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Animal Models Of Cognitive Impairment

Author : Edward D. Levin
ISBN : 9781420004335
Genre : Science
File Size : 67. 46 MB
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The costs associated with a drug’s clinical trials are so significant that it has become necessary to validate both its safety and efficacy in animal models prior to the continued study of the drug in humans. Featuring contributions from distinguished researchers in the field of cognitive therapy research, Animal Models of Cognitive Impairment examines some of the most popular and successful animal archetypes used in the context of drug discovery. It provides integrated coverage of the latest research concerning neuronal systems relevant to cognitive function and dysfunction, assimilating reviews of this research within the context of each chapter. This approach is unique in that it brings together molecular and neurochemical methodologies, behavioral applications in translational models, and clinical applications. The book comprehensively discusses a wide variety of animal models of cognitive impairment, including genetic, lesion, pharmacological, and aging related impairments. It also explores the significance of this research in regards to the treatment of various addictions and disorders such as stroke, autism, Alzheimer’s, schizophrenia, and ADHD. Edited by two renowned authorities in the field, Animal Models of Cognitive Impairment is a timely book that provides integrated coverage of cutting-edge research that concerns neuronal systems relevant to cognitive function and dysfunction.

Animal Models Of Human Cognitive Aging

Author : Jennifer L. Bizon
ISBN : 9781597454223
Genre : Medical
File Size : 49. 34 MB
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Significant improvements in lifestyle and medical science are leading to an ever increasing elderly population in the United States and other developed nations. The U.S census bureau estimates that the number of people over 65 will nearly double by 2030, and that the elderly will comprise nearly one-fifth of the world’s entire population within the next 20 years. In Animal Models of Human Cognitive Aging, Jennifer Bizon, Alisa Woods, and a panel of international authorities comprehensively discuss the use of animal models as a tool for understanding cognitive changes associated with the aging process. The book provides substantive background on the newest and most widely used animal models in studies of cognition and aging, while detailing the normal and pathological processes of brain aging of humans in relation to those models. Additional chapters comprehensively review frontal cortical deficits and executive function in primates as related to humans, and the use of transgenic modulation in mice to model Alzheimer’s and other age-related diseases. Groundbreaking and authoritative, Animal Models of Human Cognitive Aging provides a valuable resource for Neuroscientists, Gerontological Scientists and all aging medicine researchers, while serving as a primer for understanding current brain aging studies.

Animal Models For Neurological Disorders

Author : Anil Kumar
ISBN : 9789815039696
Genre : Science
File Size : 24. 48 MB
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Animal disease models are a vital tool to study diseases and associated conditions. Studies on animal models can, in some cases, be used as a basis for modeling and understanding human diseases. Biomedical scientists face a challenge to choose the correct animal model to study disease pathology, and neurological diseases are no exception to this rule. Animal Models for Neurological Disorders covers different animal models which have been used for studying neurological disorders. 13 topical chapters have been contributed by a group of experts on the subject with an aim to cover emerging experimental models of a range of neurological diseases encountered in the clinic including Alzheimer’s disease, psychosis, Parkinson’s, Huntington’s disease, vascular dementia, schizophrenia, multiple sclerosis and brain tumors, among others. The chapters also inform readers about relevant clinical correlations in each disease model where appropriate. Animal Models for Neurological Disorders is intended for all scholarly researchers and students of biomedical sciences, pharmacology, medicine (oncology, neurology, psychiatry), pharmacy, biochemistry, and biotechnology. The organized contents of the book also serve as a quick reference point for scientists working in applied areas of neuroscience including the study of neurodegenerative diseases and cognitive dysfunction in living organisms.

