Strategies for Developing Animal Models of Neurotoxicant-Induced Neurodegenerative Disorders

1994 ◽  
pp. 17-38 ◽  
Author(s):  
Paul R. Solomon ◽  
Maryellen Groccia-Ellison ◽  
Mark E. Stanton ◽  
William W. Pendlebury
Keyword(s):  
Animal Models ◽  
Neurodegenerative Disorders

scholarly journals Editorial: Contribution of Translational Animal Models to the Systems Biology of Neurodegenerative Disorders

2020 ◽  
Vol 11 ◽  
Author(s):  
Wael M. Y. Mohamed ◽  
Mohamed M. Salama ◽  
Maha M. El Batsh ◽  
Eyleen L. Goh
Keyword(s):  
Systems Biology ◽  
Animal Models ◽  
Neurodegenerative Disorders

scholarly journals Viewpoint: Mechanisms of Action and Therapeutic Potential of Neurohormetic Phytochemicals

Dose-Response ◽  
2007 ◽  
Vol 5 (3) ◽  
pp. dose-response.0 ◽  
Author(s):  
Mark. P. Mattson ◽  
Tae Gen Son ◽  
Simonetta Camandola
Keyword(s):  
Animal Models ◽  
Neurodegenerative Disorders ◽  
Histone Deacetylases ◽  
Therapeutic Potential ◽  
Antioxidant Properties ◽  
Disease Process ◽  
Antioxidant Response ◽  
Mechanisms Of Action ◽  
Cellular Stress Response ◽  
Vegetables And Fruits

The nervous system is of fundamental importance in the adaptive (hormesis) responses of organisms to all types of stress, including environmental “toxins”. Phytochemicals present in vegetables and fruits are believed to reduce the risk of several major diseases including cardiovascular disease, cancers and neurodegenerative disorders. Although antioxidant properties have been suggested as the basis of health benefits of phytochemicals, emerging findings suggest a quite different mechanism of action. Many phytochemicals normally function as toxins that protect the plants against insects and other damaging organisms. However, at the relatively low doses consumed by humans and other mammals these same “toxic” phytochemicals activate adaptive cellular stress response pathways that can protect the cells against a variety of adverse conditions. Recent findings have elucidated hormetic mechanisms of action of phytochemicals (e.g., resveratrol, curcumin, sulforaphanes and catechins) using cell culture and animal models of neurological disorders. Examples of hormesis pathways activated by phytochemicals include the transcription factor Nrf-2 which activates genes controlled by the antioxidant response element, and histone deacetylases of the sirtuin family and FOXO transcription factors. Such hormetic pathways stimulate the production of antioxidant enzymes, protein chaperones and neurotrophic factors. In several cases neurohormetic phytochemicals have been shown to suppress the disease process in animal models relevant to neurodegenerative disorders such as Alzheimer's and Parkinson's diseaess, and can also improve outcome following a stroke. We are currently screening a panel of biopesticides in order to establish hormetic doses, neuroprotective efficacy, mechanisms of action and therapeutic potential as dietary supplements.

scholarly journals Challenges and future perspectives for 3D cerebral organoids as a model for complex brain disorders

2019 ◽  
Vol 2 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Pike-See Cheah ◽  
John O. Mason ◽  
King Hwa Ling
Keyword(s):  
Bipolar Disorder ◽  
Animal Models ◽  
Human Brain ◽  
Neurodegenerative Disorders ◽  
Neural Circuitry ◽  
Brain Diseases ◽  
Brain Disorders ◽  
Future Perspectives ◽  
Human Material ◽  
Underlying Mechanisms

The human brain is made up of billions of neurons and glial cells which are interconnected and organized into specific patterns of neural circuitry, and hence is arguably the most sophisticated organ in human, both structurally and functionally. Studying the underlying mechanisms responsible for neurological or neurodegenerative disorders and the developmental basis of complex brain diseases such as autism, schizophrenia, bipolar disorder, Alzheimer’s and Parkinson’s disease has proven challenging due to practical and ethical limitations on experiments with human material and the limitations of existing biological/animal models. Recently, cerebral organoids have been proposed as a promising and revolutionary model for understanding complex brain disorders and preclinical drug screening.

