stress<sup>[2]</sup>. Therefore, tau proteins play an important role in the pathogenesis of cognitive disorders. The relationship between morphine dependence and cognitive dysfunction is now reviewed.</span>

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 The Neuroprotective Effects of Carvacrol on Ethanol-Induced Hippocampal Neurons Impairment via the Antioxidative and Antiapoptotic Pathways

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Peng Wang ◽  
Qian Luo ◽  
Hui Qiao ◽  
Hui Ding ◽  
Yonggang Cao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Cognitive Dysfunction ◽  
Hippocampal Neurons ◽  
Morris Water Maze Test ◽  
Oxidative Stress Biomarkers ◽  
Neuroprotective Effects ◽  
Stress Injury

Chronic alcohol consumption causes hippocampal neuronal impairment, which is associated with oxidative stress and apoptosis. Carvacrol is a major monoterpenic phenol found in essential oils from the family Labiatae and has antioxidative stress and antiapoptosis actions. However, the protective effects of carvacrol in ethanol-induced hippocampal neuronal impairment have not been fully understood. We explored the neuroprotective effects of carvacrol in vivo and in vitro. Male C57BL/6 mice were exposed to 35% ethanol for 4 weeks to establish ethanol model in vivo, and hippocampal neuron injury was simulated by 200 mM ethanol in vitro. Morris water maze test was performed to evaluate the cognitive dysfunction. The oxidative stress injury of hippocampal neurons was evaluated by measuring the levels of oxidative stress biomarkers. Histopathological examinations and western blot were performed to evaluate the apoptosis of neurons. The results showed that carvacrol attenuates the cognitive dysfunction, oxidative stress, and apoptosis of the mice treated with ethanol and decreases hippocampal neurons apoptosis induced by ethanol in vitro. In addition, western blot analysis revealed that carvacrol modulates the protein expression of Bcl-2, Bax, caspase-3, and p-ERK, without influence of p-JNK and p-p38. Our results suggest that carvacrol alleviates ethanol-mediated hippocampal neuronal impairment by antioxidative and antiapoptotic effects.

scholarly journals Unique Responses of Differentiating Neuronal Growth Cones to Inhibitory Cues Presented by Oligodendrocytes

1998 ◽  
Vol 142 (1) ◽  
pp. 191-202 ◽  
Author(s):  
A. Shibata ◽  
M.V. Wright ◽  
S. David ◽  
L. McKerracher ◽  
P.E. Braun ◽  
...  
Keyword(s):  
Growth Cone ◽  
Hippocampal Neurons ◽  
Dendritic Growth ◽  
System Development ◽  
Axonal Growth ◽  
Growth Cones ◽  
Nervous System Development ◽  
Environmental Cues ◽  
Growth Cone Collapse ◽  
Neuronal Growth Cones

During central nervous system development, neurons differentiate distinct axonal and dendritic processes whose outgrowth is influenced by environmental cues. Given the known intrinsic differences between axons and dendrites and that little is known about the response of dendrites to inhibitory cues, we tested the hypothesis that outgrowth of differentiating axons and dendrites of hippocampal neurons is differentially influenced by inhibitory environmental cues. A sensitive growth cone behavior assay was used to assess responses of differentiating axonal and dendritic growth cones to oligodendrocytes and oligodendrocyte- derived, myelin-associated glycoprotein (MAG). We report that &gt;90% of axonal growth cones collapsed after contact with oligodendrocytes. None of the encounters between differentiating, MAP-2 positive dendritic growth cones and oligodendrocytes resulted in growth cone collapse. The insensitivity of differentiating dendritic growth cones appears to be acquired since they develop from minor processes whose growth cones are inhibited (nearly 70% collapse) by contact with oligodendrocytes. Recombinant MAG(rMAG)-coated beads caused collapse of 72% of axonal growth cones but only 29% of differentiating dendritic growth cones. Unlike their response to contact with oligodendrocytes, few growth cones of minor processes were inhibited by rMAG-coated beads (20% collapsed). These results reveal the capability of differentiating growth cones of the same neuron to partition the complex molecular terrain they navigate by generating unique responses to particular inhibitory environmental cues.

