Microarray analysis of nonhuman primates: validation of experimental models in neurological disorders

2003 ◽  
Vol 17 (8) ◽  
pp. 1-19 ◽  
Author(s):  
Markéta Marvanová ◽  
Jean Ménager ◽  
Erwan Bezard ◽  
Ronald E. Bontrop ◽  
Laurent Pradier ◽  
...  
Keyword(s):  
Microarray Analysis ◽  
Neurological Disorders ◽  
Nonhuman Primates ◽  
Experimental Models

Advances in the Experimental Models of HIV-Associated Neurological Disorders

2021 ◽  
Author(s):  
Susmita Sil ◽  
Palsamy Periyasamy ◽  
Annadurai Thangaraj ◽  
Fang Niu ◽  
Divya T. Chemparathy ◽  
...  
Keyword(s):  
Neurological Disorders ◽  
Experimental Models

scholarly journals Experimental Models of Autoimmune Demyelinating Diseases in Nonhuman Primates

2017 ◽  
Vol 55 (1) ◽  
pp. 27-41 ◽  
Author(s):  
Lev Stimmer ◽  
Claire-Maëlle Fovet ◽  
Ché Serguera
Keyword(s):  
Nonhuman Primates ◽  
Rhesus Macaques ◽  
Acute Disseminated Encephalomyelitis ◽  
Experimental Models ◽  
Diagnostic Methods ◽  
Demyelinating Diseases ◽  
Protective Mechanisms ◽  
Common Marmosets ◽  
Neuro Inflammation ◽  
Underlying Mechanisms

Human idiopathic inflammatory demyelinating diseases (IIDD) are a heterogeneous group of autoimmune inflammatory and demyelinating disorders of the central nervous system (CNS). These include multiple sclerosis (MS), the most common chronic IIDD, but also rarer disorders such as acute disseminated encephalomyelitis (ADEM) and neuromyelitis optica (NMO). Great efforts have been made to understand the pathophysiology of MS, leading to the development of a few effective treatments. Nonetheless, IIDD still require a better understanding of the causes and underlying mechanisms to implement more effective therapies and diagnostic methods. Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model to study the pathophysiology of IIDD. EAE is principally induced through immunization with myelin antigens combined with immune-activating adjuvants. Nonhuman primates (NHP), the phylogenetically closest relatives of humans, challenged by similar microorganisms as other primates may recapitulate comparable immune responses to that of humans. In this review, the authors describe EAE models in 3 NHP species: rhesus macaques ( Macaca mulatta), cynomolgus macaques ( Macaca fascicularis), and common marmosets ( Callithrix jacchus), evaluating their respective contribution to the understanding of human IIDD. EAE in NHP is a heterogeneous disease, including acute monophasic and chronic polyphasic forms. This diversity makes it a versatile model to use in translational research. This clinical variability also creates an opportunity to explore multiple facets of immune-mediated mechanisms of neuro-inflammation and demyelination as well as intrinsic protective mechanisms. Here, the authors review current insights into the pathogenesis and immunopathological mechanisms implicated in the development of EAE in NHP.

Mitochondrial CHCHD2 and CHCHD10: Roles in Neurological Diseases and Therapeutic Implications

2019 ◽  
Vol 26 (2) ◽  
pp. 170-184
Author(s):  
Wei Zhou ◽  
Dongrui Ma ◽  
Eng-King Tan
Keyword(s):  
Neurological Disorders ◽  
Neurological Diseases ◽  
Mitochondrial Gene ◽  
Experimental Models ◽  
Loss Of Function ◽  
Motor Neuron Diseases ◽  
Therapeutic Implications ◽  
Mitochondrial Inner Membrane ◽  
Mitochondrial Defects ◽  
Neurological Conditions

CHCHD2 mutations have been identified in various neurological diseases such as Parkinson’s disease (PD), frontotemporal dementia (FTD), and Alzheimer’s disease (AD). It is also the first mitochondrial gene whose mutations lead to PD. CHCHD10 is a homolog of CHCHD2; similar to CHCHD2, various mutations of CHCHD10 have been identified in a broad spectrum of neurological disorders, including FTD and AD, with a high frequency of CHCHD10 mutations found in motor neuron diseases. Functionally, CHCHD2 and CHCHD10 have been demonstrated to interact with each other in mitochondria. Recent studies link the biological functions of CHCHD2 to the MICOS complex (mitochondrial inner membrane organizing system). Multiple experimental models suggest that CHCHD2 maintains mitochondrial cristae and disease-associated CHCHD2 mutations function in a loss-of-function manner. However, both CHCHD2 and CHCHD10 knockout mouse models appear phenotypically normal, with no obvious mitochondrial defects. Strategies to maintain or enhance mitochondria cristae could provide opportunities to correct the associated cellular defects in disease state and unravel potential novel targets for CHCHD2-linked neurological conditions.