Animal Models of Neurodegenerative Diseases

2016 ◽  
Author(s):  
David Baglietto-Vargas ◽  
Rahasson R. Ager ◽  
Rodrigo Medeiros ◽  
Frank M. LaFerla
Keyword(s):  
Animal Models ◽  
Life Expectancy ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Human Disease ◽  
Molecular Mechanisms ◽  
Preclinical Studies ◽  
Pathological Features ◽  
The Past ◽  
The Brain

The incidence and prevalence of neurodegenerative disorders (e.g., Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD), etc.) are growing rapidly due to increasing life expectancy. Researchers over the past two decades have focused their efforts on the development of animal models to dissect the molecular mechanisms underlying neurodegenerative disorders. Existing models, however, do not fully replicate the symptomatic and pathological features of human diseases. This chapter focuses on animal models of AD, as this disorder is the most prevalent of the brain degenerative conditions afflicting society. In particular, it briefly discusses the current leading animal models, the translational relevance of the preclinical studies using such models, and the limitations and shortcomings of using animals to model human disease. It concludes with a discussion of potential means to improve future models to better recapitulate human conditions.

Beclin 1 Complex and Neurodegenerative Disorders

2020 ◽  
pp. 236-260
Author(s):  
Ozaifa Kareem ◽  
Ghulam Nabi Bader ◽  
Faheem Hyder Pottoo ◽  
Mohd. Amir ◽  
Md. Abul Barkat ◽  
...  
Keyword(s):  
Animal Models ◽  
Complex Formation ◽  
Neurodegenerative Disorders ◽  
Protein Sorting ◽  
Biological Macromolecules ◽  
Autophagy Induction ◽  
Effector Caspase ◽  
Vacuolar Protein ◽  
Insight Into

Beclin1 is the mammalian orthologue of yeast Atg6/vacuolar protein sorting-30 (VPS30). Beclin1 interacts with various biological macromolecules like ATG14, BIF-1, NRBF2, RUBICON, UVRAG, AMBRA1, HMGB1, PINK1, and PARKIN. Such interactions promote Beclin1-PI3KC3 complex formation. Autophagy is blocked in apoptosis owing to the breakdown of Beclin1 by caspase whereas autophagy induction inhibits effector caspase degradation, therefore, blocks apoptosis. Thus, the Beclin1 is an essential biomolecular species for cross-regulation between autophagy and apoptosis. Various studies carried out in neurodegenerative animal models associated with aggregated proteins have confirmed that multifunctional Beclin1 protein is necessary for neuronal integrity. The role of Beclin1 protein has been investigated and was reported in various human neurodegeneration disorders. This chapter aims to provide an insight into the role of Beclin1 in the development of neurodegenerative disorders.

scholarly journals Parkinson’s Disease and Autophagy

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Ana María Sánchez-Pérez ◽  
Berta Claramonte-Clausell ◽  
Juan Vicente Sánchez-Andrés ◽  
María Trinidad Herrero
Keyword(s):  
Cell Death ◽  
Animal Models ◽  
Neurodegenerative Disease ◽  
Causal Relationship ◽  
Neurodegenerative Disorders ◽  
Therapeutic Strategy ◽  
Neuroprotective Effects ◽  
Autophagy Induction ◽  
Effective Therapeutic Strategy ◽  
The Brain

It is generally accepted that a correlation between neurodegenerative disease and protein aggregation in the brain exists; however, a causal relationship has not been elucidated. In neurons, failure of autophagy may result in the accumulation of aggregate-prone proteins and subsequent neurodegeneration. Thus, pharmacological induction of autophagy to enhance the clearance of intracytoplasmic aggregate-prone proteins has been considered as a therapeutic strategy to ameliorate pathology in cell and animal models of neurodegenerative disorders. However, autophagy has also been found to be a factor in the onset of these diseases, which raises the question of whether autophagy induction is an effective therapeutic strategy, or, on the contrary, can result in cell death. In this paper, we will first describe the autophagic machinery, and we will consider the literature to discuss the neuroprotective effects of autophagy.

Age- and Sex-Dependent Laterality of Rat Hippocampal Cholinergic System in Relation to Animal Models of Neurodevelopmental and Neurodegenerative Disorders

2004 ◽  
Vol 29 (4) ◽  
pp. 671-680 ◽  
Author(s):  
Zdena Krištofikov´ ◽  
František Št'astný ◽  
Věra Bubeníková ◽  
Rastislav Druga ◽  
Jan Klaschka ◽  
...  
Keyword(s):  
Animal Models ◽  
Neurodegenerative Disorders ◽  
Cholinergic System ◽  
Age And Sex
Sign in / Sign up

Export Citation Format

Share Document