Maria Antonietta Ajmone-Cat, Emanuele Cacci, and Luisa Minghetti
- Published in print:
- 2009
- Published Online:
- January 2010
- ISBN:
- 9780195326697
- eISBN:
- 9780199864874
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195326697.003.0013
- Subject:
- Neuroscience, Molecular and Cellular Systems
Inflammation is a self-defensive reaction that may develop into a chronic state and become a causative factor in the pathogenesis of a broad range of disabling diseases. Similar to peripheral ...
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Inflammation is a self-defensive reaction that may develop into a chronic state and become a causative factor in the pathogenesis of a broad range of disabling diseases. Similar to peripheral inflammation, brain inflammation is increasingly being viewed as a target for treating neurological diseases, not only infectious and immune-mediated disorders such as meningitis or multiple sclerosis but also stroke, trauma, and neurodegenerative diseases that were originally not considered to be inflammatory. Microglial cells, the resident macrophages of brain parenchyma, are generally viewed as major sources of pro-inflammatory and potentially neurotoxic molecules in the damaged brain, However, a direct link between activated microglia and tissue damage has not been univocally demonstrated in vivo, and recent studies have rather documented exacerbation of injury following selective microglial ablation or anti-inflammatory treatments. Recent studies have implicated inflammation in the regulation of adult neurogenesis, thus broadening the therapeutic potential of strategies aimed at controlling neuroinflammation. This chapter summarizes the main evidence supporting both detrimental and protective roles of inflammation in acute and chronic brain diseases.Less
Inflammation is a self-defensive reaction that may develop into a chronic state and become a causative factor in the pathogenesis of a broad range of disabling diseases. Similar to peripheral inflammation, brain inflammation is increasingly being viewed as a target for treating neurological diseases, not only infectious and immune-mediated disorders such as meningitis or multiple sclerosis but also stroke, trauma, and neurodegenerative diseases that were originally not considered to be inflammatory. Microglial cells, the resident macrophages of brain parenchyma, are generally viewed as major sources of pro-inflammatory and potentially neurotoxic molecules in the damaged brain, However, a direct link between activated microglia and tissue damage has not been univocally demonstrated in vivo, and recent studies have rather documented exacerbation of injury following selective microglial ablation or anti-inflammatory treatments. Recent studies have implicated inflammation in the regulation of adult neurogenesis, thus broadening the therapeutic potential of strategies aimed at controlling neuroinflammation. This chapter summarizes the main evidence supporting both detrimental and protective roles of inflammation in acute and chronic brain diseases.
Walter Glannon
- Published in print:
- 2011
- Published Online:
- May 2011
- ISBN:
- 9780199734092
- eISBN:
- 9780199894475
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780199734092.003.0017
- Subject:
- Philosophy, Moral Philosophy
This chapter examines neural cell replacement therapy for neurodegenerative diseases and spinal cord injury. While neural transplantation has the potential to regenerate the brain, results from ...
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This chapter examines neural cell replacement therapy for neurodegenerative diseases and spinal cord injury. While neural transplantation has the potential to regenerate the brain, results from clinical trials testing the procedure over the last twenty years have not been very promising. The goal of decelerating neural degeneration and restoring brain function is still an unrealized possibility. The chapter points out that the underlying pathophysiology of neurodegenerative diseases may limit or preclude the regenerative potential of transplanting cells into the brain. In addition, the chapter explores some of the social and psychological implications of two hypothetical scenarios: one in which regeneration of the brain does not keep pace with regeneration of the body; and one in which it does.Less
This chapter examines neural cell replacement therapy for neurodegenerative diseases and spinal cord injury. While neural transplantation has the potential to regenerate the brain, results from clinical trials testing the procedure over the last twenty years have not been very promising. The goal of decelerating neural degeneration and restoring brain function is still an unrealized possibility. The chapter points out that the underlying pathophysiology of neurodegenerative diseases may limit or preclude the regenerative potential of transplanting cells into the brain. In addition, the chapter explores some of the social and psychological implications of two hypothetical scenarios: one in which regeneration of the brain does not keep pace with regeneration of the body; and one in which it does.