scholarly journals Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Marisela Méndez-Armenta ◽  
Concepción Nava-Ruíz ◽  
Daniel Juárez-Rebollar ◽  
Erika Rodríguez-Martínez ◽  
Petra Yescas Gómez
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Neurological Disorders ◽  
Neuronal Apoptosis ◽  
Experimental Models ◽  
State Failure ◽  
Radical Production ◽  
Induction Of Apoptosis ◽  
Models Of Epilepsy

Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy.

scholarly journals Probing the Dynamics of Neuronal Proteins In Vivo Using Non-Canonical Amino Acids Tagging

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Kevin P. Lin ◽  
Aya M. Saleh ◽  
Kathryn R. Jacobson ◽  
Sarah Calve ◽  
Tamara L. Kinzer-Ursem
Keyword(s):  
Neurological Disorders ◽  
Temporal Dynamics ◽  
Click Reaction ◽  
Neurological Diseases ◽  
Experimental Models ◽  
Selective Enrichment ◽  
Neuronal Proteins ◽  
Canonical Amino Acid ◽  
Brain Tissues

Background and Hypothesis: More than 600 neurological disorders have been identified, each with varying degrees of complexity and level of molecular understanding. However, current approaches are inadequate to capture the complex progressive nature of most neurological diseases. Therefore, developing techniques capable of probing the temporal dynamics of neuronal proteins in rodents, the most commonly used experimental models, is imperative for proper understanding of mechanisms driving neurological disorders. In this project, a protein labeling technique that enables selective labeling of newly synthesized proteins in vivo is utilized. In this technique, the non-canonical amino acid azidohomoalanine (AHA) is injected into mice to achieve global proteome labeling. AHA is an azide-tagged methionine (Met) analog that is incorporated into the nascent proteins using endogenous translational mechanisms. The azide functional group of AHA allows selective enrichment of the newly synthesized proteins from brain tissues via click-chemistry using alkynebearing affinity tags. This will be followed by detecting the AHA-labeled protein using mass spectrometry. We hypothesize that this labeling technique will help map the dynamics of the brain proteome in health and disease. This will ultimately provide insights into mechanisms underlying complex neurological diseases. Experimental Design or Project Methods: C57Bl/6 murine dams were injected with 0.1 mg/g AHA for two days. Brain tissues were harvested, homogenized and lysates were reacted with biotin-alkyne using copper-catalyzed click reaction. Biotinylated proteins were then enriched using NeutrAvidin beads and eluted by boiling in 2% SDS. Results: Tissues were fractionated into different subcellular components (cytosolic, nuclear, membrane, cytoskeletal, and extracellular matrix) using buffers of different stringency. Western blot analysis of clicked tissues using Streptavidin-fluorophore indicated effective incorporation of AHA into different cellular fractions of brain tissues. Additionally, the analysis of eluted proteins revealed successful enrichment and elution of AHA-labeled proteins. Conclusion and Potential Impact: Successful incorporation of AHA in nascent neuronal proteins can lead to a comprehensive quantitative approach for elucidating changes in the regulation of neuronal proteins in disease states.

Essential oils in experimental models of neuropsychiatric disorders: A review

2021 ◽  
Vol 19 ◽  
Author(s):  
Luciana Cristina B. Fernandes ◽  
Ianara Mendonça Costa ◽  
Marco Aurelio M. Freire ◽  
Francisca Overlânia V. Lima ◽  
Francisca Idalina Neta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Cerebral Ischemia ◽  
Essential Oils ◽  
Neurological Disorders ◽  
Biological Effects ◽  
Neuroprotective Effect ◽  
Experimental Models ◽  
Sensory Loss ◽  
Cochrane Library

Background: Neural cells undergo functional or sensory loss due to neurological disorders. In addition to environmental or genetic factors, oxidative stress is a major contributor to neurodegeneration. In this context, there has been a growing interest in investigating the effects of essential oils (EOs) in recent years, especially in the treatment of neuropathologies. The chemical and biological effects of EOs have led to important treatment tools for the management of various neurological disorders. Objective: In the present study we performed a systematic review that sought to comprehend the neuroprotective effects of different EOs. Method: This work is a systematic review where an electronic search was performed on PubMed, Science direct, Cochrane Library and SciELO (Scientific Electronic Library Online) databases, covering the last 10 years, using “Essential oil” and “Neuroprotective effect” as reference terms. Results: A total of 9 articles were identified, in which the efficacy of EOs was described in experimental models of anxiety, dementia, oxidative stress, cerebral ischemia, Alzheimer’s disease and oxidative toxicity. Conclusion: EOs from different species of medicinal plants have shown positive responses in neurological disorders such as anxiety, dementia, oxidative stress, cerebral ischemia and oxidative toxicity. Thus, EOs emerges with the potential to be used as alternative agents in the treatment of neurological disorders.

