John Bayley
- Published in print:
- 2011
- Published Online:
- September 2012
- ISBN:
- 9780199289905
- eISBN:
- 9780191728471
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780199289905.003.0003
- Subject:
- Philosophy, History of Philosophy, Moral Philosophy
This chapter presents a short memoir of Iris Murdoch as lecturer and traveller—and her relations, among other things, to God, to power (and Elias Canetti), and to what Philippa Foot has called ...
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This chapter presents a short memoir of Iris Murdoch as lecturer and traveller—and her relations, among other things, to God, to power (and Elias Canetti), and to what Philippa Foot has called “Natural Goodness”.Less
This chapter presents a short memoir of Iris Murdoch as lecturer and traveller—and her relations, among other things, to God, to power (and Elias Canetti), and to what Philippa Foot has called “Natural Goodness”.
Margaret Lock
- Published in print:
- 2013
- Published Online:
- October 2017
- ISBN:
- 9780691149783
- eISBN:
- 9781400848461
- Item type:
- book
- Publisher:
- Princeton University Press
- DOI:
- 10.23943/princeton/9780691149783.001.0001
- Subject:
- Anthropology, Social and Cultural Anthropology
Due to rapidly aging populations, the number of people worldwide experiencing dementia is increasing, and the projections are grim. Despite billions of dollars invested in medical research, no ...
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Due to rapidly aging populations, the number of people worldwide experiencing dementia is increasing, and the projections are grim. Despite billions of dollars invested in medical research, no effective treatment has been discovered for Alzheimer's disease, the most common form of dementia. This book exposes the predicaments embedded in current efforts to slow down or halt Alzheimer's disease through early detection of pre-symptomatic biological changes in healthy individuals. Based on a meticulous account of the history of Alzheimer's disease and extensive in-depth interviews, the book highlights the limitations and the dissent associated with biomarker detection. It argues that basic research must continue, but should be complemented by a public health approach to prevention that is economically feasible, more humane, and much more effective globally than one exclusively focused on an increasingly harried search for a cure.Less
Due to rapidly aging populations, the number of people worldwide experiencing dementia is increasing, and the projections are grim. Despite billions of dollars invested in medical research, no effective treatment has been discovered for Alzheimer's disease, the most common form of dementia. This book exposes the predicaments embedded in current efforts to slow down or halt Alzheimer's disease through early detection of pre-symptomatic biological changes in healthy individuals. Based on a meticulous account of the history of Alzheimer's disease and extensive in-depth interviews, the book highlights the limitations and the dissent associated with biomarker detection. It argues that basic research must continue, but should be complemented by a public health approach to prevention that is economically feasible, more humane, and much more effective globally than one exclusively focused on an increasingly harried search for a cure.
Gary L. Wenk
- Published in print:
- 2010
- Published Online:
- September 2010
- ISBN:
- 9780195388541
- eISBN:
- 9780199863587
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195388541.003.0002
- Subject:
- Neuroscience, Behavioral Neuroscience, Neuroendocrine and Autonomic
The actions of the neurotransmitter acetylcholine influence the function of many brain regions. Within these regions, acetylcholine allows you to learn and remember, to regulate your attention and ...
