scholarly journals Proteomics Analyses for the Global Proteins in the Brain Tissues of Different Human Prion Diseases

2015 ◽  
Vol 14 (4) ◽  
pp. 854-869 ◽  
Author(s):  
Qi Shi ◽  
Li-Na Chen ◽  
Bao-Yun Zhang ◽  
Kang Xiao ◽  
Wei Zhou ◽  
...  
Keyword(s):  
Prion Diseases ◽  
The Brain ◽  
Brain Tissues

Proteomic Analyses for the Global S-Nitrosylated Proteins in the Brain Tissues of Different Human Prion Diseases

2015 ◽  
Vol 53 (8) ◽  
pp. 5079-5096 ◽  
Author(s):  
Li-Na Chen ◽  
Qi Shi ◽  
Bao-Yun Zhang ◽  
Xiao-Mei Zhang ◽  
Jing Wang ◽  
...  
Keyword(s):  
Prion Diseases ◽  
Proteomic Analyses ◽  
The Brain ◽  
Brain Tissues

scholarly journals INTERRELATION OF PRIONS WITH NON-CODING RNAS

2018 ◽  
Vol 22 (4) ◽  
pp. 415-424
Author(s):  
R. N. Mustafin ◽  
E. K. Khusnutdinova
Keyword(s):  
Prion Diseases ◽  
Noncoding Rnas ◽  
Transmissible Spongiform Encephalopathies ◽  
Regulatory Effect ◽  
Spongiform Encephalopathies ◽  
Neuronal Stem Cells ◽  
Non Coding Rnas ◽  
The Brain ◽  
Brain Tissues

Prions are alternative infectious conformations for some cellular proteins. For the protein PrPC(PrP – prion protein, С – common), a prion conformation, called PrPSc(S – scrapie), is pathological. For example, in mammals the PrPScprion causes transmissible spongiform encephalopathies accumulating in the brain tissues of PrPScaggregates that have amyloid properties. MicroRNAs and long non-coding RNAs can be translated into functional peptides. These peptides can have a regulatory effect on genes from which their non-coding RNAs are transcribed. It has been assumed that prions, like peptides, due to the presence of specific domains, can also activate certain non-coding RNAs. Some of the activated non-coding RNAs can catalyze the formation of new prions from normal protein, playing their role in the pathogenesis of prion diseases. Confirmation of this assumption is the presence of the association of alleles of microRNA with the development of the disease, which indicates the role of the specific sequences of noncoding RNAs in the catalysis of prion formation. In the brain tissues of patients with prion diseases, as well as in exosomes containing an abnormal PrPScisoform, changes in the levels of microRNA have been observed. A possible cause is the interaction of the spatial domains of PrPScwith the sequences of the non-coding RNA genes, which causes a change in their expression. MicroRNAs, in turn, affect the synthesis of long non-coding RNAs. We hypothesize that long noncoding RNAs and possibly microRNAs can interact with PrPCcatalyzing its transformation into PrPSc. As a result, the number of PrPScincreases exponentially. In the brain of animals and humans, transposon activity has been observed, which has a regulatory effect on the differentiation of neuronal stem cells. Transposons form the basis of domain structures of long non-coding RNAs. In addition, they are important sources of microRNA. Since prion diseases can arise as sporadic and hereditary cases, and hereditary predisposition is important for the development of pathology, we hypothesize the role of individual features of activation of transposons in the pathogenesis of prion diseases. The activation of transposons in the brain at certain stages of development, as well as under the influence of stress, is reflected in the peculiarities of expression of specific non-coding RNAs that are capable of catalyzing the transition of the PrPCprotein to PrPSc. Research in this direction can be the basis for targeted anti-microRNA therapy of prion diseases.

