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1. |
Title Page / Table of Contents |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 125-128
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ISSN:1420-8008
DOI:10.1159/000106707
出版商:S. Karger AG
年代:1994
数据来源: Karger
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2. |
Introduction |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 129-129
L.A. Carlson,
C.G. Gottfries,
B. Winblad,
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PDF (176KB)
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ISSN:1420-8008
DOI:10.1159/000106708
出版商:S. Karger AG
年代:1994
数据来源: Karger
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3. |
Vascular Dementia: A Radical Redefinition |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 130-132
Vladimir Hachinski,
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摘要:
‘Vascular dementia’ may be the leading cause of cognitive impairment in the world, yet there is little agreement as to what this concept encompasses or how it is defined. A critical review reaches the conclusion that the concept of ‘vascular dementia’ has become obsolete. ‘Vascular’ is too generic, and fails to identify specific etiologies which may be subject to current and future preventive measures. ''Dementia'' identifies patients too late to do much about their problem. An alternate approach is suggested. Identify patients across the whole spectrum of vascular cognitive impairment, from high risk with no deficit (''brain-at-risk stage'') to full-blown dementia. Describe the cognitive impairment in terms of standardized neuropsychological measures, and relate the dementia to the specific vascular cause, so that the appropriate preventive measures can be
ISSN:1420-8008
DOI:10.1159/000106709
出版商:S. Karger AG
年代:1994
数据来源: Karger
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4. |
How Does Cerebrovascular Disease Cause Dementia? |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 133-136
Michael D. O'Brien,
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摘要:
There are several factors that might be important in the development of dementia due to cerebrovascular disease. These include the volume of infarcted brain, the bilaterality and symmetry of lesions, the strategic location of small lesions, the number of lesions, the extent and density of white matter lesions and the coexistence of other pathologies, particularly Alzheimer''s disease. No one factor is solely related to dementia and in most patients several of these factors combine to exceed the critical threshold for normal cognition. It is the extent of the disease which determines the development of dementia, rather than its etiology. Conversely, the possibility of treatment depends more on the etiology of the vascular disease than on the extent.
ISSN:1420-8008
DOI:10.1159/000106710
出版商:S. Karger AG
年代:1994
数据来源: Karger
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5. |
Risk Factors for Vascular Dementia: A Review |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 137-144
Ingmar Skoog,
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摘要:
In recent years, interest in vascular causes of dementia has increased and it has been proposed that vascular dementia (VAD) may be more common than previously supposed. This may have important implications, because VAD at present may be more amenable to prevention and treatment than Alzheimer''s disease (AD). Several vascular factors have been related to cognitive decline and dementia in the elderly, including stroke and white matter disease. However, while numerous case-control studies have been concerned with the risk factors for AD, studies on risk factors for VADs are rare. The problems inherent in the diagnostic criteria make it difficult to interpret the results from the few studies that have been performed. Generally, risk factors for multi-infarct dementia are supposed to be the same as those for stroke, and include hypertension, diabetes mellitus, advanced age, male sex, smoking and cardiac diseases. White matter dementia has mainly been related to hypertension. Recent research suggests that vascular factors may also be important in AD, especially in the late-onset type. In stroke patients, dementia has been associated with higher age, less formal education, cerebral atrophy, left-sided or bilateral infarcts, volume of macroscopic infarcts, bilateral symptoms, previous stroke and white matter lesions. The pathogenetic mechanism through which these factors cause dementia is still not clear. Furthermore, it is not known if risk factors for VAD differ from those found in stroke patients. There is now an urgent need for further research on risk factors for VAD and on factors related to dementia in subjects with cerebrovascular disorders.
ISSN:1420-8008
DOI:10.1159/000106711
出版商:S. Karger AG
年代:1994
数据来源: Karger
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6. |
Pathology and Pathophysiology of Cerebrovascular Dementia: Pure Subgroups of Obstructive and Hypoperfusive Etiology |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 145-147
Arne Brun,
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摘要:
The brains of 175 consecutive autopsy cases of dementia, clinically studied prospectively, were analyzed pathoanatomically with regard to type, size and site of lesions. Pure groups of vascular dementia caused by large or small vessel disease and by hypoperfusion could be defined. The infarcts were either complete with a more or less pronounced incomplete perifocal component or of an incomplete type only. Incomplete infarction appears to be an important and yet little appreciated cause of brain dysfunction. These groups could be used as a basis for a pathoanatomical classification of vascular dementias. Vascular dementia is much more common than generally assumed.
ISSN:1420-8008
DOI:10.1159/000106712
出版商:S. Karger AG
年代:1994
数据来源: Karger
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7. |
White Matter Changes: Neurobehavioral Manifestations of Binswanger's Disease and Clinical Correlates in Alzheimer's Disease |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 148-152
David A. Bennett,
David W. Gilley,
Sarha Lee,
Elizabeth J. Cochran,
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摘要:
Although white matter lesions (WMLs) are among the most common structural neuroimaging changes found on computed tomography and magnetic resonance imaging of older persons with dementia, their presence should not be misconstrued as proof that vascular disease is causing or contributing to the dementia. We report the results of several studies examining the neurobehavioral manifestations of persons meeting explicit operational criteria for Binswanger''s disease (BD) and the clinical correlates of white matter changes in persons with autopsy-proven Alzheimer''s disease (AD). The findings suggest that relative to persons with AD of comparable dementia severity, persons with BD have less profound impairments in episodic memory, more depressive symptomatology and a more variable rate of cognitive decline; among persons with AD, some WMLs are associated with incontinence and gait disturbance, but they do not appear to contribute to dementia severity.