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The actions of the neurotransmitter acetylcholine influence the function of many brain regions. Within these regions, acetylcholine allows you to learn and remember, to regulate your attention and mood, and to control how well you can move. Thus, anything that affects the function of acetylcholine neurons has the potential to affect all of these brain and body functions. In the brains of people with Alzheimer's disease acetylcholine neurons very slowly die. Because of this these people have difficulty paying attention or remembering almost everything. Blocking the actions of acetylcholine can have a wide range of consequences, a fact that was recognized by Homer, voodoo priests, and witches during the darks ages. Various nuts, mushrooms, and plants, such as the infamous tobacco leaf, contain chemicals that can either mimic or antagonize the actions of acetylcholine in the brain; the consequences of which include feelings of happiness, relaxation, and well-being as well as dramatic hallucinations that lead to the adventures of Alice in Wonderland.Less
The actions of the neurotransmitter acetylcholine influence the function of many brain regions. Within these regions, acetylcholine allows you to learn and remember, to regulate your attention and mood, and to control how well you can move. Thus, anything that affects the function of acetylcholine neurons has the potential to affect all of these brain and body functions. In the brains of people with Alzheimer's disease acetylcholine neurons very slowly die. Because of this these people have difficulty paying attention or remembering almost everything. Blocking the actions of acetylcholine can have a wide range of consequences, a fact that was recognized by Homer, voodoo priests, and witches during the darks ages. Various nuts, mushrooms, and plants, such as the infamous tobacco leaf, contain chemicals that can either mimic or antagonize the actions of acetylcholine in the brain; the consequences of which include feelings of happiness, relaxation, and well-being as well as dramatic hallucinations that lead to the adventures of Alice in Wonderland.
Gary L. Wenk
- Published in print:
- 2010
- Published Online:
- September 2010
- ISBN:
- 9780195388541
- eISBN:
- 9780199863587
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195388541.003.0009
- Subject:
- Neuroscience, Behavioral Neuroscience, Neuroendocrine and Autonomic
No drugs or nutrients are currently available that can reverse the primary cause of cognitive decline: normal aging. Also, it is currently impossible to enhance the function of a normal brain. These ...
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No drugs or nutrients are currently available that can reverse the primary cause of cognitive decline: normal aging. Also, it is currently impossible to enhance the function of a normal brain. These facts have not deterred con artists from placing numerous advertisements on the Internet that claim their products are effective brain boosters or cognition enhancers. In general, these products take advantage of the ability of stimulants to enhance performance. The classic brain stimulants such as coffee, amphetamine, or nicotine, might improve performance, but they do not raise one's IQ score and they do not stop age-related cognitive decline. Overall, the best way to slow the process of aging in your brain and body is to eat less food. A lot less food! Also, stop wasting money on drugs with benefits that are too good to be true: they will not make you wiser or healthier, only poorer.Less
No drugs or nutrients are currently available that can reverse the primary cause of cognitive decline: normal aging. Also, it is currently impossible to enhance the function of a normal brain. These facts have not deterred con artists from placing numerous advertisements on the Internet that claim their products are effective brain boosters or cognition enhancers. In general, these products take advantage of the ability of stimulants to enhance performance. The classic brain stimulants such as coffee, amphetamine, or nicotine, might improve performance, but they do not raise one's IQ score and they do not stop age-related cognitive decline. Overall, the best way to slow the process of aging in your brain and body is to eat less food. A lot less food! Also, stop wasting money on drugs with benefits that are too good to be true: they will not make you wiser or healthier, only poorer.
Rachel Mistur, Lisa Mosconi, Remigiusz Switalski, Susan De Santi, Yi Li, Lidia Glodzik, Miroslaw Brys, Wai Tsui, Henry Rusinek, and Mony J. de Leon
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0011
- Subject:
- Neuroscience, Techniques, Development
Reductions in the cerebral metabolic rate of glucose (CMRglc), a measure of neuronal function, have proven to be a promising tool in the early diagnosis of Alzheimer's disease (AD). FDG-PET imaging ...