Elias K. Michaelis
- Published in print:
- 2012
- Published Online:
- September 2012
- ISBN:
- 9780199592388
- eISBN:
- 9780199949922
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780199592388.003.0004
- Subject:
- Neuroscience, Disorders of the Nervous System, Behavioral Neuroscience
The phenomenon of selective neuronal vulnerability to neurological diseases or insults, such as ischemia-reperfusion, brain trauma, and ageing-associated neurodegeneration, was described in the ...
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The phenomenon of selective neuronal vulnerability to neurological diseases or insults, such as ischemia-reperfusion, brain trauma, and ageing-associated neurodegeneration, was described in the hippocampus nearly a century ago. The hippocampus has been the focus for many of the studies designed to identify the stresses to which neurons respond differentially, as well as the molecular, cellular and physiological mechanisms that may be responsible for such differential response patterns. Although final conclusions have not yet been reached on the mechanisms for differential neuronal responses to stress and disease, genomic and proteomic analyses, in conjunction with biochemical and physiological measurements, are beginning to point to endogenous differences between vulnerable and resistant populations of neurons. Collectively, these studies have identified differential patterns of energy metabolism, generation of reactive oxygen species, handling of transient intracellular calcium elevations, and the activity of the neurotransmitter glutamate, as some of the key processes that lead to selective sensitivity to neurological stresses. The genomic and proteomic analyses have revealed that differences in gene expression related to inflammatory and immune responses and responses to oxidative stress represent endogenous processes differentially expressed in neurons selectively vulnerable to stresses. The same is true for genes involved in DNA, RNA, and protein repair. Cells that are more resistant to stresses and disease conditions express genes for energy generation, nervous system development, and synaptic transmission at higher levels than those found in vulnerable neurons. The molecular pathways identified above and described in this chapter may eventually determine the targets for future therapeutic interventions for neurodegenerative diseases.Less
The phenomenon of selective neuronal vulnerability to neurological diseases or insults, such as ischemia-reperfusion, brain trauma, and ageing-associated neurodegeneration, was described in the hippocampus nearly a century ago. The hippocampus has been the focus for many of the studies designed to identify the stresses to which neurons respond differentially, as well as the molecular, cellular and physiological mechanisms that may be responsible for such differential response patterns. Although final conclusions have not yet been reached on the mechanisms for differential neuronal responses to stress and disease, genomic and proteomic analyses, in conjunction with biochemical and physiological measurements, are beginning to point to endogenous differences between vulnerable and resistant populations of neurons. Collectively, these studies have identified differential patterns of energy metabolism, generation of reactive oxygen species, handling of transient intracellular calcium elevations, and the activity of the neurotransmitter glutamate, as some of the key processes that lead to selective sensitivity to neurological stresses. The genomic and proteomic analyses have revealed that differences in gene expression related to inflammatory and immune responses and responses to oxidative stress represent endogenous processes differentially expressed in neurons selectively vulnerable to stresses. The same is true for genes involved in DNA, RNA, and protein repair. Cells that are more resistant to stresses and disease conditions express genes for energy generation, nervous system development, and synaptic transmission at higher levels than those found in vulnerable neurons. The molecular pathways identified above and described in this chapter may eventually determine the targets for future therapeutic interventions for neurodegenerative diseases.
James W. Fawcett, Anne E. Rosser, and Stephen B. Dunnett
- Published in print:
- 2002
- Published Online:
- March 2012
- ISBN:
- 9780198523376
- eISBN:
- 9780191724534
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198523376.003.0006
- Subject:
- Neuroscience, Techniques
Most dementias are associated with a widespread pattern of atrophy in the forebrain, which is most apparent as a reduction in the weight of the brain measured post-mortem. As the brain undergoes loss ...