Experimental models of spatial neglect

e-Neuroforum ◽  
2012 ◽  
Vol 18 (1) ◽  
Author(s):  
M. Wilke ◽  
P. Dechent ◽  
C. Schmidt-Samoa
Keyword(s):  
Nonhuman Primates ◽  
Brain Activity ◽  
Brain Regions ◽  
Experimental Models ◽  
Spatial Neglect ◽  
Distributed Network ◽  
Healthy Individuals ◽  
Detailed Understanding ◽  
Brain Circuits ◽  
The Brain

AbstractSpatial neglect is a debilitating neuropsy­chological disorder that is characterized by an impaired or lost ability to explore the space contralateral to the lesion and to re­act to stimuli presented on this side. Lesion sites that have been implicated in spatial ne­glect form a widely distributed network con­sisting of a number of cortical (i.e., frontopa­rietal) and subcortical (i.e., thalamic) areas that are activated during attention and vi­suomotor tasks in healthy individuals. While detailed understanding of the brain circuits and mechanisms involved in spatial neglect is a prerequisite for the development of ef­fective therapies, this has proven to be dif­ficult in human patients because of the size and variability of lesion sites. Therefore, ex­perimental models where predefined brain regions can be systematically inactivated are of great advantage. Neglect models have been developed in nonhuman primates in whom it is possible to pharmacologically in­activate small brain regions and in humans by means of noninvasive stimulation/inacti­vation methods such as transcranial magnet­ic stimulation. In this article, we discuss theo­ries about the mechanisms of spatial neglect such as the hemispheric imbalance model and the supporting experimental evidence, with an emphasis on imaging experiments that have explored the effects of lesions on dynamic brain activity.

scholarly journals Neuronal delivery of antibodies has therapeutic effects in animal models of botulism

2021 ◽  
Vol 13 (575) ◽  
pp. eabd7789
Author(s):  
Patrick M. McNutt ◽  
Edwin J. Vazquez-Cintron ◽  
Luis Tenezaca ◽  
Celinia A. Ondeck ◽  
Kyle E. Kelly ◽  
...  
Keyword(s):  
Neuromuscular Transmission ◽  
Botulinum Neurotoxin ◽  
Nonhuman Primates ◽  
Symptomatic Treatment ◽  
Experimental Models ◽  
Therapeutic Effects ◽  
Single Domain Antibody ◽  
Domain Antibody ◽  
Molecular Toxicity ◽  
Intracellular Targets

Botulism is caused by a potent neurotoxin that blocks neuromuscular transmission, resulting in death by asphyxiation. Currently, the therapeutic options are limited and there is no antidote. Here, we harness the structural and trafficking properties of an atoxic derivative of botulinum neurotoxin (BoNT) to transport a function-blocking single-domain antibody into the neuronal cytosol where it can inhibit BoNT serotype A (BoNT/A1) molecular toxicity. Post-symptomatic treatment relieved toxic signs of botulism and rescued mice, guinea pigs, and nonhuman primates after lethal BoNT/A1 challenge. These data demonstrate that atoxic BoNT derivatives can be harnessed to deliver therapeutic protein moieties to the neuronal cytoplasm where they bind and neutralize intracellular targets in experimental models. The generalizability of this platform might enable delivery of antibodies and other protein-based therapeutics to previously inaccessible intraneuronal targets.

Comparative Enamel Histology of Primate Teeth

1979 ◽  
Vol 58 (2_suppl) ◽  
pp. 1002-1003 ◽  
Author(s):  
D.G. Gantt
Keyword(s):  
Comparative Studies ◽  
Nonhuman Primates ◽  
Experimental Models ◽  
Primate Species ◽  
Dental Tissues ◽  
The Past ◽  
Ultra Structure ◽  
Systemic Stress

The use of nonhuman primates as experimental models has markedly increased during the past decade. However, very little is known about primate dental tissues, especially enamel. Comparative studies of the enamel from 25 primate species reveal a wide variation in (1) the thickness of enamel, (2) microstructure and ultra-structure, and (3) the species' capacity to respond to systemic stress. These data provide a baseline of information presently not available to the dental researcher.

Microarray analysis of xenograft-derived cancer cell lines representing multiple experimental models of human prostate cancer

2003 ◽  
Vol 37 (4) ◽  
pp. 209-221 ◽  
Author(s):  
Gennadi V. Glinsky ◽  
Anja Krones-Herzig ◽  
Anna B. Glinskii ◽  
Gerhard Gebauer
Keyword(s):  
Prostate Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Microarray Analysis ◽  
Cancer Cell Lines ◽  
Experimental Models ◽  
Human Prostate ◽  
Human Prostate Cancer
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