摘要:

The raphe serotonin system was studied in patients with senile dementia of the Alzheimer type (SDAT) or with Parkinson's disease and compared with normal controls. Postmortem brain stems were cut in coronal sections from the red nucleus to the decussation of the pyramidal tract and were reacted with PH8 antibodies (PH8) which cross-react with tryptophan hydroxylase, the synthesizing enzyme for serotonin. In addition, adjacent sections were reacted with antibodies against tyrosine hydroxylase (TH) to detect catecholamine neurons in the locus ceruleus (LC), with monoamine oxidase (MAO) A antibodies, which labeled most neurons in the LC, or with MAO B antibodies which labeled a subpopulation of neurons in the raphe nuclei. A computer-based-image-analysis system was used for counting cell numbers and, in addition, 3-dimensional reconstructions of all raphe nuclei were made with this program. In SDAT, a loss of PH8-immunoreactive (PH8-i) neurons was detected in the raphe nuclei. This loss was most pronounced in the ventrolateral division of the dorsal raphe nucleus and was correlated to the cortical pathology and age of the patients. In addition the number of TH-immunoreactive (TH-i) neurons was reduced in the LC, with the rostral parts of the nucleus being the most severely affected. A comparison of the morphological changes in SDAT revealed that, in the same cases, the greatest neuronal alterations were found in the TH-i neurons in the LC rather than in the PH8-i neurons in the raphe nuclei. This reduction of TH-i neurons was matched by a loss of MAO A-immunoreactive (MAO A-i) neurons in the LC in SDAT. Similarly, the loss of PH8-i neurons was accompanied by a loss of MAO B-immunoreactive neurons in the raphe nuclei. In Parkinson's disease two different types of pathologies were found in the raphe nuclei; in one case with dementia a reduction of PH8-i neurons was seen in the ventrolateral and caudal subnucleus of the dorsal raphe. In two other cases with depression, severe cell loss was found in the raphe obscurus. All these Parkinson cases showed a considerable reduction of TH-i and MAO A-i neurons in the LC. Thus, the catecholamine lesions of the LC are more severe than the serotonin lesions of the raphe in SDAT patients and this was true of Parkinson patients as well. The relationships of catecholamine neurons with the MAO A enzyme localization and of serotonin neurons with the MAO B enzyme were also confirmed.

ISSN:1420-8008    

DOI:10.1159/000107026

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

The raphe serotonin system was studied in patients with senile dementia of the Alzheimer type (SDAT) or with Parkinson's disease and compared with normal controls. Postmortem brain stems were cut in coronal sections from the red nucleus to the decussation of the pyramidal tract and were reacted with PH8 antibodies (PH8) which cross-react with tryptophan hydroxylase, the synthesizing enzyme for serotonin. In addition, adjacent sections were reacted with antibodies against tyrosine hydroxylase (TH) to detect catecholamine neurons in the locus ceruleus (LC), with monoamine oxidase (MAO) A antibodies, which labeled most neurons in the LC, or with MAO B antibodies which labeled a subpopulation of neurons in the raphe nuclei. A computer-based-image-analysis system was used for counting cell numbers and, in addition, 3-dimensional reconstructions of all raphe nuclei were made with this program. In SDAT, a loss of PH8-immunoreactive (PH8-i) neurons was detected in the raphe nuclei. This loss was most pronounced in the ventrolateral division of the dorsal raphe nucleus and was correlated to the cortical pathology and age of the patients. In addition the number of TH-immunoreactive (TH-i) neurons was reduced in the LC, with the rostral parts of the nucleus being the most severely affected. A comparison of the morphological changes in SDAT revealed that, in the same cases, the greatest neuronal alterations were found in the TH-i neurons in the LC rather than in the PH8-i neurons in the raphe nuclei. This reduction of TH-i neurons was matched by a loss of MAO A-immunoreactive (MAO A-i) neurons in the LC in SDAT. Similarly, the loss of PH8-i neurons was accompanied by a loss of MAO B-immunoreactive neurons in the raphe nuclei. In Parkinson's disease two different types of pathologies were found in the raphe nuclei; in one case with dementia a reduction of PH8-i neurons was seen in the ventrolateral and caudal subnucleus of the dorsal raphe. In two other cases with depression, severe cell loss was found in the raphe obscurus. All these Parkinson cases showed a considerable reduction of TH-i and MAO A-i neurons in the LC. Thus, the catecholamine lesions of the LC are more severe than the serotonin lesions of the raphe in SDAT patients and this was true of Parkinson patients as well. The relationships of catecholamine neurons with the MAO A enzyme localization and of serotonin neurons with the MAO B enzyme were also confirmed.