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Most dementias are associated with a widespread pattern of atrophy in the forebrain, which is most apparent as a reduction in the weight of the brain measured post-mortem. As the brain undergoes loss of cells, there is a thinning of the neocortex, and an associated flattening of the sulci on the surface of the brain and the ventricles in its depths. Dementia can come about through a number of different causes. In a series of studies in the 1950s and 1960s, Sir Martin Roth and his colleagues at the University of Newcastle undertook a systematic evaluation of the nature of the post-mortem pathology in a large series of patients dying (both with and without dementia) in a psychogeriatric hospital. These studies highlighted the fact that the cognitive disturbances of senile dementia can be associated with a number of distinct patterns of neuropathology, associated with different causes and disease processes.Less
Most dementias are associated with a widespread pattern of atrophy in the forebrain, which is most apparent as a reduction in the weight of the brain measured post-mortem. As the brain undergoes loss of cells, there is a thinning of the neocortex, and an associated flattening of the sulci on the surface of the brain and the ventricles in its depths. Dementia can come about through a number of different causes. In a series of studies in the 1950s and 1960s, Sir Martin Roth and his colleagues at the University of Newcastle undertook a systematic evaluation of the nature of the post-mortem pathology in a large series of patients dying (both with and without dementia) in a psychogeriatric hospital. These studies highlighted the fact that the cognitive disturbances of senile dementia can be associated with a number of distinct patterns of neuropathology, associated with different causes and disease processes.
Zachary A. Miller and Bruce L. Miller
- Published in print:
- 2011
- Published Online:
- January 2012
- ISBN:
- 9780199732142
- eISBN:
- 9780199918485
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780199732142.003.0079
- Subject:
- Psychology, Cognitive Psychology
Philosophers have hypothesized that one of the defining characteristics of being human is the production and appreciation of art. Beginning in the early 20th century, observations following isolated ...
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Philosophers have hypothesized that one of the defining characteristics of being human is the production and appreciation of art. Beginning in the early 20th century, observations following isolated strokes or brain surgery supported theories that artistic behaviors were mediated by complex interactions between the frontal and parietal lobes. While these findings were instrumental in establishing the foundations of functional neuroanatomy, the association between artistic behavior and brain circuitry remained crude at best. With advances in molecular biology, improved clinical measures, and sophisticated neuroimaging techniques, the study of neurodegenerative disease has become a powerful method for investigating behavior. Already, the study of neurodegenerative disease has yielded significant insights into the process of artistic behavior. In this chapter we present an overview of visuospatial functional anatomy, how neurodegenerative disease affects artistic sensibility, and detail the paradoxical functional facilitation of artistic ability in patients diagnosed with frontotemporal dementia. Specifically, the behaviors we document developed in the setting of profound and isolated speech dysfunction, a condition known as primary progressive aphasia. Based on the specific aphasia subtype - semantic dementia versus progressive nonfluent aphasia - the quality of these patient’s artistic interest appeared to differ. Taken together, we believe that patients suffering from the language variants of frontotemporal lobar degeneration are uniquely positioned to provide the greatest insights yet into aesthetic choice and artistic creation.Less
Philosophers have hypothesized that one of the defining characteristics of being human is the production and appreciation of art. Beginning in the early 20th century, observations following isolated strokes or brain surgery supported theories that artistic behaviors were mediated by complex interactions between the frontal and parietal lobes. While these findings were instrumental in establishing the foundations of functional neuroanatomy, the association between artistic behavior and brain circuitry remained crude at best. With advances in molecular biology, improved clinical measures, and sophisticated neuroimaging techniques, the study of neurodegenerative disease has become a powerful method for investigating behavior. Already, the study of neurodegenerative disease has yielded significant insights into the process of artistic behavior. In this chapter we present an overview of visuospatial functional anatomy, how neurodegenerative disease affects artistic sensibility, and detail the paradoxical functional facilitation of artistic ability in patients diagnosed with frontotemporal dementia. Specifically, the behaviors we document developed in the setting of profound and isolated speech dysfunction, a condition known as primary progressive aphasia. Based on the specific aphasia subtype - semantic dementia versus progressive nonfluent aphasia - the quality of these patient’s artistic interest appeared to differ. Taken together, we believe that patients suffering from the language variants of frontotemporal lobar degeneration are uniquely positioned to provide the greatest insights yet into aesthetic choice and artistic creation.
Adriana Simon Coitinho and Glaucia N. M. Hajj
- Published in print:
- 2009
- Published Online:
- January 2010
- ISBN:
- 9780195326697
- eISBN:
- 9780199864874
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195326697.003.0001
- Subject:
- Neuroscience, Molecular and Cellular Systems
Prions are infectious particles composed only of proteins. Their importance resides in the concept that information transmission between two organisms can be devoid of nucleic acid. Prions are also ...