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Reductions in the cerebral metabolic rate of glucose (CMRglc), a measure of neuronal function, have proven to be a promising tool in the early diagnosis of Alzheimer's disease (AD). FDG-PET imaging demonstrates progressive CMRglc reductions in AD patients, the extent and topography of which correlate with symptom severity. There is increasing evidence that hypometabolism appears during the preclinical stages of AD and can predict decline years before the onset of symptoms. This chapter provides an overview of FDG-PET results in individuals at risk for developing dementia, including presymptomatic individuals carrying mutations responsible for early-onset familial AD, patients with mild cognitive impairment (MCI), nondemented carriers of the Apolipoprotein E (ApoE) e4 allele, cognitively normal subjects with a family history of AD, subjects with subjective memory complaints, and the normal elderly followed longitudinally until they expressed the clinical symptoms of AD. Finally, this chapter discusses the potential to combine different PET tracers and cerebrospinal fluid (CSF) markers of pathology to improve the early detection of AD.Less
Reductions in the cerebral metabolic rate of glucose (CMRglc), a measure of neuronal function, have proven to be a promising tool in the early diagnosis of Alzheimer's disease (AD). FDG-PET imaging demonstrates progressive CMRglc reductions in AD patients, the extent and topography of which correlate with symptom severity. There is increasing evidence that hypometabolism appears during the preclinical stages of AD and can predict decline years before the onset of symptoms. This chapter provides an overview of FDG-PET results in individuals at risk for developing dementia, including presymptomatic individuals carrying mutations responsible for early-onset familial AD, patients with mild cognitive impairment (MCI), nondemented carriers of the Apolipoprotein E (ApoE) e4 allele, cognitively normal subjects with a family history of AD, subjects with subjective memory complaints, and the normal elderly followed longitudinally until they expressed the clinical symptoms of AD. Finally, this chapter discusses the potential to combine different PET tracers and cerebrospinal fluid (CSF) markers of pathology to improve the early detection of AD.
Eric Salmon, Fabienne Collette, and Gaëtan Garraux
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0015
- Subject:
- Neuroscience, Techniques, Development
Functional neuroimaging in neurodegenerative dementias provides 3D representations of brain activity that are relatively characteristic of the underlying phenotypic distribution of cerebral lesions. ...
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Functional neuroimaging in neurodegenerative dementias provides 3D representations of brain activity that are relatively characteristic of the underlying phenotypic distribution of cerebral lesions. They are not specific for a given brain pathology and the heterogeneity of brain diseases must always be considered. However, when methodologies are optimized, the values for sensitivity, specificity, and early diagnostic accuracy approach 80%. A lot of studies have shown that Alzheimer's disease can be distinguished from depression, vascular dementia or frontotemporal dementia, and Lewy body dementia when two techniques are used. General recommendations are to rely on multiple key regions and to combine different neuroimaging techniques to make a differential diagnosis among dementias.Less
Functional neuroimaging in neurodegenerative dementias provides 3D representations of brain activity that are relatively characteristic of the underlying phenotypic distribution of cerebral lesions. They are not specific for a given brain pathology and the heterogeneity of brain diseases must always be considered. However, when methodologies are optimized, the values for sensitivity, specificity, and early diagnostic accuracy approach 80%. A lot of studies have shown that Alzheimer's disease can be distinguished from depression, vascular dementia or frontotemporal dementia, and Lewy body dementia when two techniques are used. General recommendations are to rely on multiple key regions and to combine different neuroimaging techniques to make a differential diagnosis among dementias.
António J. Bastos-Leite and Philip Scheltens
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0016
- Subject:
- Neuroscience, Techniques, Development
Magnetic resonance imaging (MRI) has opened up the way to diagnose dementia in vivo. It provides clear evidence for hippocampal atrophy in Alzheimer's disease (AD), lobar atrophy in frontotemporal ...
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Magnetic resonance imaging (MRI) has opened up the way to diagnose dementia in vivo. It provides clear evidence for hippocampal atrophy in Alzheimer's disease (AD), lobar atrophy in frontotemporal lobar degeneration (FTLD), vascular changes in VaD, and specific findings in some rare forms of dementia. In addition, the traditional role of excluding space-occupying lesions has been kept and the combination of both aspects has rendered MRI indispensable in the diagnostic work-up.Less
Magnetic resonance imaging (MRI) has opened up the way to diagnose dementia in vivo. It provides clear evidence for hippocampal atrophy in Alzheimer's disease (AD), lobar atrophy in frontotemporal lobar degeneration (FTLD), vascular changes in VaD, and specific findings in some rare forms of dementia. In addition, the traditional role of excluding space-occupying lesions has been kept and the combination of both aspects has rendered MRI indispensable in the diagnostic work-up.
