Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph Method

A graph method was employed to analyse spatial neuronal patterns of pontine nuclei with ascending aminergic projections to the forebrain (nucleus centralis superior (NCS), raphes dorsalis (NRD) and locus coeruleus (LC)), in Alzheimer disease (AD), Huntington disease (HD), and vascular (VD) as well a...

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Main Authors: Yan Yang, Konrad Beyreuther, Horst P. Schmitt
Format: Article
Language:English
Published: Wiley 1999-01-01
Series:Analytical Cellular Pathology
Online Access:http://dx.doi.org/10.1155/1999/256382
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author Yan Yang
Konrad Beyreuther
Horst P. Schmitt
author_facet Yan Yang
Konrad Beyreuther
Horst P. Schmitt
author_sort Yan Yang
collection DOAJ
description A graph method was employed to analyse spatial neuronal patterns of pontine nuclei with ascending aminergic projections to the forebrain (nucleus centralis superior (NCS), raphes dorsalis (NRD) and locus coeruleus (LC)), in Alzheimer disease (AD), Huntington disease (HD), and vascular (VD) as well as “mixed‐type” (VA) dementia, compared with non‐demented controls (CO) and a small sample of brains from schizophrenics (“dementia praecox” (DP)). The quantitative evaluations by the “minimal spanning tree (MST)” were complemented by rough neurofibrillary tangle (NFT) counts and by semiquantitative immunohistochemical assessment of amyloid deposition, neuritic plaque formation, and cellular gliosis. The AD cases showed a significant decline of neuronal density in all nuclei examined, as compared with controls and DP. Neuronal loss was not significant in VD, while the mixed cases with both vascular and Alzheimer‐type pathology exhibited pronounced changes of neuronal density. Amyloid deposition occurred almost exclusively in AD and VA, as a rule, being of moderate degree, except for two presenile AD cases where it was marked. NFT were significantly increased in all nuclei in AD and in the VA cases, while they only occasionally appeared beyond age 55 in HD, DP and CO. The four HD cases showed in the NCS and NRD neuronal loss as severe as in AD. This neuronal loss implicates impairment of serotoninergic and noradrenergic neuromodulation as one basic mechanism promoting dementia in AD, VA and perhaps in HD.
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spelling doaj-art-d80cd450e570479c8e1a9a70f0b6af722025-08-20T03:23:52ZengWileyAnalytical Cellular Pathology0921-89121878-36511999-01-01193-412513810.1155/1999/256382Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph MethodYan Yang0Konrad Beyreuther1Horst P. Schmitt2Department of Neuropathology, University of Heidelberg, GermanyCenter for Molecular Biology, University of Heidelberg, GermanyDepartment of Neuropathology, University of Heidelberg, GermanyA graph method was employed to analyse spatial neuronal patterns of pontine nuclei with ascending aminergic projections to the forebrain (nucleus centralis superior (NCS), raphes dorsalis (NRD) and locus coeruleus (LC)), in Alzheimer disease (AD), Huntington disease (HD), and vascular (VD) as well as “mixed‐type” (VA) dementia, compared with non‐demented controls (CO) and a small sample of brains from schizophrenics (“dementia praecox” (DP)). The quantitative evaluations by the “minimal spanning tree (MST)” were complemented by rough neurofibrillary tangle (NFT) counts and by semiquantitative immunohistochemical assessment of amyloid deposition, neuritic plaque formation, and cellular gliosis. The AD cases showed a significant decline of neuronal density in all nuclei examined, as compared with controls and DP. Neuronal loss was not significant in VD, while the mixed cases with both vascular and Alzheimer‐type pathology exhibited pronounced changes of neuronal density. Amyloid deposition occurred almost exclusively in AD and VA, as a rule, being of moderate degree, except for two presenile AD cases where it was marked. NFT were significantly increased in all nuclei in AD and in the VA cases, while they only occasionally appeared beyond age 55 in HD, DP and CO. The four HD cases showed in the NCS and NRD neuronal loss as severe as in AD. This neuronal loss implicates impairment of serotoninergic and noradrenergic neuromodulation as one basic mechanism promoting dementia in AD, VA and perhaps in HD.http://dx.doi.org/10.1155/1999/256382
spellingShingle Yan Yang
Konrad Beyreuther
Horst P. Schmitt
Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph Method
Analytical Cellular Pathology
title Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph Method
title_full Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph Method
title_fullStr Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph Method
title_full_unstemmed Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph Method
title_short Spatial Analysis of the Neuronal Density of Aminergic Brainstem Nuclei in Primary Neurodegenerative and Vascular Dementia: A Comparative Immunocytochemical and Quantitative Study Using a Graph Method
title_sort spatial analysis of the neuronal density of aminergic brainstem nuclei in primary neurodegenerative and vascular dementia a comparative immunocytochemical and quantitative study using a graph method
url http://dx.doi.org/10.1155/1999/256382
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