Human And Animal Models For Translational Research On Neurodegeneration Challenges And Opportunities From South America

Author : Agustín Ibáñez
ISBN : 9782889454945
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Neurodegenerative diseases are the most frequent cause of dementia, representing a burden for public health systems (especially in middle and middle-high income countries). Although most research on this issue is concentrated in first-world centers, growing efforts in South America are affording important breakthroughs. This emerging agenda poses new challenges for the region but also new opportunities for the field. This book aims to integrate the community of experts across the globe and the region, and to establish new challenges and developments for future investigation. We present research focused on neurodegenerative research in South America. We introduce studies assessing the interplay among genetic, neural, and behavioral dimensions of these diseases, as well as articles on vulnerability factors, comparisons of findings from various countries, and works promoting multicenter and collaborative networking. More generally, our book covers a broad scope of human-research approaches (behavioral assessment, neuroimaging, electromagnetic techniques, brain connectivity, peripheral measures), animal methodologies (genetics, epigenetics, proteomics, metabolomics, other molecular biology tools), species (all human and non-human animals, sporadic, and genetic versions), and article types (original research, review, and opinion papers). Through this wide-ranging proposal, we hope to introduce a fresh approach to the challenges and opportunities of research on neurodegeneration in South America.

Animal Models Of Behavior Genetics

Author : Jonathan C. Gewirtz
ISBN : 9781493937776
Genre : Medical
File Size : 31. 48 MB
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This stimulating analysis reviews the broad potential of animal models to foster a deeper understanding of human pathology, strengthen connections between genetic and behavioral studies, and develop more effective treatments for mental disorders. Widely-studied and lesser-used species are examined in models that capture features along the continuum of normative and pathological behavior. The models highlight genetic causes of core features, or endophenotypes, of developmental, internalizing, and externalizing disorders, as well as dementia. Expert contributors address questions ranging from how suitable species are chosen for study to the costs and benefits of using inbred versus outbred strains, and the effects of housing environment on subject animals. Larger issues addressed include how to evaluate the applicability of animal behavioral models to the human condition and how these models can harness emerging molecular technologies to further our understanding of the genetic basis of mental illness. Included in the coverage: Mating and fighting in Drosophila. Attachment and social bonding. Impulsivity in rodents and humans. Animal models of cognitive decline. Animal models of social cognition. Future directions for animal models in behavioral genetics. A detailed map of where this evolving field is headed, Animal Models of Behavior Genetics shows geneticists, molecular biologists, and cognitive neuroscientists paths beyond established concepts toward a more knowledgeable and collaborative future.

Animal Models For The Study Of Human Disease

Author : Joachim Wistuba
ISBN : 9780128072219
Genre : Medical
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Klinefelter syndrome (KS) is a frequent (0.2%) sex chromosomal disorder in males presenting with a 47,XXY karyotype. This condition is associated with infertility, hypogonadism, and metabolic and cognitive impairments. As experimental research is restrictive in patients, animal models for KS are needed to explore its molecular and genetic basis. Supernumerary X chromosomes due to meiotic nondisjunctions sporadically also occur in males of other mammalian species and provoke the same or at least some of the features observed in patients. However, as the condition is linked to infertility, the generation and availability of a substantial number of experimental animals cannot be fulfilled using individuals with the naturally occurring syndrome. Breeding of B6Ei.Lt-Y∗ mice carrying a mutated Y chromosome provides a sufficient number of males with a supernumerary X chromosome that resembles the human disorder and permits the design and performance of the complex investigations needed to elucidate the mechanisms at the heart of the pathology. This chapter reviews the insights obtained into studies into KS over the past decades and highlights the contribution made by the animal model.

Zebrafish Model Of Cognitive Dysfunction

Author : Brandon Kar Meng
ISBN : OCLC:1154169226
Genre : Science
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Cognitive dysfunction is an impairment in one or more of the six cognitive domains (complex attention, executive function, learning and memory, language, perceptual motor and social cognition). The effect of pharmacological interventions can be studied using animal models of cognitive dysfunction, which are typically split into pharmacological, developmental and genetic models. Rodents are the most commonly used animal species for modelling cognitive dysfunction, although multiple models and test locations are often recommended to improve validity. Researchers thus unfortunately need to balance the validity of their experimental designs with financial, logistical and cost constraints. Zebrafish could be the answer to this conundrum as one of their many advantages over rodents is their high breeding rate which makes high-throughput screening more feasible and thus increases cost-effectiveness. The popularity of zebrafish has been increasing in recent times, as measured by the increasing number of zebrafish research publications. It is thus unsurprising that several zebrafish models of cognitive dysfunction have already been developed, together with zebrafish tests designed to measure zebrafish cognitive performance. Future research will undoubtedly lead to the development of new zebrafish models of cognitive dysfunction, as well as validate current ones to pave the way for widespread adoption.