Adriane Mayda, Mitsuhiro Yoshita, and Charles DeCarli
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0017
- Subject:
- Neuroscience, Techniques, Development
Both advancing age and cognitive impairment are associated with increased prevalence of various brain diseases, with Alzheimer's disease (AD) and cerebrovascular disease (CVD) being the most common. ...
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Both advancing age and cognitive impairment are associated with increased prevalence of various brain diseases, with Alzheimer's disease (AD) and cerebrovascular disease (CVD) being the most common. Abnormalities of cerebral white matter commonly seen on a magnetic resonance image (MRI) as white matter hyperintensities (WMH) are non-specific, but are increased with aging, CVD, and as a possible consequence of AD. In this chapter, we review current scientific evidence regarding the impact of white matter changes, particularly WMH, on cognition with aging and in the setting of cognitive impairment syndromes such as mild cognitive impairment (MCI) and AD.Less
Both advancing age and cognitive impairment are associated with increased prevalence of various brain diseases, with Alzheimer's disease (AD) and cerebrovascular disease (CVD) being the most common. Abnormalities of cerebral white matter commonly seen on a magnetic resonance image (MRI) as white matter hyperintensities (WMH) are non-specific, but are increased with aging, CVD, and as a possible consequence of AD. In this chapter, we review current scientific evidence regarding the impact of white matter changes, particularly WMH, on cognition with aging and in the setting of cognitive impairment syndromes such as mild cognitive impairment (MCI) and AD.
Frank Jessen and Harald Hampel
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0019
- Subject:
- Neuroscience, Techniques, Development
The rapid development of novel treatment targets for Alzheimer's disease (AD) requires tools to assess the effects of these treatments on disease progression. Structural neuroimaging with CCT and ...
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The rapid development of novel treatment targets for Alzheimer's disease (AD) requires tools to assess the effects of these treatments on disease progression. Structural neuroimaging with CCT and magnetic resonance imaging (MRI) has been extensively applied in patients with AD over the last two decades. Today longitudinal MRI is integrated in the majority of clinical trials with novel compounds that aim at modifying the disease process. This makes MRI one of the major surrogate marker candidates in AD. A surrogate marker according to the definition of the regulatory agencies must correlate with the disease process and with drug-induced modifications of the disease. Beyond this, effects on the surrogate marker need to predict future clinical outcomes. Brain volume measures obtained from structural imaging studies in AD reflect the underlying pathology and correlate with clinical symptoms cross-sectionally and longitudinally. The effects of drugs on brain volume measures and the prediction of clinical outcomes by brain volume changes, however, are not yet sufficiently defined.Less
The rapid development of novel treatment targets for Alzheimer's disease (AD) requires tools to assess the effects of these treatments on disease progression. Structural neuroimaging with CCT and magnetic resonance imaging (MRI) has been extensively applied in patients with AD over the last two decades. Today longitudinal MRI is integrated in the majority of clinical trials with novel compounds that aim at modifying the disease process. This makes MRI one of the major surrogate marker candidates in AD. A surrogate marker according to the definition of the regulatory agencies must correlate with the disease process and with drug-induced modifications of the disease. Beyond this, effects on the surrogate marker need to predict future clinical outcomes. Brain volume measures obtained from structural imaging studies in AD reflect the underlying pathology and correlate with clinical symptoms cross-sectionally and longitudinally. The effects of drugs on brain volume measures and the prediction of clinical outcomes by brain volume changes, however, are not yet sufficiently defined.
John Darrell, Van Horn, and Arthur W. Toga
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0021
- Subject:
- Neuroscience, Techniques, Development
Large-scale archives of primary neuroimaging data of older populations are an essential element for contemporary research into normal and disease processes associated with aging. In this chapter, we ...