scholarly journals The Disabled 1 Phosphotyrosine-Binding Domain Binds to the Internalization Signals of Transmembrane Glycoproteins and to Phospholipids

1999 ◽  
Vol 19 (7) ◽  
pp. 5179-5188 ◽  
Author(s):  
Brian W. Howell ◽  
Lorene M. Lanier ◽  
Ronald Frank ◽  
Frank B. Gertler ◽  
Jonathan A. Cooper
Keyword(s):  
Hippocampal Neurons ◽  
System Development ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Nervous System Development ◽  
Amino Terminal ◽  
Density Lipoprotein Receptor ◽  
The Disabled ◽  
Phosphorylated Peptide ◽  
Ptb Domain

ABSTRACT Disabled gene products are important for nervous system development in drosophila and mammals. In mice, the Dab1 protein is thought to function downstream of the extracellular protein Reln during neuronal positioning. The structures of Dab proteins suggest that they mediate protein-protein or protein-membrane docking functions. Here we show that the amino-terminal phosphotyrosine-binding (PTB) domain of Dab1 binds to the transmembrane glycoproteins of the amyloid precursor protein (APP) and low-density lipoprotein receptor families and the cytoplasmic signaling protein Ship. Dab1 associates with the APP cytoplasmic domain in transfected cells and is coexpressed with APP in hippocampal neurons. Screening of a set of altered peptide sequences showed that the sequence GYXNPXY present in APP family members is an optimal binding sequence, with approximately 0.5 μM affinity. Unlike other PTB domains, the Dab1 PTB does not bind to tyrosine-phosphorylated peptide ligands. The PTB domain also binds specifically to phospholipid bilayers containing phosphatidylinositol 4P (PtdIns4P) or PtdIns4,5P2 in a manner that does not interfere with protein binding. We propose that the PTB domain permits Dab1 to bind specifically to transmembrane proteins containing an NPXY internalization signal.

scholarly journals The influence of diet patterns on Alzheimer’s risk: a concise systematic review

2021 ◽  
Vol 14 (3) ◽  
Author(s):  
Sayonara Carrijo Machado ◽  
Idiberto José Zotarelli Filho
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disorder ◽  
Cognitive Disorders ◽  
Health Concern ◽  
Eating Patterns ◽  
Diet Patterns ◽  
Age Related ◽  
Neurochemical Changes ◽  
The Relationship ◽  
Over Time

Alzheimer's disease (AD) is a progressive neurodegenerative disorder responsible for the main cause of dementia, and the increasing worldwide prevalence of AD is a major public health concern. Studies suggest that diet and nutrition may be important modifiable risk factors for AD. In addition, intestinal microbial metabolites and their effects on host neurochemical changes can increase or decrease the risk of AD. The aim of this literature review article is to discuss the relationship between dietary patterns, foods, gut microbiota, micro and macronutrients, and cognitive disorders, especially Alzheimer's. The results show that the excessive generation and accumulation of reactive pro-oxidant species over time can damage proteins, lipids, carbohydrates, and nucleic acids. Over time, this oxidative stress can contribute to a variety of age-related degenerative diseases. Therefore, antioxidant foods and healthy eating patterns, such as the Mediterranean diet, can contribute to reducing oxidative stress and consequently reducing the risk of Alzheimer's.

scholarly journals Role of Numb in Dendritic Spine Development with a Cdc42 GEF Intersectin and EphB2

2006 ◽  
Vol 17 (3) ◽  
pp. 1273-1285 ◽  
Author(s):  
Takashi Nishimura ◽  
Tomoya Yamaguchi ◽  
Akinori Tokunaga ◽  
Akitoshi Hara ◽  
Tomonari Hamaguchi ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Hippocampal Neurons ◽  
Neuronal Development ◽  
System Development ◽  
Direct Interaction ◽  
Nervous System Development ◽  
Nucleotide Exchange ◽  
Spine Development