Handbook Of Animal Models In Alzheimer S Disease

Author : G. Casadesus
ISBN : 9781607507338
Genre : Medical
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Animals have been used to model diseases or test new treatments since around 300 BC, and undoubtedly our ability to model disease in animals – including transgenic animals – has provided major breakthroughs in all fields of biomedical research. Due to their complexity and plurality of pathology and symptomatology, the study of neurodegenerative diseases relies heavily on animal models. These models have been developed in many species in the attempt to undercover the complex nature of the disease mechanisms involved. The ultimate goal is to test promising therapies and to manage, prevent or cure neurodegenerative disease. But because most animal models in this area do not reproduce the full phenotypical disease spectrum and the etiology and clinical presentation of neurodegenerative diseases differ from one patient to the next, the testing of these diseases in animal models often translates poorly to indices of efficacy when applied to the clinical population. Written by experts in the field with these advances and challenges in mind, this handbook provides an updated overview of the animal models being developed and used to study complex disease dynamics. The first part of the book presents an overview of animal models of various species and includes a review of new invertebrate animal models to study neurodegeneration. The second section presents the use of animal models to pinpoint disease mechanisms, and the last part of the handbook examines the various therapeutic interventions being used in models of neurodegenerative disease.

Neuropathological Changes In Mouse Models Of Cardiovascular Diseases

Author : Diewertje Ilse Bink
ISBN : OCLC:1041852500
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Mild cognitive impairment and dementia are common disorders in the elderly. As the life span of the population in the Western world is increasing, the prevalence of cognitive disorders and the social and economic burden that coincide with that will increase. Recent data indicate that cardiovascular diseases are largely associated with an increased risk of dementia. The presence of atherosclerosis, heart failure, hypertension and small vessel disease are all associated with neuropathological changes and increased cognitive decline. Exploring the link between cardiovascular diseases and cognitive decline is important, since it could identify treatment targets for patients with cognitive impairment and dementia. The main hypothesis of this thesis is that different cardiovascular diseases in mice contribute to the development of neuropathological changes related to cognitive impairment and dementia. To test this hypothesis animal models with comparable etiology and neuropathology are needed in order to perform mechanistic studies and study cause-consequence relationships. In chapter 2 we reviewed the literature on mouse models of cardiovascular disease with reported cerebral changes in order to get an insight in which animal models are suited for vascular cognitive impairment or dementia research. These included models for atherosclerosis, heart failure, hypoperfusion, hypertension and small vessel disease. In chapter 3 we explored the distribution of atherosclerotic plaques in the common carotid artery, intracranial carotid artery and circle of Willis in different atherosclerotic mouse models. In chapter 4-6 we used mouse models of atherosclerosis, heart failure and hypoperfusion to study the effect of these cardiovascular diseases on brain pathology.

Various Animal Models To Check Learning And Memory A Review

Author : Avneet Gupta
ISBN : 3847322222
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Learning is defined as the acquisition of information and skills or in other words it is the process by which new information is acquired. Subsequent retention of the information is called memory, which is the process by which acquired knowledge is retained. But oxidative stress and vascular dysfunction are recognized as important contributing factors in the pathogenesis of Alzheimer's disease (AD) and other dementia of vascular origin. AD is a progressive neurodegenerative disorder associated with loss of neurons in distinct brain areas and cord and AD shows cognitive dysfunctions. Deficit in learning and memory have long been recognized as severe and consistent neurological disorder associated with numerous psychiatric and neurodegenerative states. Moreover, a marked compromise of processes has become an integral part of aging. Normal aging is associated with a decline in functions such as sensory and motor performance, and at times, this decline is accompanied by cognitive dysfunction So, the present study is therefore focused on discussing different animal models for Learning and memory. These animal models provide help for measure cognitive functions in animals.