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Large-scale archives of primary neuroimaging data of older populations are an essential element for contemporary research into normal and disease processes associated with aging. In this chapter, we describe the role of digital atlases of the human brain in aging research and how these resources are created, point to several such formal atlases that may be used for neuroimage data processing, as well as discuss why atlases require periodic revision. We also discuss neuroimaging data repositories related specifically to aging and to age-related disease, the role of databases in making inferences concerning functional activation, and their potential for data mining, meta-analysis, and model construction.Less
Large-scale archives of primary neuroimaging data of older populations are an essential element for contemporary research into normal and disease processes associated with aging. In this chapter, we describe the role of digital atlases of the human brain in aging research and how these resources are created, point to several such formal atlases that may be used for neuroimage data processing, as well as discuss why atlases require periodic revision. We also discuss neuroimaging data repositories related specifically to aging and to age-related disease, the role of databases in making inferences concerning functional activation, and their potential for data mining, meta-analysis, and model construction.
Yaakov Stern
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0006
- Subject:
- Neuroscience, Techniques, Development
The concept of reserve has been proposed to account for the disjunction between the degree of brain damage and its clinical outcome. After reviewing epidemiologic data supporting the concept of ...
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The concept of reserve has been proposed to account for the disjunction between the degree of brain damage and its clinical outcome. After reviewing epidemiologic data supporting the concept of cognitive reserve, this chapter focuses on methodologic approaches for imaging studies intended to delineate the neural underpinnings of cognitive reserve (CR). It suggests three interrelated questions that can guide this research: Do old and young individuals use the same or different networks to mediate task performance? If they use the same network, can CR be related to individual differences in network efficiency and capacity? If they use different networks, can CR be related to this compensatory activation? Finally it raises the possibility that CR might be mediated by a generalized network that is independent of the specific demands of the task at hand.Less
The concept of reserve has been proposed to account for the disjunction between the degree of brain damage and its clinical outcome. After reviewing epidemiologic data supporting the concept of cognitive reserve, this chapter focuses on methodologic approaches for imaging studies intended to delineate the neural underpinnings of cognitive reserve (CR). It suggests three interrelated questions that can guide this research: Do old and young individuals use the same or different networks to mediate task performance? If they use the same network, can CR be related to individual differences in network efficiency and capacity? If they use different networks, can CR be related to this compensatory activation? Finally it raises the possibility that CR might be mediated by a generalized network that is independent of the specific demands of the task at hand.
Susan Y. Bookheimer
- Published in print:
- 2009
- Published Online:
- February 2010
- ISBN:
- 9780195328875
- eISBN:
- 9780199864836
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195328875.003.0009
- Subject:
- Neuroscience, Techniques, Development
The pathological changes that give rise to Alzheimer's disease (AD) begin years and potentially decades before disease onset. This is well demonstrated using a range of in vivo imaging tools ...
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The pathological changes that give rise to Alzheimer's disease (AD) begin years and potentially decades before disease onset. This is well demonstrated using a range of in vivo imaging tools including PET, structural MRI, and functional MRI. In particular, individuals with a genetic risk for AD show similar PET and MRI abnormalities as do Alzheimer's subjects, though to a lesser extent. Studying subjects with a genetic risk for AD prior to the onset of clinically significant memory loss adds to our understanding of the pathological processes leading to AD and may distinguish between those likely to develop the disease and those experiencing normal age-related brain changes. This chapter reviews the major genetic risk factors for AD and discusses the range of imaging abnormalities associated with genetic risk and early manifestations of AD.Less
The pathological changes that give rise to Alzheimer's disease (AD) begin years and potentially decades before disease onset. This is well demonstrated using a range of in vivo imaging tools including PET, structural MRI, and functional MRI. In particular, individuals with a genetic risk for AD show similar PET and MRI abnormalities as do Alzheimer's subjects, though to a lesser extent. Studying subjects with a genetic risk for AD prior to the onset of clinically significant memory loss adds to our understanding of the pathological processes leading to AD and may distinguish between those likely to develop the disease and those experiencing normal age-related brain changes. This chapter reviews the major genetic risk factors for AD and discusses the range of imaging abnormalities associated with genetic risk and early manifestations of AD.
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.