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Prions are infectious particles composed only of proteins. Their importance resides in the concept that information transmission between two organisms can be devoid of nucleic acid. Prions are also well-known as the etiological agents of several neurodegenerative diseases of animals and humans called transmissible spongiform encephalopathies (TSEs). Literature on prion-associated diseases, transmission mechanisms, and the related normal isoform of the protein has grown impressively in the last few years, making it very difficult to cover all aspects of prion in depth in this chapter. This chapter therefore focuses on the history, symptoms, mechanisms of transmission and diagnosis of prion diseases, and currently proposed therapies. The roles of the normal isoform of the prion in physiology are also discussed, along with neuroinvasion and pathogenicity.Less
Prions are infectious particles composed only of proteins. Their importance resides in the concept that information transmission between two organisms can be devoid of nucleic acid. Prions are also well-known as the etiological agents of several neurodegenerative diseases of animals and humans called transmissible spongiform encephalopathies (TSEs). Literature on prion-associated diseases, transmission mechanisms, and the related normal isoform of the protein has grown impressively in the last few years, making it very difficult to cover all aspects of prion in depth in this chapter. This chapter therefore focuses on the history, symptoms, mechanisms of transmission and diagnosis of prion diseases, and currently proposed therapies. The roles of the normal isoform of the prion in physiology are also discussed, along with neuroinvasion and pathogenicity.
Nancy J. Rothwell (ed.)
- Published in print:
- 1997
- Published Online:
- March 2012
- ISBN:
- 9781872748795
- eISBN:
- 9780191724381
- Item type:
- book
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9781872748795.001.0001
- Subject:
- Neuroscience, Disorders of the Nervous System
This new edition covers recent advances in understanding immunological and inflammatory responses in the nervous system, research driven by the potential to use knowledge of the molecules and ...
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This new edition covers recent advances in understanding immunological and inflammatory responses in the nervous system, research driven by the potential to use knowledge of the molecules and mechanisms involved to intervene in, and arrest, neurodegenerative disease processes. This book covers developmental aspects of immune/inflammatory responses in the CNS and basic aspects of glial function, as well as inflammatory mediators and their mechanisms of action, clinical importance, and sites of infection. There is also coverage of the major diseases of the CNS, including stroke, brain injury, multiple sclerosis, and Alzheimer's disease. Throughout, the focus is on the underlying basic neuroscience, clinical relevance and the potential for therapeutic interventions. This book aims to contribute to the understanding and improving of the diagnosis of neuroimmune diseases and determining therapeutic measures.Less
This new edition covers recent advances in understanding immunological and inflammatory responses in the nervous system, research driven by the potential to use knowledge of the molecules and mechanisms involved to intervene in, and arrest, neurodegenerative disease processes. This book covers developmental aspects of immune/inflammatory responses in the CNS and basic aspects of glial function, as well as inflammatory mediators and their mechanisms of action, clinical importance, and sites of infection. There is also coverage of the major diseases of the CNS, including stroke, brain injury, multiple sclerosis, and Alzheimer's disease. Throughout, the focus is on the underlying basic neuroscience, clinical relevance and the potential for therapeutic interventions. This book aims to contribute to the understanding and improving of the diagnosis of neuroimmune diseases and determining therapeutic measures.
Nancy Rothwell and Sarah Loddick (eds)
- Published in print:
- 2002
- Published Online:
- March 2012
- ISBN:
- 9780198509806
- eISBN:
- 9780191724596
- Item type:
- book
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198509806.001.0001
- Subject:
- Neuroscience, Disorders of the Nervous System
This new edition covers advances in understanding immunological and inflammatory responses in the nervous system, research driven by the potential to use knowledge of the molecules and mechanisms ...
More
This new edition covers advances in understanding immunological and inflammatory responses in the nervous system, research driven by the potential to use knowledge of the molecules and mechanisms involved to intervene in, and arrest, neurodegenerative disease processes. This book covers developmental aspects of immune/inflammatory responses in the central nervous system (CNS), basic aspects of glial function, as well as inflammatory mediators, their mechanisms of action, clinical importance, and sites of infection. There is also coverage of the major diseases of the CNS, including stroke, brain injury, multiple sclerosis, and Alzheimer's disease. Throughout, the focus is on the underlying basic neuroscience, clinical relevance, and the potential for therapeutic interventions. The book will be useful for improving the diagnosis of neuroimmune diseases and determining therapeutic measures.Less
This new edition covers advances in understanding immunological and inflammatory responses in the nervous system, research driven by the potential to use knowledge of the molecules and mechanisms involved to intervene in, and arrest, neurodegenerative disease processes. This book covers developmental aspects of immune/inflammatory responses in the central nervous system (CNS), basic aspects of glial function, as well as inflammatory mediators, their mechanisms of action, clinical importance, and sites of infection. There is also coverage of the major diseases of the CNS, including stroke, brain injury, multiple sclerosis, and Alzheimer's disease. Throughout, the focus is on the underlying basic neuroscience, clinical relevance, and the potential for therapeutic interventions. The book will be useful for improving the diagnosis of neuroimmune diseases and determining therapeutic measures.