Numb has been implicated in cortical neurogenesis during nervous system development, as a result of its asymmetric partitioning and antagonizing Notch signaling. Recent studies have revealed that Numb functions in clathrin-dependent endocytosis by binding to the AP-2 complex. Numb is also expressed in postmitotic neurons and plays a role in axonal growth. However, the functions of Numb in later stages of neuronal development remain unknown. Here, we report that Numb specifically localizes to dendritic spines in cultured hippocampal neurons and is implicated in dendritic spine morphogenesis, partially through the direct interaction with intersectin, a Cdc42 guanine nucleotide exchange factor (GEF). Intersectin functions as a multidomain adaptor for proteins involved in endocytosis and cytoskeletal regulation. Numb enhanced the GEF activity of intersectin toward Cdc42 in vivo. Expression of Numb or intersectin caused the elongation of spine neck, whereas knockdown of Numb and Numb-like decreased the protrusion density and its length. Furthermore, Numb formed a complex with EphB2 receptor-type tyrosine kinase and NMDA-type glutamate receptors. Knockdown of Numb suppressed the ephrin-B1-induced spine development and maturation. These results highlight a role of Numb for dendritic spine development and synaptic functions with intersectin and EphB2.

The effect of folic acid as an antioxidant on the hypothalamic monoamines in experimentally induced hypothyroid rat

2011 ◽  
Vol 28 (3) ◽  
pp. 253-261 ◽  
Author(s):  
Wafaa Ibrahim ◽  
Ehab Tousson ◽  
Thanaa El-Masry ◽  
Nadia Arafa ◽  
Mohamed Akela
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Folic Acid ◽  
Group Treatment ◽  
System Development ◽  
Critical Role ◽  
Nervous System Development ◽  
Control Group ◽  
Albino Rats ◽  
Pubertal Stage

Thyroid hormones are recognized as key metabolic hormones that play a critical role in the central nervous system development throughout life. In the present study, we studied the biochemical changes of hypothalamus of hypothyroid rats at post-pubertal stage, and the possible ameliorating effect of folic acid. A total of 50 male albino rats were equally divided into five groups; the first and second groups were the control and folic acid groups, respectively, while the third group was the hypothyroid group in which rats received daily 6- n-propyl-2-thiouracil (PTU) in drinking water for 6 weeks to induce hypothyroidism. The fourth and fifth groups were hypothyroid rats treated with folic acid for 4 weeks during and after receiving PTU, respectively, and were dissected after 6 and 10 weeks, respectively. There was a significant increase in plasma total homocysteine, malondialdehyde (MDA), oxidized glutathione\reduced glutathione and total nitric oxide and hypothalamic MDA, serotonin and norepinephrine in the hypothyroid rats group as compared to the control group. This reflects hyperhomocysteinaemia and oxidative stress associated with hypothyroid state. On the other hand, hypothalamic total nitric oxide and dopamine in the hypothyroid rats group were significantly decreased when compared to the control group. Treatment of hypothyroid rats with folic acid improves the oxidative stress and hypothalamic monoamines. Our results revealed that, folic acid treatment was better if it is administered as an adjuvant after returning to the euthyroid state.

scholarly journals OXIDATIVE STRESS IN ALZHEIMER’S DISEASE–EVALUATING THE AMYLOID BETA HYPOTHESIS

2021 ◽  
pp. 32-38
Author(s):  
SWETHA G. ◽  
ANJALI RAJ ◽  
SANIYA TABASSUM ◽  
DOUGLAS ZORINMAWIA CHHAKCHHUAK
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pyramidal Neurons ◽  
Senile Plaques ◽  
Redox Balance ◽  
Tau Proteins ◽  
Significant Component ◽  
And Behavior ◽  
The Relationship