Senile Dementia Of The Alzheimer Type

Author : Jörg Traber
ISBN : 9783642706448
Genre : Medical
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Society is showing increasing concern for disorders related to aging that lead to a loss of brain function. In view of the enormous proportion of elderly people in our society today, brain aging is more than ever subject to challenge to us all, not only politicians and health authorities, but every individual who is confronted with the difficult situation of watching the mental powers of apparently healthy elderly friends, neighbours, or relatives fail, often with alarming rapidity. This challenge is directed especially toward us scientists. As one of our colleagues succinctly put it 2 years ago at the close of our First International Symposium on Brain Aging: "Do something. We are not dealing here with just another disease; we are concerned with human dignity. " More than any statistics, these words convinced me that Tropon's decision to leave the field of classic CNS pharmacology and move into the field of gerontopsychopharmacology was the right one, even though we knew that success would be uncertain and that, even if it finally comes it will be many years hence. At this point, let me add a personal comment: each one of us is judged by his or her own success. We live in a competitive society where success counts. This applies not only to the businessman, but also to the scientist, in particular, to those in industry.

Part I Targeted Intervention For Cognitive Impairment Identified In The Young Adult Rat And Part Ii A Novel Role For The Er Membrane Acetylcoa Transporter At 1 In The Development Of Autism