Renée L. Beard
- Published in print:
- 2016
- Published Online:
- January 2017
- ISBN:
- 9781479800117
- eISBN:
- 9781479855377
- Item type:
- book
- Publisher:
- NYU Press
- DOI:
- 10.18574/nyu/9781479800117.001.0001
- Subject:
- Social Work, Health and Mental Health
Alzheimer’s is ubiquitous. Stories of the heart-wrenching drudgery of care giving, escalating incidence rates, and the new path to a cure just around the corner are everywhere. Yet we rarely see or ...
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Alzheimer’s is ubiquitous. Stories of the heart-wrenching drudgery of care giving, escalating incidence rates, and the new path to a cure just around the corner are everywhere. Yet we rarely see or hear from anyone actually living with AD. The negative portrayals, apocalyptic projections, and promise of cures in the mass media and medical outlets are grossly inaccurate. But they are also an assault on the identities of those with Alzheimer’s. Drawing on an 18-month ethnography observing cognitive evaluations and post-diagnosis interviews with nearly 100 forgetful individuals, this book aims to chip away at this pervasive and persistent destructive trend by revealing what life with memory loss is really like. While diagnosed seniors are ultimately socialized into medicalized interpretations of their forgetfulness, most participants achieve a graceful balance between accepting the medical label and resisting the social stigma that accompanies it. In contrast to what we are led to believe, people with early AD actively and deliberately navigate their lives. Interviews with specialty clinicians and staff from the Alzheimer’s Association reveal that a biomedical ethos generates tensions that constrain the roles older forgetful people can play within these settings. Clinicians and Association staff perpetuate “myths” about “self-loss,” “impending cures,” and the economic and emotional “burden” even if they do not personally believe them. Living with AD ultimately requires managing stigma and presumptions of incompetence in addition to the associated symptoms. Unfortunately, we, the well-meaning public, and not their dementia become the major barrier to a happy life for those affected.Less
Alzheimer’s is ubiquitous. Stories of the heart-wrenching drudgery of care giving, escalating incidence rates, and the new path to a cure just around the corner are everywhere. Yet we rarely see or hear from anyone actually living with AD. The negative portrayals, apocalyptic projections, and promise of cures in the mass media and medical outlets are grossly inaccurate. But they are also an assault on the identities of those with Alzheimer’s. Drawing on an 18-month ethnography observing cognitive evaluations and post-diagnosis interviews with nearly 100 forgetful individuals, this book aims to chip away at this pervasive and persistent destructive trend by revealing what life with memory loss is really like. While diagnosed seniors are ultimately socialized into medicalized interpretations of their forgetfulness, most participants achieve a graceful balance between accepting the medical label and resisting the social stigma that accompanies it. In contrast to what we are led to believe, people with early AD actively and deliberately navigate their lives. Interviews with specialty clinicians and staff from the Alzheimer’s Association reveal that a biomedical ethos generates tensions that constrain the roles older forgetful people can play within these settings. Clinicians and Association staff perpetuate “myths” about “self-loss,” “impending cures,” and the economic and emotional “burden” even if they do not personally believe them. Living with AD ultimately requires managing stigma and presumptions of incompetence in addition to the associated symptoms. Unfortunately, we, the well-meaning public, and not their dementia become the major barrier to a happy life for those affected.
Jens R. Nyengaard, Karl-Anton Dorph-Petersen, and Yong Tang
- Published in print:
- 2004
- Published Online:
- September 2009
- ISBN:
- 9780198505280
- eISBN:
- 9780191723766
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198505280.003.0006
- Subject:
- Neuroscience, Techniques
Significant disagreements exist among previous morphometric studies of synapse number in relation to memory deficits associated with aging and diseases such as Alzheimer's disease. There may be a ...