ISSN:1420-8008    

DOI:10.1159/000315533

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

The raphe serotonin system was studied in patients with senile dementia of the Alzheimer type (SDAT) or with Parkinson's disease and compared with normal controls. Postmortem brain stems were cut in coronal sections from the red nucleus to the decussation of the pyramidal tract and were reacted with PH8 antibodies (PH8) which cross-react with tryptophan hydroxylase, the synthesizing enzyme for serotonin. In addition, adjacent sections were reacted with antibodies against tyrosine hydroxylase (TH) to detect catecholamine neurons in the locus ceruleus (LC), with monoamine oxidase (MAO) A antibodies, which labeled most neurons in the LC, or with MAO B antibodies which labeled a subpopulation of neurons in the raphe nuclei. A computer-based-image-analysis system was used for counting cell numbers and, in addition, 3-dimensional reconstructions of all raphe nuclei were made with this program. In SDAT, a loss of PH8-immunoreactive (PH8-i) neurons was detected in the raphe nuclei. This loss was most pronounced in the ventrolateral division of the dorsal raphe nucleus and was correlated to the cortical pathology and age of the patients. In addition the number of TH-immunoreactive (TH-i) neurons was reduced in the LC, with the rostral parts of the nucleus being the most severely affected. A comparison of the morphological changes in SDAT revealed that, in the same cases, the greatest neuronal alterations were found in the TH-i neurons in the LC rather than in the PH8-i neurons in the raphe nuclei. This reduction of TH-i neurons was matched by a loss of MAO A-immunoreactive (MAO A-i) neurons in the LC in SDAT. Similarly, the loss of PH8-i neurons was accompanied by a loss of MAO B-immunoreactive neurons in the raphe nuclei. In Parkinson's disease two different types of pathologies were found in the raphe nuclei; in one case with dementia a reduction of PH8-i neurons was seen in the ventrolateral and caudal subnucleus of the dorsal raphe. In two other cases with depression, severe cell loss was found in the raphe obscurus. All these Parkinson cases showed a considerable reduction of TH-i and MAO A-i neurons in the LC. Thus, the catecholamine lesions of the LC are more severe than the serotonin lesions of the raphe in SDAT patients and this was true of Parkinson patients as well. The relationships of catecholamine neurons with the MAO A enzyme localization and of serotonin neurons with the MAO B enzyme were also confirmed.