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ISBN : OCLC:944972210
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Part I: Targeted intervention for cognitive impairment identified in the young-adult rat: Behavioral and pharmacological treatments for cognitive impairments associated with the aging process are becoming a growing focus of concern as the elderly population continues to expand worldwide. Studies of cognitive impairment are typically designed to study cognitive decline in aged animals in order to identify molecular changes that occur in the aging brain. However, studies investigating cognitive impairments in young animals and tracking cognition over the lifetime are rare. Furthermore, young rats ubiquitously perform very well on established versions of commonly used paradigms such as the Morris Water Maze (MWM), suggesting that more challenging tasks may be required to reveal subtle differences in young animals. Current evidence suggests that environmental enrichment can improve learning and memory, and is effective at ameliorating symptoms associated with various disease states, but the age at which enrichment can be effective and the length of enrichment necessary remain unclear. Furthermore, the impacts of environmental enrichment on synaptic plasticity and the molecular mechanisms behind environmental enrichment have not been elucidated. A compelling body of evidence suggests that group 1 metabotropic glutamate receptors (mGluR1/5) are vital for hippocampal synaptic plasticity and learning and memory formation, and it has been suggested that this effect is mediated by activation of the extracellular signal related kinase (ERK) and mammalian target of rapamycin (mTOR) pathways. The experiments in this thesis were designed to develop behavioral paradigms sensitive enough to reveal subtle differences in hippocampal dependent learning and memory in young rodents in order to track performance over their lifespan. The experiments were further designed to determine the impact of environmental enrichment on cognition, synaptic plasticity, and mGluR dependent signaling pathways in young-adult rodents. First, we show that a novel one-day version of the Morris water maze and novel object recognition can be used to identify subtle cognitive impairments early in life. We have found that these two tasks reliably separate young rats into inferior and superior learners, are highly correlated, and that performance on these tasks early in life is predictive of performance at 12 months of age. Furthermore, we have found that repeated training in this task selectively improves the performance of inferior learners, suggesting that behavioral training from an early age may provide a buffer against age-related cognitive decline. Second, we show that 4 months of environmental enrichment improves cognitive performance in young-adult rats and enhances hippocampal LTP. We demonstrate that this LTP is dependent on mGluR5 signaling, activation of ERK and mTOR signaling cascades, and sustained phosphorylation of p70s6 kinase, thus providing a potential target mechanism for future studies of cognitive enhancement in the rodent. Taken together, the results of these studies provide valuable insight into novel means of preventing cognitive impairment by targeting affected populations from a young age. The results of these studies further provide potential molecular mechanisms that may be targeted for cognitive enhancement. In addition to environmental enrichment, gene therapy is a promising therapeutic technique for interventions in numerous disease states. Indeed, AAV has proven to be successful for gene therapy in a number of animal models of disease, and is currently being used in human clinical trials for various conditions such as Lieber congenital amaurosis, hemophilia, muscular dystrophy, Parkinson's disease, and Alzheimer's disease. MRI contrast agents such as gadoteridol have been used to track the distribution of therapeutic drugs in real