Dementia is defined by the debilitation of cognition and behavior of individuals more than 65 y. Alzheimer's disease (AD) is the most pervasive pervasive form of dementia, afflicting around 47 million individuals worldwide. Oxidative damage is a significant component in the pathophysiology of Alzheimer's disease (AD). Assessment of Alzheimer's disease mind has shown a lot of oxidative harm, related with both trademark pathologies (senile plaques and neurofibrillary tangles) just as in typical seeming pyramidal neurons. By the by, the process that eventually causes disruption of redox balance and furthermore the origin of the free radicals are as yet hazy. There is likewise the accessibility of proof that oxidative stress may enhance the conglomeration and production of Aβ and furthermore help the polymerization just as phosphorylation of tau, subsequently making a pernicious cycle that invigorates the development and even commencement of Alzheimer's. These neurotic trademarks have complex proportional collaborations with cholinergic abrasions. This review may give complemental data for understanding the relationship between oxidative stress, amyloid plaques, tau proteins and cholinergic system in processing of AD.

scholarly journals Tauopathy and cognitive impairment in experimental diabetes mellitus

2017 ◽  
Vol 20 (3) ◽  
pp. 181-184 ◽  
Author(s):  
Mariia V. Matveeva ◽  
Yulia G. SamoiIova ◽  
Natalia G. Zhukova ◽  
Oksana A. Oleynik ◽  
Maria A. Rotkank
Keyword(s):  
Diabetes Mellitus ◽  
Cognitive Impairment ◽  
Glucose Metabolism ◽  
Tau Protein ◽  
Cognitive Disorders ◽  
Effective Strategies ◽  
Increased Risk ◽  
Glycation End Products ◽  
Stress Formation ◽  
The Relationship

Currently, diabetes mellitus (DM) is the most common metabolic disorder, which is manifested by hyperglycemia and leads to vascular and cognitive impairment. Mechanisms of cognitive dysfunction in patients with DM remain highly unclear, thus complicating the search for effective strategies for the prevention and treatment of dementia. Recently, scientists have discussed the issues regarding the relationship between DM and Alzheimers disease (AD), such as risk factors that trigger the cascade of pathological reactions. Patients with DM show an increased risk of developing AD. Similarly, patients with AD have been shown to have impaired insulin and glucose metabolism. Both these diseases have common nosology, pathology and biochemical basics, including oxidative stress, formation of advanced glycation end products, dysregulation of glucose metabolism and altered insulin signaling pathways. The microtubule-associated tau protein is involved in one of the causative mechanisms underlying the development of AD. We provide an overview of the major domestic and foreign data analyses regarding tau protein and the development of cognitive disorders in experimental DM.

Neuropsychology of Multiple Sclerosis: Looking Back and Moving Forward

2017 ◽  
Vol 23 (9-10) ◽  
pp. 832-842 ◽  
Author(s):  
Ralph H.B. Benedict ◽  
John DeLuca ◽  
Christian Enzinger ◽  
Jeroen J.G. Geurts ◽  
Lauren B. Krupp ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cognitive Dysfunction ◽  
Test Performance ◽  
Cognitive Rehabilitation ◽  
Cognitive Disorders ◽  
Cognitive Test ◽  
Functional Reserve ◽  
Cognitive Test Performance ◽  
The Relationship

AbstractThe neuropsychological aspects of multiple sclerosis (MS) have evolved over the past three decades. What was once thought to be a rare occurrence, cognitive dysfunction is now viewed as one of the most disabling symptoms of the disease, with devastating effects on patients’ quality of life. This selective review will highlight major innovations and scientific discoveries in the areas of neuropathology, neuroimaging, diagnosis, and treatment that pertain to our understanding of the neuropsychological aspects of MS. Specifically, we focus on the recent discovery that MS produces pathogical lesions of gray matter (GM) that have consequences for cognitive functions. Methods for imaging these GM lesions in MS are discussed along with multimodal imaging studies that integrate structural and functional imaging methods to provide a better understanding of the relationship between cognitive test performance and functional reserve. Innovations in the screening and comprehensive assessment of cognitive disorders are presented along with recent research that examines cognitive dysfunction in pediatric MS. Results of innovative outcome studies in cognitive rehabilitation are discussed. Finally, we highlight trends for potential future innovations over the next decade. (JINS, 2017, 23, 832–842)

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