Increases of Galectin-1 and its S-nitrosylated form in the Brain Tissues of Scrapie-Infected Rodent Models and Human Prion Diseases

2016 ◽  
Vol 54 (5) ◽  
pp. 3707-3716 ◽  
Author(s):  
Yan-Jun Guo ◽  
Qi Shi ◽  
Xiao-Dong Yang ◽  
Jian-Le Li ◽  
Yue Ma ◽  
...  
Keyword(s):  
Prion Diseases ◽  
Rodent Models ◽  
The Brain ◽  
Brain Tissues

Characterization of Ischemic Stroke in CT Images using Image Processing

2017 ◽  
Vol 7 (9) ◽  
pp. 18
Author(s):  
Amal Alzain ◽  
Suhaib Alameen ◽  
Rani Elmaki ◽  
Mohamed E. M. Gar-Elnabi
Keyword(s):  
Ischemic Stroke ◽  
White Matter ◽  
Classification Accuracy ◽  
Ct Images ◽  
Gray Level ◽  
Level Variation ◽  
Interactive Data ◽  
The Brain ◽  
Brain Tissues

This study concern to characterize the brain tissues to ischemic stroke, gray matter, white matter and CSF using texture analysisto extract classification features from CT images. The First Order Statistic techniques included sevenfeatures. To find the gray level variation in CT images it complements the FOS features extracted from CT images withgray level in pixels and estimate the variation of thesubpatterns. analyzing the image with Interactive Data Language IDL software to measure the grey level of images. The results show that the Gray Level variation and   features give classification accuracy of ischemic stroke 97.6%, gray matter95.2%, white matter 97.3% and the CSF classification accuracy 98.0%. The overall classification accuracy of brain tissues 97.0%.These relationships are stored in a Texture Dictionary that can be later used to automatically annotate new CT images with the appropriate brain tissues names.

scholarly journals Distribution of microRNA profiles in pre-clinical and clinical forms of murine and human prion disease

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Lesley Cheng ◽  
Camelia Quek ◽  
Xia Li ◽  
Shayne A. Bellingham ◽  
Laura J. Ellett ◽  
...  
Keyword(s):  
Prion Disease ◽  
Molecular Subtype ◽  
Prion Diseases ◽  
Clinical Stage ◽  
Clinical Samples ◽  
Serum Samples ◽  
Prion Infection ◽  
Clinical Forms ◽  
Therapeutic Development ◽  
The Brain

AbstractPrion diseases are distinguished by long pre-clinical incubation periods during which prions actively propagate in the brain and cause neurodegeneration. In the pre-clinical stage, we hypothesize that upon prion infection, transcriptional changes occur that can lead to early neurodegeneration. A longitudinal analysis of miRNAs in pre-clinical and clinical forms of murine prion disease demonstrated dynamic expression changes during disease progression in the affected thalamus region and serum. Serum samples at each timepoint were collected whereby extracellular vesicles (EVs) were isolated and used to identify blood-based biomarkers reflective of pathology in the brain. Differentially expressed EV miRNAs were validated in human clinical samples from patients with human sporadic Creutzfeldt-Jakob disease (sCJD), with the molecular subtype at codon 129 either methionine-methionine (MM, n = 14) or valine-valine (VV, n = 12) compared to controls (n = 20). EV miRNA biomarkers associated with prion infection predicted sCJD with an AUC of 0.800 (85% sensitivity and 66.7% specificity) in a second independent validation cohort (n = 26) of sCJD and control patients with MM or VV subtype. This study discovered clinically relevant miRNAs that benefit diagnostic development to detect prion-related diseases and therapeutic development to inhibit prion infectivity.

A fingerprint of amyloid plaques in a bitransgenic animal model of Alzheimer's disease obtained by statistical unmixing analysis of hyperspectral Raman data

The Analyst ◽  
2019 ◽  
Vol 144 (23) ◽  
pp. 7049-7056 ◽  
Author(s):  
Emerson A. Fonseca ◽  
Lucas Lafetá ◽  
Renan Cunha ◽  
Hudson Miranda ◽  
João Campos ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Amyloid Plaques ◽  
Model Of Alzheimer’S Disease ◽  
The Brain ◽  
Brain Tissues

We have found different Raman signatures of AB fibrils and in brain tissues from unmixed analysis, providing a detailed image of amyloid plaques in the brain, with the potential to be used as biomarkers.