time, allowing visualization of the volume of spread across various structures. However, the effect of gadoteridol on the spread of the injected drugs has not been thoroughly investigated. In a third study, we conducted experiments to determine whether coinfusion with gadoteridol impacts the spread of rAAV in the injected tissue. We show that rAAV1 but not rAAV5 transduction efficiency is significantly increased by co-infusion with gadoteridol, and that gadoteridol has no deleterious effects on behavior. This provides a safe method to enable targeting of larger brain regions with fewer injection sites and thus reduce surgery time, an important variable to consider especially when working with aged or fragile animal models of neurological disease. Part II: A novel role for the ER membrane acetylCoA transporter AT-1 in the development of autism AcetylCoA is an essential substrate for a wide range of biochemical reactions that occur within the cell. The production of cytosolic acetylCoA relies predominantly on the conversion of citrate from the mitochondria and CoA by ATP-citrate lyase (Acly), and the condensation of free acetate from the peroxisome and CoA by acetylCoA synthetase (AceCS). AcetylCoA is then imported into the lumen of the ER by the ER membrane transporter AT-1 (also known as SLC33A1), where it serves as the donor of the acetyl group in the Nε-lysine acetylation of ER-resident and -transiting proteins. Previous studies form our laboratory have revealed that the ER acetylation machinery regulates two essential and intimately related functions of the ER: (i) "positive" selection of correctly folded nascent polypeptides (as part of quality control) and (ii) tight regulation of autophagy (as part of ER Associated Degradation type II). A balance between these two functions must be maintained to ensure ER homeostasis. The acetylation machinery of the ER has been linked to a variety of human conditions, including hereditary spastic paraplegia, Alzheimer's disease (AD), and Autism spectrum disorder (ASD). In particular, an S113R mutation in AT-1 has been identified in patients with a familial form of spastic paraplegia ΝϚʹ“�� Μρο ιαβ ϝαπ γδκμλπϟοαϟδγ ϟϝαϟ ϟϝζπ κρϟαϟζμλ ζλ ΑϞ�» νοδσδλϟπ γζκδοζφαϟζμλ με ϟϝδ ϟοαλπνμοϟδο αλγ ϐαρπδπ γδϐοδαπδγ ζλειρτ με Αϐδϟυι�μΑ ζλϟμ ϟϝδ ΔΟ� ςϝζϐϝ ιδαγπ ϟμ αβδοοαλϟ ζλγρϐϟζμλ με αρϟμνϝαϛυ ζλ ϐδιιπ αλγ ζλ αλζκαι κμγδιπ� Ϟϝζπ ζλπρεεζϐζδλϐυ με ΑϞ�»ζλ ϟϝδ αλζκαι οδπριϟπ ζλ λδρομγδϛδλδοαϟζμλ� ζλειακκαϟζμλ� αλγ νομνδλπζϟυ ϟμ ζλεδϐϟζμλπ αλγ ϐαλϐδο� Πϟργζδπ εομκ μρο ιαβ ϝασδ αιπμ οδσδαιδγ ϟϝαϟ ϟϝδ αϐϟζσζϟυ με ΑϞ�» αλγ ϟϝδ ΑϞαπδπ αοδ ζλϟζκαϟδιυ ιζλθδγ ϟμ ϟϝδ ναϟϝμϛδλδπζπ με Αιφϝδζκδοπͅ γζπδαπδ� Ϟϝδ αϐϟζσζϟυ με ΑϞ�» οδϛριαϟδπ ϟϝδ αϐδϟυιαϟζμλ πϟαϟρπ με ΒΑ�Δ�»� ϟϝδ οαϟδ� ιζκζϟζλϛ πϟδν ζλ ϟϝδ νομγρϐϟζμλ με Α�ø� Ζλϝζβζϟζμλ με ϟϝδ ΑϞαπδπ ϝαπ βδδλ πϝμςλ ϟμ γζκζλζπϝ ΒΑ�Δ�» ιδσδιπ αλγ ιδαγ ϟμ πρβπδξρδλϟ γδϐοδαπδγ ιδσδιπ με Α�ø� Α�ø αϛϛοδϛαϟδπ� αλγ λδρομλαι νιαξρδπ� Εροϟϝδοκμοδ� ζλϝζβζϟζμλ με ϟϝδ ΑϞαπδπ ϝαπ βδδλ πϝμςλ ϟμ ζκνομσδ πυλανϟζϐ νιαπϟζϐζϟυ� ιδαολζλϛ αλγ κδκμου� αλγ ιζεδπναλ ζλ α κμρπδ κμγδι με ΑΓ� Εζλαιιυ� α γρνιζϐαϟζμλ με ΑϞ�» ϝαπ βδδλ οδνμοϟδγ ζλ ναϟζδλϟπ ςζϟϝ αρϟζπκ πνδϐϟορκ γζπμογδο �ΑΠΓ� αλγ ζλϟδιιδϐϟραι γζπαβζιζϟυ �Αρϟζπκ Γαϟαβαπδ· αιπμ Πςζππϝδικ Θ�� δϟ αι� ΑΠϜϚ Αλλραι Κδδϟζλϛ� Μϐϟμβδο »��““� “«»ʹ� Παλ Γζδϛμ� �Α�� Ϝμςδσδο� ϟϝδ κδϐϝαλζπκπ βδϝζλγ ϟϝζπ ϐμοοδιαϟζμλ αλγ ϝμς ΑϞ�» καυ ϐμλϟοζβρϟδ ϟμ ϟϝδ ναϟϝμϛδλδπζπ με ΑΠΓ αοδ λμϟ ϐιδαο� Ζλ ϟϝζπ ϟϝδπζπ� ςδ πμρϛϝϟ ϟμ ζλσδπϟζϛαϟδ ϟϝδ ϐμλπδξρδλϐδπ με ζλϐοδαπδγ αϐϟζσζϟυ με ΑϞ�»� �δ ϛδλδοαϟδγ αλ ΑϞ�» Ϟϛ κμρπδ κμγδι ϟϝαϟ πδιδϐϟζσδιυ μσδοδτνοδππδπ ΑϞ�» ζλ λδρομλπ� Ϟϝδπδ αλζκαιπ γδκμλπϟοαϟδ ϐμϛλζϟζσδ γδεζϐζϟπ� αρϟζπϟζϐ�ιζθδ πμϐζαι βδϝασζμο� αβδοοαλϟ πυλανϟζϐ νιαπϟζϐζϟυ� ζλϐοδαπδγ γδλγοζϟζϐ πνζλδ αλγ βοαλϐϝ εμοκαϟζμλ� αλγ ςζγδπνοδαγ νομϟδμκζϐ ϐϝαλϛδπ� Ζλ αγγζϟζμλ� ςδ εμρλγ ϟϝαϟ ΑϞ�» Ϟϛ αλζκαιπ γζπνιαυ ζλϐοδαπδγ δτνοδππζμλ με κζϟμϐϝμλγοζαι δλφυκδπ οδιαϟδγ ϟμ αϐδϟυι�μΑ νομγρϐϟζμλ� πρϛϛδπϟζλϛ ϟϝαϟ ζλϐοδαπδγ ειρτ με αϐδϟυι�μΑ ζλϟμ ϟϝδ ΔΟ ϐαρπδπ ϐμκνδλπαϟμου αϐϟζσζϟυ με ϟϝδ κζϟμϐϝμλγοζα�

