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Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease
by
Morris, John C.
, Price, Joseph L.
in
Aged
/ Aging
/ Aging - pathology
/ Alzheimer Disease - pathology
/ Alzheimer Disease - physiopathology
/ Alzheimer Disease - psychology
/ Alzheimer's disease
/ Cerebral Cortex - pathology
/ Cerebral Cortex - physiopathology
/ Diagnosis, Differential
/ Disease Progression
/ Humans
/ Middle Aged
/ Neurofibrillary Tangles - pathology
/ Plaque, Amyloid - pathology
2001
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Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease
by
Morris, John C.
, Price, Joseph L.
in
Aged
/ Aging
/ Aging - pathology
/ Alzheimer Disease - pathology
/ Alzheimer Disease - physiopathology
/ Alzheimer Disease - psychology
/ Alzheimer's disease
/ Cerebral Cortex - pathology
/ Cerebral Cortex - physiopathology
/ Diagnosis, Differential
/ Disease Progression
/ Humans
/ Middle Aged
/ Neurofibrillary Tangles - pathology
/ Plaque, Amyloid - pathology
2001
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Do you wish to request the book?
Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease
by
Morris, John C.
, Price, Joseph L.
in
Aged
/ Aging
/ Aging - pathology
/ Alzheimer Disease - pathology
/ Alzheimer Disease - physiopathology
/ Alzheimer Disease - psychology
/ Alzheimer's disease
/ Cerebral Cortex - pathology
/ Cerebral Cortex - physiopathology
/ Diagnosis, Differential
/ Disease Progression
/ Humans
/ Middle Aged
/ Neurofibrillary Tangles - pathology
/ Plaque, Amyloid - pathology
2001
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Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease
Journal Article
Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease
2001
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Overview
The results of studies from the Washington University Alzheimer Disease (AD) Research Center and those from other centers and investigators regarding the neuropathologic correlates of normal aging and early-stage AD are reviewed. We conclude that widespread amyloid plaques in the neocortex best distinguishes very early stage AD, including \"MCI\" stage, and preclinical stages, from healthy brain aging. Other AD lesions, including increased formation of neurofibrillary tangles and neuronal degeneration appear to result from the amyloid-initiated pathologic process, although they may have a more immediate effect on expression and severity of dementia. These data provide strong support for anti-amyloid intervention as a preventive therapy for AD. It is now critical to develop methods to detect preclinical AD during life.
Publisher
Springer Nature B.V
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