ISSN:1420-8008    

DOI:10.1159/000315534

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

The distribution of MAO A and B immunoreactivity was studied in the postmortem hippocampus, cerebellum and temporal cortex of normal controls and in patients with senile dementia of the Alzheimer type (SDAT). In normal control, neurons, glia cells, cellular processes and the walls of blood vessels were found to be MAO-immunoreactive (MAO-i). In the hippocampus of control cases, a subpopulation of small nonpyramidal neurons was MAO A-i. In addition, the somata of granule and pyramidal cells were densely surrounded by MAO B-i cellular processes. In the cerebellum, fine MAO A and B-i cellular processes and small varicosities were found in the cortex and in the dentate nucleus. In the normal temporal cortex, glia cells and cellular processes were MAO A-i and MAO B-i in all lamina. In SDAT, some changes of MAO immunoreactivity were encountered in all of the examined brain areas. The hippocampal MAO A-i neurons were well preserved in the dentate gyrus. However, large MAO B-i glia cells were found in the Ammon's horn, subiculum and entorhinal cortex, where they formed cell clusters or patches with increased MAO B immunoreactivity. Bodian-stained sections of the same hippocampi showed neuritic plaques in a similar number and regional distribution as the patches of increased MAO B immunoreactivity. In the cerebellar cortex of SDAT patients, plexuses of thick MAO A-i processes as well as patches of increased MAO B immunoreactivity with clusters of large MAO B-i glia cells were found. In the temporal cortex of SDAT cases, proliferation of large MAO B-i glia cells was detected. These glia cells formed numerous patches of increased MAO B immunoreactivity which were predominantly found in the upper cortical layers, similar to the distribution of neuritic plaques.

ISSN:1420-8008    

DOI:10.1159/000107027

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

The distribution of MAO A and B immunoreactivity was studied in the postmortem hippocampus, cerebellum and temporal cortex of normal controls and in patients with senile dementia of the Alzheimer type (SDAT). In normal control, neurons, glia cells, cellular processes and the walls of blood vessels were found to be MAO-immunoreactive (MAO-i). In the hippocampus of control cases, a subpopulation of small nonpyramidal neurons was MAO A-i. In addition, the somata of granule and pyramidal cells were densely surrounded by MAO B-i cellular processes. In the cerebellum, fine MAO A and B-i cellular processes and small varicosities were found in the cortex and in the dentate nucleus. In the normal temporal cortex, glia cells and cellular processes were MAO A-i and MAO B-i in all lamina. In SDAT, some changes of MAO immunoreactivity were encountered in all of the examined brain areas. The hippocampal MAO A-i neurons were well preserved in the dentate gyrus. However, large MAO B-i glia cells were found in the Ammon's horn, subiculum and entorhinal cortex, where they formed cell clusters or patches with increased MAO B immunoreactivity. Bodian-stained sections of the same hippocampi showed neuritic plaques in a similar number and regional distribution as the patches of increased MAO B immunoreactivity. In the cerebellar cortex of SDAT patients, plexuses of thick MAO A-i processes as well as patches of increased MAO B immunoreactivity with clusters of large MAO B-i glia cells were found. In the temporal cortex of SDAT cases, proliferation of large MAO B-i glia cells was detected. These glia cells formed numerous patches of increased MAO B immunoreactivity which were predominantly found in the upper cortical layers, similar to the distribution of neuritic plaques.

ISSN:1420-8008    

DOI:10.1159/000315540

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

The somatostatinergic innervation, and by comparison that of neuropeptide Y, was examined by immunocytochemistry, in the hippocampal formation of 6 patients with clinically and neuropathologically confirmed diagnosis of Alzheimer's disease (AD) and 4 matched controls. The quantitative assessment of the somatostatin and neuropeptide Y immunoreactive cell perikarya was conducted on regularly spaced sections covering the span of the whole hippocampus and parahippocampal cortex. The estimated total number of somatostatin or neuropeptide Y containing neurons was similar in the hippocampal formation of patients with AD and controls. By contrast, the density of the somatostatinergic fibers and terminals as estimated by the optical density of the somatostatin neuropil, significantly decreased by 30-45% in all the hippocampal subregions and the parahippocampal cortex, whereas the density of the neuropeptide Y immunoreactive neuropil significantly decreased (45%) only in the parahippocampal cortex. Numerous enlarged fibers containing somatostatin or neuropeptide Y, some of which were observed within senile plaques, were detected in the brain of patients with AD. These data suggest that in AD, somatostatin and neuropeptide Y containing cell bodies in the hippocampus and parahippocampal gyrus are anatomically preserved, in spite of an altered terminal field.