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ISBN : 9781614998761
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Neurodegeneration And Alzheimer S Disease

Author : Ralph N. Martins
ISBN : 9781119356790
Genre : Technology & Engineering
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Understanding the impact of diet, exercise, genetics, and hormones on the risk and development of Alzheimer’s and other neurogenerative diseases Diet is widely known to impact on neurological function. Nevertheless, academic texts discussing this relationship are relatively few in number. This book therefore fills an important gap in the current literature. Opening with an overview of neurodegenerative diseases, particularly Alzheimer’s disease, the text then focuses on explaining the means by which glycemic control and lipid metabolism – and associated nutritional and lifestyle variables – may factor into such disorders’ prevention and treatment. An international group of experts in the fields of food science and neurodegeneration have contributed chapters that examine Alzheimer’s disease within a broad range of contexts. Offering dietary, genetic, and hormonal perspectives, the authors explore topics ranging from sugar consumption to digestive fermentation, and Alzheimer’s disease animal models to the cognition-enhancing effects of physical exercise. Also included are overviews of the latest research into current and developing methods of treatment and diagnosis, as well as differential diagnostics. This groundbreaking book: Explores how glucose metabolism, insulin resistance, lipid metabolism, and high intake of refined carbohydrates are linked to Alzheimer's disease Discusses how genetic makeup can impact risk of Alzheimer’s and Parkinson’s disease Examines cognitive changes in neurodegeneration, lists current tests for determining cognitive impairment, and provides information concerning differential diagnosis Discusses potential advantages of increasing antioxidant and micronutrient intake Reviews hormonal influences on neurodegeneration Examines the links between protein intake and Alzheimer’s disease. Neurodegeneration and Alzheimer's Disease is an essential resource for researchers, medical practitioners, dietitians, and students with an interest in neurological diseases and their diagnosis and risk factors, as well as diet-related conditions such as diabetes and obesity. Lifestyle and diet influence neurodegeneration risk, and a better understanding of this evidence amongst health professionals will hopefully lead to greater public awareness of how to reduce the likelihood of these widespread conditions.

Animal Models For The Study Of Human Disease

Author : Mengqi Chen
ISBN : 9780128072158
Genre : Medical
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Alzheimer’s disease (AD) is a major and increasing burden on families, communities, and national health budgets. Despite intensive and extended research, there is still widespread debate about its cause(s), and no effective treatments exist. Familial (inherited, mainly early onset) and sporadic (mainly late onset) forms of the disease exist, and it is uncertain to what extent they are related. Transgenic mouse models have dominated the investigation of this disease, but their validity can be questioned. Numerous alternative models exist that can provide valuable information on the molecular and cellular basis of AD. In this chapter, we review the various invertebrate, nonmammalian vertebrate, and mammalian models and how these have been used to investigate this disease. We examine the strengths and weaknesses of these various model systems. Of course, animal models never completely reflect the true nature of a human disease, but progress in understanding and finding preventative and ameliorative treatments for AD is hindered by the lack of a convincing hypothesis for the cause of this complex condition.

Cell And Animal Models In Aging And Dementia Research

Author : Siegfried Hoyer
ISBN : 9783709193501
Genre : Medical
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Although age has been recognized as a risk factor for late-onset dementia of Alzheimer type, its etiology is unknown as yet. Several age-related metabolic abnormalities may thus become important for the pathogenesis of the late-onset form. Studies at the cellular/molecular level in brain tissue are possible post mortem, but lack information on the beginning of the disorder. In this supplement, different approaches are dealt with how to induce structural and/or metabolic abnormalities in relevant cell cultures, in brain slices and in experimental animals, and how behavioral changes parallel the metabolic variations.

Cognitive Impairment In Plb1 Mice

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ISBN : OCLC:921223267
Genre : Alzheimer's disease
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AD is a particular form of dementia with a complex aetiology. A necessary step to understand the disease in greater detail is the development of correct animal models. To date, animal models do not fully encapsulate endophenotypes of AD so that further improvements are warranted. Our group has recently developed a genetically improved and pathologically extended novel mouse model of AD, the PLB line. It consists of a multitude of directly comparable genetic lines due to selective knock-in of human APP and Tau mutant gene, which can be selectively excised by cross breeding with deleter mice. Through this process, 5 different genetic lines were generated termed PLB1Double (expressing mutant APP and Tau), PLB1WT, PLB1Triple (expressing human APP, Tau and presenilin 1), PLB2Tau, and PLB2APP and exposed to social interaction and social recognition tasks, and novel object recognition as well as novel object location tasks with a short-term delay. Animals were tested aged 5 and 12 months in cross-sectional designs. The results show impairments in social recognition at the age of 5 months in the PLB1Triple, PLB2Tau and PLB1Double but not in PLB2APP, which performed like PLB1WT. Social recognition but not sociability was compromised in PLB1WT mice at 12 month of age precluding a meaningful readout at this age. In object recognition, however, all AD models apart from PLB1Triple expressed a trend for object memory at 6 months, but this was only preserved in PLB2APP mice at 12 months; all other groups failed to recall the object over 5 minute delays. Spatial memory for object location was observed in controls at 6 and 12 months, but not in any other genotype or age group. Towards this end, our date seem to suggest that lines with underlying tau pathology present with a more severe recognition memory phenotype relative to APP containing lines.