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Significant disagreements exist among previous morphometric studies of synapse number in relation to memory deficits associated with aging and diseases such as Alzheimer's disease. There may be a number of methodological reasons for these conflicting results including lack of unbiased sampling design; use of two-dimensional sampling and model-based methods; reporting of densities; and ignorance of postmortem changes. This chapter describes a design-based stereological approach that can overcome these problems.Less
Significant disagreements exist among previous morphometric studies of synapse number in relation to memory deficits associated with aging and diseases such as Alzheimer's disease. There may be a number of methodological reasons for these conflicting results including lack of unbiased sampling design; use of two-dimensional sampling and model-based methods; reporting of densities; and ignorance of postmortem changes. This chapter describes a design-based stereological approach that can overcome these problems.
Helmut Kettenmann and Bruce R. Ransom (eds)
- Published in print:
- 2004
- Published Online:
- May 2009
- ISBN:
- 9780195152227
- eISBN:
- 9780199865024
- Item type:
- book
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195152227.001.0001
- Subject:
- Neuroscience, Development, Disorders of the Nervous System
This book details the basic biology and function of glial cells. It covers the entire field of glial research from the basic molecular and cellular properties of these cells to their involvement in ...
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This book details the basic biology and function of glial cells. It covers the entire field of glial research from the basic molecular and cellular properties of these cells to their involvement in neurological diseases including stroke, Alzheimer's Disease, and multiple sclerosis. This edition includes new chapters on transmitter release by extocytosis from glia, glia derived stem cells, glia synaptic transmission, glia and axon guidance, an entirely new section on mechanisms of glial injury, and several new chapters on the roles of glia in different diseases. It covers the fields of neuroanatomy, neurochemistry, neurophysiology, molecular neurobiology, neurology, neurosurgery, psychiatry, neuropathology, neuro-oncology, and physiatry.Less
This book details the basic biology and function of glial cells. It covers the entire field of glial research from the basic molecular and cellular properties of these cells to their involvement in neurological diseases including stroke, Alzheimer's Disease, and multiple sclerosis. This edition includes new chapters on transmitter release by extocytosis from glia, glia derived stem cells, glia synaptic transmission, glia and axon guidance, an entirely new section on mechanisms of glial injury, and several new chapters on the roles of glia in different diseases. It covers the fields of neuroanatomy, neurochemistry, neurophysiology, molecular neurobiology, neurology, neurosurgery, psychiatry, neuropathology, neuro-oncology, and physiatry.
Fabrizio Benedetti
- Published in print:
- 2008
- Published Online:
- September 2009
- ISBN:
- 9780199559121
- eISBN:
- 9780191724022
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780199559121.003.0005
- Subject:
- Neuroscience, Molecular and Cellular Systems
In depression, a fluoxetine treatment and a placebo treatment affect similar brain regions. In addition, covert (unexpected) administration of anti-anxiety drugs is less effective than overt ...
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In depression, a fluoxetine treatment and a placebo treatment affect similar brain regions. In addition, covert (unexpected) administration of anti-anxiety drugs is less effective than overt (expected) administration, which indicates the key role of expectation in anti-anxiety therapy. In dementia, the disruption of prefrontal executive control in Alzheimer's disease may decrease the magnitude of placebo responses, and expectations appear to be particularly important when associated to the effects of drugs of abuse. In general, placebo effects appear to be powerful in psychotherapy and, interestingly, the brain areas involved in the psychotherapeutic outcome are different from those involved in the placebo effect, which suggests different underlying mechanisms.Less
In depression, a fluoxetine treatment and a placebo treatment affect similar brain regions. In addition, covert (unexpected) administration of anti-anxiety drugs is less effective than overt (expected) administration, which indicates the key role of expectation in anti-anxiety therapy. In dementia, the disruption of prefrontal executive control in Alzheimer's disease may decrease the magnitude of placebo responses, and expectations appear to be particularly important when associated to the effects of drugs of abuse. In general, placebo effects appear to be powerful in psychotherapy and, interestingly, the brain areas involved in the psychotherapeutic outcome are different from those involved in the placebo effect, which suggests different underlying mechanisms.