ISSN:1420-8008    

DOI:10.1159/000107028

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

The somatostatinergic innervation, and by comparison that of neuropeptide Y, was examined by immunocytochemistry, in the hippocampal formation of 6 patients with clinically and neuropathologically confirmed diagnosis of Alzheimer's disease (AD) and 4 matched controls. The quantitative assessment of the somatostatin and neuropeptide Y immunoreactive cell perikarya was conducted on regularly spaced sections covering the span of the whole hippocampus and parahippocampal cortex. The estimated total number of somatostatin or neuropeptide Y containing neurons was similar in the hippocampal formation of patients with AD and controls. By contrast, the density of the somatostatinergic fibers and terminals as estimated by the optical density of the somatostatin neuropil, significantly decreased by 30-45% in all the hippocampal subregions and the parahippocampal cortex, whereas the density of the neuropeptide Y immunoreactive neuropil significantly decreased (45%) only in the parahippocampal cortex. Numerous enlarged fibers containing somatostatin or neuropeptide Y, some of which were observed within senile plaques, were detected in the brain of patients with AD. These data suggest that in AD, somatostatin and neuropeptide Y containing cell bodies in the hippocampus and parahippocampal gyrus are anatomically preserved, in spite of an altered terminal field.

ISSN:1420-8008    

DOI:10.1159/000315541

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

Angiotensin-converting enzyme (ACE), choline acetyltransferase and acetylcholinesterase were measured in seven cortical regions from the brains of 11 neurologically normal controls, 15 cases of dementia of the Alzheimer type, 6 cases of Parkinson dementia, and 12 cases with other neurological diseases. The groups did not differ significantly in age or postmortem delay. As expected, the cholinergic enzyme activities were significantly correlated with each other and were both markedly reduced in the Alzheimer and Parkinson dementia groups. Overall, ACE activity was not correlated with either of the cholinergic enzymes, and was not significantly affected by clinical category. The activity did, however, show significant regional variation and appeared somewhat higher in females than in males. The mean cortical ACE activity showed a statistically significant increase with age.

ISSN:1420-8008    

DOI:10.1159/000107029

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

The effect of tacrine (THA), the cholinesterase inhibitor, and Ginkgo biloba extract (EGb) on the sodium-dependent high-affinity choline uptake (HACU) into hippocampal synaptosomes was studies in vivo in model experiments after long-term administration in old rats (THA 5 or 10 mg/kg/day p.o. for 3 months; EGb 50 or 100 mg/kg/day p.o. for 30 days) and in vitro tests. EGb increased HACU both in vivo and in vitro experiments. On the contrary, THA induced a decrease of HACU under both conditions, suggesting a negative impact on the cholinergic neuronal activity.

ISSN:1420-8008    

DOI:10.1159/000107030

出版商:S. Karger AG    

年代:1992

数据来源: Karger

摘要:

By using single- or double-color immunohistochemistry of β-amyloid peptide, complement proteins C4d, C3d, and C5b-9, and the HLA-DR marker LN-3, differences were detected in the extent of complement activation in the two major types of cerebellar β-amyloid peptide deposit, diffuse and compacted senile plaques. Both types of deposit were highly co-localized with immunoreactivity of complement protein C4d, an early stage complement fragment. However, immunoreactivity of C3d, an intermediate stage complement fragment, co-localized predominantly with compacted plaques and could only occasionally be found in diffuse plaques. Immunoreactivity for C5b-9, the membrane attack complex formed as a final step in full complement activation and responsible for lysis of bystander cells, could only be detected unequivocally in compacted plaques, not in diffuse plaques. The failure of full complement activation in diffuse plaques, which greatly predominate in the Alzheimer's cerebellum, may underlie the relative paucity of cerebellar pathology and clinical symptomatology in Alzheimer's disease.

ISSN:1420-8008    

DOI:10.1159/000107031

出版商:S. Karger AG    

年代:1992

数据来源: Karger