Proteomic analysis of the brain tissues from a transgenic mouse model of amyloid β oligomers

2012 ◽  
Vol 61 (3) ◽  
pp. 347-355 ◽  
Author(s):  
Masaoki Takano ◽  
Kouji Maekura ◽  
Mieko Otani ◽  
Keiji Sano ◽  
Tooru Nakamura-Hirota ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Proteomic Analysis ◽  
Amyloid Β ◽  
Transgenic Mouse Model ◽  
The Brain ◽  
Brain Tissues

scholarly journals ПОВЕДІНКОВА АКТИВНІСТЬ ЩУРІВ І РІВЕНЬ ЕНДОТОКСИКОЗУ МОЗКУ НА ТЛІ ГІДРАЗИНОВОГО ГЕПАТИТУ

2019 ◽  
Vol 76 (2) ◽  
pp. 78-84
Author(s):  
O. A. Makarenko ◽  
T. V. Hladkyi ◽  
A. V. Maikova ◽  
T. V. Mohylevska
Keyword(s):  
Open Field ◽  
Urease Activity ◽  
Toxic Hepatitis ◽  
Male Rats ◽  
Behavioural Activity ◽  
Animal Physiology ◽  
Malondialdehyde Content ◽  
Experimental Formation ◽  
The Brain ◽  
Brain Tissues

Hepatic encephalopathy is a frequent complication and manifestation of liver diseases, and a consequence of liver failure. Our research aims at studying behavioral and emotional activity, as well as identification of the degree of endotoxicosis of brain tissues of rats at the background of modelling in them of toxic chronic hydrazine hepatitis. The research was carried out at the Department of Human and Animal Physiology of Odessa National Mechnykov University on laboratory male rats, aged 8-10 months. The animals were divided into 2 groups, 6 animals in each, control (intact animals) and experimental (formation of a model of toxic hydrazine hepatitis) ones. The functional state of the brain of rats was evaluated by studying the behavioral and emotional activities of animals with the methods of "Open field" and "T- shaped labyrinth". In brain homogenates, the activity of a number of enzymes was determined, which could indicate the cause of changes in the functioning of the nervous system: the activity of lysozyme, urease, elastase, catalase, the content of malondialdehyde. It was discovered that formation of toxic hepatitis in rats is accompanied by inhibition of orientation and behavioural activity – on 50-70 %, exploratory – on 40-60 % and emotional – on 30 % in “open field” test, considerable aggravation of dynamics of rate and quality of learning problem solving in T-shaped labyrinth. Modeling of hepatitis in rats led to the decrease in lysozyme activity by 22.1%, catalase activity by 30.8%, detection of urease activity in the brain, as well as an increase in elastase activity by 44.6% and malondialdehyde content by 21.5%.в At the background of hepatitis in homogenates of brain tissues urease activity has been detected, activity of inflammation markers and enzymes-destructors increases, with activity of indices of antioxidant brain system decreasing. Change of behavioural activity of rats at the background of toxic hepatitis is caused by the development of endotoxicosis, which results from impairment of the function of liver detoxification.

THE SPREAD OF PRION DISEASES IN THE BRAIN — MODELS OF REACTION AND TRANSPORT ON NETWORKS

2009 ◽  
Vol 17 (04) ◽  
pp. 623-641 ◽  
Author(s):  
FRANZISKA MATTHÄUS
Keyword(s):  
Disease Progression ◽  
Prion Diseases ◽  
Reaction Diffusion ◽  
Sudden Onset ◽  
Reaction Diffusion Equations ◽  
Diffusion Term ◽  
Network Decomposition ◽  
Fast Progression ◽  
The Brain ◽  
Infective Agent

In this paper we will present a modeling approach to describe the progression and the spread of prion diseases in the brain. Although there exist a number of mathematical models for the interaction of prions with their native counterpart, prion transport and spread is usually neglected. The concentration dynamics of prions, and thus the dynamics of the disease progression, however, are influenced by prion transport, especially in a medium as complex as the brain. Therefore, we focus here on the interaction between prion concentration dynamics and prion transport. The model is constructed by combining a model of prion-prion interaction with transport on networks. The approach leads to a system of reaction-diffusion equations, whereby the diffusion term is discrete. The equations are solved numerically on domains given as large networks. We show that the prion concentration grows faster on networks characterized by a higher degree heterogeneity. Furthermore, we introduce cell death as a consequence of increasing prion concentration, leading to network decomposition. We show that infectious diseases destroy networks similarly to targeted attacks, namely by affecting the nodes with the highest degree first. Relating the incubation period and disease progression to the process of network decomposition, we find that, interestingly, a long incubation time followed by sudden onset and fast progression of the disease does not need to be reflected in the overall concentration dynamics of the infective agent.

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