John Paul Eberhard
- Published in print:
- 2009
- Published Online:
- May 2009
- ISBN:
- 9780195331721
- eISBN:
- 9780199864058
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195331721.003.0005
- Subject:
- Neuroscience, Behavioral Neuroscience, Techniques
This chapter discusses the relationship between how memory helps to form the experiences we have of places and spaces. This includes special considerations in designing facilities for the aging ...
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This chapter discusses the relationship between how memory helps to form the experiences we have of places and spaces. This includes special considerations in designing facilities for the aging population, and those with Alzheimer's. A number of hypotheses are described that result from research in cognitive neuroscience applied to experiences with aging.Less
This chapter discusses the relationship between how memory helps to form the experiences we have of places and spaces. This includes special considerations in designing facilities for the aging population, and those with Alzheimer's. A number of hypotheses are described that result from research in cognitive neuroscience applied to experiences with aging.
Agnieszka Jaworska
- Published in print:
- 2004
- Published Online:
- September 2009
- ISBN:
- 9780198567219
- eISBN:
- 9780191724084
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198567219.003.0007
- Subject:
- Neuroscience, Behavioral Neuroscience
This chapter presents a case study that illustrates the interplay between ethical conceptual analysis and neuroscientific findings in the resolution of moral dilemmas that arise in Alzheimer's ...
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This chapter presents a case study that illustrates the interplay between ethical conceptual analysis and neuroscientific findings in the resolution of moral dilemmas that arise in Alzheimer's disease. It defends the philosophical view that the immediate interests of an individual cannot be overridden as long as the individual possesses the capacity to value. In the context of each particular neurodegenerative disease, this recommendation must be guided by a scientifically informed assessment of when in the course of the disease the capacity to value could possibly be lost, and when it is likely to be retained. In the case of Alzheimer's disease, neuroscientific evidence indicates that the capacity to value is slowly and gradually weakened, and in some cases may not be completely lost until relatively far along in the disease's progression. Similar neuroethical analyses must be carried out for other diseases and disorders, and will probably yield different results.Less
This chapter presents a case study that illustrates the interplay between ethical conceptual analysis and neuroscientific findings in the resolution of moral dilemmas that arise in Alzheimer's disease. It defends the philosophical view that the immediate interests of an individual cannot be overridden as long as the individual possesses the capacity to value. In the context of each particular neurodegenerative disease, this recommendation must be guided by a scientifically informed assessment of when in the course of the disease the capacity to value could possibly be lost, and when it is likely to be retained. In the case of Alzheimer's disease, neuroscientific evidence indicates that the capacity to value is slowly and gradually weakened, and in some cases may not be completely lost until relatively far along in the disease's progression. Similar neuroethical analyses must be carried out for other diseases and disorders, and will probably yield different results.
Robert Veerhuis, Jeroen J.M. Hoozemans, Annachiara Cagnin, Piet Eikelenboom, and Richard B. Banati
- Published in print:
- 2004
- Published Online:
- May 2009
- ISBN:
- 9780195152227
- eISBN:
- 9780199865024
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195152227.003.0045
- Subject:
- Neuroscience, Development, Disorders of the Nervous System
This chapter focuses on the contribution of activated microglia to the progression of Alzheimer's disease (AD) at various stages of the pathological cascade. Clusters of activated microglia occur ...
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This chapter focuses on the contribution of activated microglia to the progression of Alzheimer's disease (AD) at various stages of the pathological cascade. Clusters of activated microglia occur only in complement-positive amyloidβ (Aβ) plaques, and effector functions of complement include the modulation of microglial activity in vitro. It addresses the question of whether microglia are detrimental or beneficial in AD pathogenesis, especially in relation to the presence and modulating activities of activation products of the complement system.Less
This chapter focuses on the contribution of activated microglia to the progression of Alzheimer's disease (AD) at various stages of the pathological cascade. Clusters of activated microglia occur only in complement-positive amyloidβ (Aβ) plaques, and effector functions of complement include the modulation of microglial activity in vitro. It addresses the question of whether microglia are detrimental or beneficial in AD pathogenesis, especially in relation to the presence and modulating activities of activation products of the complement system.