ISSN:1420-8008
DOI:10.1159/000106713
出版商:S. Karger AG
年代:1994
数据来源: Karger
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8. |
Structural and Vasoactive Factors Influencing Intracerebral Arterioles in Cases of Vascular Dementia and Other Cerebrovascular Disease: A Review |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 153-162
Wei Wei Zhang,
Tichomir Badonic,
Anders Höög,
Ming Hui Jiang,
Kuo Chun Ma,
Jing Xiao Nie,
Yngve Olsson,
Patrick Sourander,
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摘要:
The condition of the brain parenchyma in cases of vascular dementia and other cerebrovascular conditions may be influenced by structural and functional changes of the terminal intracerebral blood vessels. Arterioles can develop obliterative lesions, capillaries and postcapillary venules can be altered, causing edema. The first part of this review is focused on expression of different types of collagens and other components of the extracellular matrix in intracerebral arterioles. The changes present in hereditary multi-infarct disease of the brain are compared with those occurring in the Binswanger type of encephalopathy and cases presenting hyalinosis of intracerebral vessels. Deposition of collagens in degenerated parts of the media and adventitia of the arterioles may contribute to impaired blood flow regulation in the brain parenchyma. Fibrillary collagens and basal laminae are probably the most important components of the hyaline material in vessels showing ‘hyalinosis’. The second part of our review concerns the possibility that the vasoactive peptide, endothelin-1, released from reactive astrocytes, can influence the function of intracerebral arterioles. Normal astrocytes do not show endothelin-1-like immunoreactivity, but in cases of infarcts, lacunes, hereditary multi-infarct disease, Binswanger''s encephalopathy and Alzheimer''s disease numerous reactive astrocytes express such immunoreactivity. If endothelin-1 is produced and released from reactive astrocytes it may reach intracerebral arterioles and induce long-lasting vasoconstriction. Endothelin-1 is the most powerful vasoconstrictor peptide known to date and has mitogenic capacity. It may promote cellular mechanisms leading to astrocytic gliosis and neovascularizat
ISSN:1420-8008
DOI:10.1159/000106714
出版商:S. Karger AG
年代:1994
数据来源: Karger
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9. |
The Neurochemistry of Vascular Dementia |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 163-167
C.G. Gottfries,
K. Blennow,
I. Karlsson,
A. Wallin,
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摘要:
Vascular dementia (VAD) is cognitive impairment caused by changes in the blood circulation of the brain. It is not synonymous with multi-infarct dementia. The latter is a subgroup of VAD. Neurochemical investigations of noninfarcted brain tissue from patients with VAD show general changes in VAD brains. The serotonin metabolism is severely reduced and so is the activity of choline acetyltransferase. Monamine oxidase B is significantly increased in the white matter. A severe decrease in myelin components indicates white matter disturbances of such a degree that they must be considered to be of pathogenetic importance. The levels of some neuropeptides in the hypothalamus are increased. This is a finding which is in agreement with clinical findings of a high activity in the hypothalamic-pituitary-adrenal axis in patients with VAD. This high activity is possibly due to a loss of serotonergic inhibitory tone on the hypothalamus in VAD brains.
ISSN:1420-8008
DOI:10.1159/000106715
出版商:S. Karger AG
年代:1994
数据来源: Karger
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10. |
Cerebral Ischemia Induces Alterations in Tau and Ubiquitin Proteins |
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Dementia and Geriatric Cognitive Disorders,
Volume 5,
Issue 3-4,
1994,
Page 168-173
D. Dewar,
D.I. Graham,
G.M. Teasdale,
J. McCulloch,
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摘要:
Excessive stimulation of glutamate receptors and elevation of intracellular calcium levels initiate the neurodegenerative process resulting from cerebral ischemia. However, the subsequent cascade of molecular changes which are of pathogenic significance is less well understood. Breakdown of the cytoskeleton may be involved in the progression from compromise of neuronal viability to irreversible damage. Alteration of the microtubule-associated protein tau, as reflected by increased Alz-50 immunoreactivity, was induced by permanent focal cerebral ischemia in vivo but only in a proportion of neurones. Alz-50 immunoreactive neurones did not exhibit the characteristics of irreversible ischemic cell damage. Increased immunoreactivity to the stress response protein ubiquitin was also induced by ischemia in a proportion of neurones. Both proteins are components of neurofibrillary tangles in Alzheimer''s disease. Alterations of the microtubule-associated protein tau may be a feature of the early stages of the ischemia-induced degeneration and the ubiquitin response may be an attempt by compromised neurones to deal with the presence of abnormal proteins.
ISSN:1420-8008
DOI:10.1159/000106716
出版商:S. Karger AG
年代:1994
数据来源: Karger
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