Studying Alzheimer S Disease Pre Clinical Stages

Author : Maria Iulita
ISBN : OCLC:911202030
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"The recent failure of major Alzheimer's disease (AD) clinical trials would indicate that, at the moment of diagnosis, the damage to the brain is likely irreversible. There is also a growing recognition that the pathological changes that lead to AD develop many years before cognitive decline. This pre-clinical stage deserves further attention, as it should offer a critical opportunity for successful treatment. Unfortunately, the investigation of this stage is complicated by the fact that current diagnostic methods cannot unequivocally identify asymptomatic individuals bound to develop dementia. In that sense, transgenic animal models offer an attractive alternative. Even better, Down's syndrome (DS) brains offer the unique opportunity to investigate the temporal development of AD pathology in humans. Due to triplication of the amyloid-[beta] (A[beta]) precursor protein (APP) in chromosome 21, all DS subjects gradually develop amyloid plaques, neurofibrillary tangles and gliosis. Therefore, taking advantage of these models, the main objective of this Thesis was to better understand the early stages of AD pathology.The progressive degeneration of basal forebrain cholinergic neurons (BFCN) is central to the manifestation of cognitive deficits in AD and DS. BFCN have a life-long dependence on nerve growth factor (NGF) for their phenotypic maintenance. Previous studies from the Cuello lab have shown deficits in NGF's extracellular metabolism in AD brains, which compromise proNGF maturation and enhance NGF degradation. The possibility that this occurs early during AD progression has not been investigated and it is relevant given the need for new disease biomarkers.Consequently, we first examined whether an NGF-metabolic deficit occurred in DS. Our investigations revealed for the first time a compromised extracellular NGF metabolism in adult DS brains and in trisomic DS mice. Importantly, alterations in NGF metabolism were detected early, in primary cultures from DS fetal cortex.The NGF metabolic cascade was further examined in the cerebro-spinal fluid (CSF) of subjects with AD and mild cognitive impairment (MCI). Matrix metallo-protease 3 (MMP-3) and tissue plasminogen activator (tPA) were identified as novel biomarker candidates in AD CSF, with significant correlations between the levels of these analytes and clinico-pathological parameters. Although these markers were normal in individuals with MCI, this group exhibited increased neuroserpin, plasminogen and TIMP-1 in CSF, compared to control subjects. Finally, taking advantage of our APP transgenic rat, we have shown that prior to amyloid plaque deposition, A[beta] peptides are present in pyramidal neurons of the cortex and hippocampus as well as in the rat CSF. The early accumulation of intracellular pathology (which includes A[beta], APP and its C-terminal fragments) was accompanied by cognitive deficits, which paralleled the evolution of A[beta] pathology. Together, these results demonstrate that the early accumulation of A[beta] is sufficient to induce CNS damage (e.g. NGF deregulation, learning and memory deficits), before the development of full-blown AD pathology. These studies may also provide clues for the development of novel neuroprotective therapies and hint at potential new biomarker candidates for the staging of individuals in the AD trajectory." --

Reelin Related Neurological Disorders And Animal Models

Author : Laura Lossi
ISBN : 9782889451111
Genre :
File Size : 48. 15 MB
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The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.

Investigating The Neuroprotective Effects Of Resistance Exercise In Animal Models Of Alzheimer S Disease And Postoperative Cognitive Dysfunction

Author : 劉艷
ISBN : OCLC:1129084465
Genre : Alzheimer's diseaselzheimer's disease
File Size : 36. 4 MB
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