Animal Models of Dementia: Ethical Considerations

2010 ◽  
pp. 15-33 ◽  
Author(s):  
I. Anna S. Olsson ◽  
Peter Sandøe
Keyword(s):  
Animal Models ◽  
Ethical Considerations

The challenges of animal models of pain

2018 ◽  
Author(s):  
Muhammad Saad Yousuf ◽  
Bradley J. Kerr
Keyword(s):  
Animal Models ◽  
Tissue Damage ◽  
Emotional Experience ◽  
Human Studies ◽  
Common Symptom ◽  
Biological Mechanisms ◽  
Ethical Considerations ◽  
Physician Consultation ◽  
Mcgill University ◽  
Unpleasant Feeling

The landmark paper discussed in this chapter is ‘Animal models of pain: progress and challenges’, published in the journal Nature Reviews Neuroscience by Jeff Mogil of McGill University in 2009. The most common symptom across various medical conditions and a major reason for seeking physician consultation is pain. It is defined as ‘an unpleasant feeling or emotional experience associated with actual or potential tissue damage’. A large percentage of the research investigating the biological mechanisms of pain is performed on animals. Human studies of pain are limited by lack of practicality, subjectivity, and ethical considerations. This influential review by Mogil discusses the progress and challenges faced in studying pain using various animal models.

Animal Models in Psychiatric Disorders of Childhood Onset

2013 ◽  
pp. 967-969
Author(s):  
Richard Paylor ◽  
Alexia M. Thomas ◽  
Surabi Veeraragavan ◽  
Shannon M. Hamilton
Keyword(s):  
Informed Consent ◽  
Animal Models ◽  
Psychiatric Disorders ◽  
Human Behavior ◽  
Face Validity ◽  
Complex Behavior ◽  
Rodent Models ◽  
Childhood Onset ◽  
Ethical Considerations ◽  
Childhood Disorders

Research to elucidate the mechanisms underlying psychiatric disorders can be challenging with regards to childhood disorders, in which human samples available to researchers are not only limited, but there are also ethical considerations regarding the ability of children to provide informed consent. Therefore animal models provide an alternative for studying the complex behavior associated with neurological and psychiatric disorders of childhood-onset. Behaviors in rodent models are likely not completely analogous to human behavior and the models must meet face validity, construct validity and predictive validity to be considered relevant. This chapter highlights the major animal models currently used in the research of childhood-onset psychiatric disorders.

scholarly journals Animal models of cerebral amyloid angiopathy

2017 ◽  
Vol 131 (19) ◽  
pp. 2469-2488 ◽  
Author(s):  
Lieke Jäkel ◽  
William E. Van Nostrand ◽  
James A.R. Nicoll ◽  
David J. Werring ◽  
Marcel M. Verbeek
Keyword(s):  
Animal Models ◽  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Ethical Considerations ◽  
Naturally Occurring ◽  
Cerebral Amyloid

Cerebral amyloid angiopathy (CAA), due to vascular amyloid β (Aβ) deposition, is a risk factor for intracerebral haemorrhage and dementia. CAA can occur in sporadic or rare hereditary forms, and is almost invariably associated with Alzheimer’s disease (AD). Experimental (animal) models are of great interest in studying mechanisms and potential treatments for CAA. Naturally occurring animal models of CAA exist, including cats, dogs and non-human primates, which can be used for longitudinal studies. However, due to ethical considerations and low throughput of these models, other animal models are more favourable for research. In the past two decades, a variety of transgenic mouse models expressing the human Aβ precursor protein (APP) has been developed. Many of these mouse models develop CAA in addition to senile plaques, whereas some of these models were generated specifically to study CAA. In addition, other animal models make use of a second stimulus, such as hypoperfusion or hyperhomocysteinemia (HHcy), to accelerate CAA. In this manuscript, we provide a comprehensive review of existing animal models for CAA, which can aid in understanding the pathophysiology of CAA and explore the response to potential therapies.

Reductionist thinking and animal models in neuropsychiatric research

2019 ◽  
Vol 42 ◽  
Author(s):  
Nicole M. Baran
Keyword(s):  
Animal Models ◽  
Mental Disorders ◽  
Environmental Factors ◽  
Neuropsychiatric Disorders ◽  
Model Organisms ◽  
Developmental Genetic ◽  
Term Study ◽  
Genetic And Environmental Factors ◽  
Mechanisms Of Plasticity

AbstractReductionist thinking in neuroscience is manifest in the widespread use of animal models of neuropsychiatric disorders. Broader investigations of diverse behaviors in non-model organisms and longer-term study of the mechanisms of plasticity will yield fundamental insights into the neurobiological, developmental, genetic, and environmental factors contributing to the “massively multifactorial system networks” which go awry in mental disorders.

Inflammational Animal Models for Schizophrenia

2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel
Keyword(s):  
Animal Model ◽  
Animal Models ◽  
Immune Activation ◽  
Microglial Activation ◽  
Treatment Options ◽  
Early Adulthood ◽  
Brain Regions ◽  
Synaptic Connections ◽  
Preventive Interventions ◽  
Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

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