Fliss Murtagh, Rachel Burman, and Polly Edmonds
- Published in print:
- 2005
- Published Online:
- November 2011
- ISBN:
- 9780198530039
- eISBN:
- 9780191730450
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198530039.003.0006
- Subject:
- Palliative Care, Patient Care and End-of-Life Decision Making, Pain Management and Palliative Pharmacology
While some aspects of breathlessness in neurological disease are common to various neurological diseases, some aspects are specific to particular ones. This chapter therefore addresses the ...
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While some aspects of breathlessness in neurological disease are common to various neurological diseases, some aspects are specific to particular ones. This chapter therefore addresses the pathophysiology of breathlessness in neurological diseases and considers the general management strategies for this symptom in this group of diseases. It also discusses the causes of shortness of breath in specific conditions such as Parkinson's disease, dementia, neurodegenerative diseases, and stroke. The chapter furthermore includes a discussion on the ethical considerations of palliative management and terminal sedation in patients with neurological disease or advanced disease.Less
While some aspects of breathlessness in neurological disease are common to various neurological diseases, some aspects are specific to particular ones. This chapter therefore addresses the pathophysiology of breathlessness in neurological diseases and considers the general management strategies for this symptom in this group of diseases. It also discusses the causes of shortness of breath in specific conditions such as Parkinson's disease, dementia, neurodegenerative diseases, and stroke. The chapter furthermore includes a discussion on the ethical considerations of palliative management and terminal sedation in patients with neurological disease or advanced disease.
Roger Dixon, Lars Backman, and Lars-Goran Nilsson (eds)
- Published in print:
- 2004
- Published Online:
- March 2012
- ISBN:
- 9780198525691
- eISBN:
- 9780191689369
- Item type:
- book
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198525691.001.0001
- Subject:
- Psychology, Cognitive Psychology
With an ever increasing population of aging people in the western world, it is more crucial than ever that we try to understand how and why cognitive competence breaks down with advancing age; why do ...
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With an ever increasing population of aging people in the western world, it is more crucial than ever that we try to understand how and why cognitive competence breaks down with advancing age; why do some people follow normal patterns of cognitive change, while others follow a path of progressive decline, with neurodegenerative diseases such as Alzheimer’s. What can be done to prevent cognitive decline or — to avoid neurodegenerative diseases? The answers, if they come, will not emerge from research within one discipline, but from work being done across a range of scientific and medical specialities. This book delves into the subjects of cognitive aging, neuroscience, pharmacology, health, genetics, sensory biology, and epidemiology. This book is about new frontiers rather than past research and accomplishments. Recently cognitive aging research has taken several new directions, linking with, and benefiting from, rapid technological and theoretical advances in these neighbouring disciplines. This book provides unique interdisciplinary coverage of the topic.Less
With an ever increasing population of aging people in the western world, it is more crucial than ever that we try to understand how and why cognitive competence breaks down with advancing age; why do some people follow normal patterns of cognitive change, while others follow a path of progressive decline, with neurodegenerative diseases such as Alzheimer’s. What can be done to prevent cognitive decline or — to avoid neurodegenerative diseases? The answers, if they come, will not emerge from research within one discipline, but from work being done across a range of scientific and medical specialities. This book delves into the subjects of cognitive aging, neuroscience, pharmacology, health, genetics, sensory biology, and epidemiology. This book is about new frontiers rather than past research and accomplishments. Recently cognitive aging research has taken several new directions, linking with, and benefiting from, rapid technological and theoretical advances in these neighbouring disciplines. This book provides unique interdisciplinary coverage of the topic.
