Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002395 (Alzheimer's disease)
 110,584 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dementia in Parkinson's disease is thought to be attributable not only to subcortical lesions but also to cortical alterations, especially frontal lobe dysfunction. To evaluate cortical function, the regional cerebral blood flow (rCBF) was estimated of 13 demented and 13 non-demented age matched patients with Parkinson's disease compared with that of 10 age matched controls using I-123 iodoamphetamine single photon emission tomography (IMP-SPECT). The rCBF of the nondemented Parkinson's patients showed no significant differences from that of the control subjects. In the demented patients, the bilateral frontal and parietal and left temporal regional blood flow was significantly less than in the controls. Four demented patients showed isolated frontal hypoperfusion, 8 showed fronto-parietal hypoperfusion, and 1 showed isolated parietal hypoperfusion. Frontal hypoperfusion was therefore present in 12 of the 13 demented patients, and this finding agrees with the frontal lobe dysfunction hypothesis. Parietal rCBF had a significant positive correlation with cortical functions such as calculation and language ability in the MMSE scores. The parietal and temporal reduction in rCBF probably reflects the presence of Alzheimer pathology, cortical Lewy body disease, or both.
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PMID:SPECT findings in Parkinson's disease associated with dementia. 143 61

Extrapyramidal, frontal release, and other neurological signs were studied in 54 demented and non-demented patients with Down's syndrome (DS). Fourteen patients were demented and five showed extrapyramidal signs, mainly of the rigid-hypokinetic spectrum and similar to Parkinsonian features in advanced Alzheimer's disease (AD). None of the non-demented patients had Parkinsonian signs. The mean age of the demented DS patients with extrapyramidal signs was significantly higher than that of the patients without. Frontal release signs were present in demented and non-demented patients. A questionnaire showed no increase in either the proportion of early- or senile-onset dementia or Parkinsonism among first- and second-degree relatives of DS patients. Parkinsonian signs appear to be present at a lower frequency in DS than in advanced AD. A speculative hypothesis about a gene dosage effect of Cu/Zn-superoxide dismutase in preventing toxic radical formation in the substantia nigra of DS patients is presented.
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PMID:Extrapyramidal features in advanced Down's syndrome: clinical evaluation and family history. 182 26

The results of a clinical study on extrapyramidal, frontal release, and other neurological signs in 54 demented and non-demented patients with Down's syndrome (DS) are presented. Fourteen patients were demented, five of them showed extrapyramidal signs, mainly of the rigid-hypokinetic spectrum and rather similar to Parkinsonian features in advanced Alzheimer's disease (AD). None of the non-demented patients had Parkinsonian signs. The mean ages of the demented DS patients with extrapyramidal signs was significantly higher than that of the patients without the respective signs. Frontal release signs were present in demented and nondemented patients. From a questionnaire neither a raised proportion of early- or senile-onset dementia nor of Parkinsonism among first- and second-degree relatives of DS patients could be traced. Parkinsonian signs seem to be present at a lower frequency in DS than in advanced AD. A speculative hypothesis about a gene dosage effect of Cu/Zn-superoxide dismutase in preventing toxic radical formation in the substantia nigra of DS patients is presented.
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PMID:Parkinsonian features in advanced Down's syndrome. 183 96

Changes in the cholinergic, serotonergic, noradrenergic, dopaminergic, GABAergic and somatostatinergic neurons were investigated to determine their roles in Alzheimer's disease (AD). Markers for these systems were analyzed in postmortem brain samples from 20 patients with AD and 14 controls. In the CSF study, markers for the cholinergic neurons (choline esterase, ChE) and for the somatostatinergic neurons (somatostatin-like immunoreactivity, SLI) were assayed for 93 and 75 probable AD patients and 29 and 19 controls, respectively. Activity of choline acetyltransferase (CAT) was decreased by 50-85% in four cortical areas and hippocampus in patients with AD, but not in other areas of the brain, indicating a profound deficit in the function of cholinergic projections ascending from the nucleus basalis to the cerebral cortex and hippocampus in AD. Muscarinic receptor binding was reduced by 18% in the frontal cortex but not in other areas of the brain in AD. Serotonin (5HT) concentrations were reduced (by 21-37%) in hippocampal cortex, hippocampus and striatum; and 5HT metabolite levels were lowered (by 39-54%) in three cortical areas, thalamus and putamen in AD patients. Concentrations of noradrenaline (NA) were reduced (18-36%) in frontal and temporal cortex and putamen. These data imply that serotonergic and noradrenergic projections are also affected in AD but less than the cholinergic neurons. Dopamine (DA) concentrations in AD patients were reduced by 18-27% in temporal and hippocampal cortex and hippocampus, while HVA, the metabolite of DA, was unaltered. Glutamic acid decarboxylase activity was not altered in AD. SLI was decreased (28-42%) in frontal, temporal and parietal cortex, but not in thalamus and putamen in patients with AD. Frontal tangle scores correlated most strongly with cortical CAT activity reduction and less so with decreases of 5HT, NA and DA, indicating a closer correlation with the cholinergic changes and severity of AD than with other neurotransmitter deficiencies. ChE activity and SLI were reduced by 20% and 35%, respectively, in CSF of the whole group of AD patients as compared to the controls. Comparison of CSF findings between four subgroups of dementia severity indicated that the SLI was already reduced in the group of mildest AD (-31%), while ChE activity was not. Although ChE activity in CSF declined in relation to dementia severity, however, the maximal reduction was only modest (-30%). On the other hand, SLI in CSF showed only a slight further reduction (up to -41%) as the dementia become more severe.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitter changes in Alzheimer's disease: implications to diagnostics and therapy. 198 17

Glucose metabolism was measured by F-18 FDG PET in 33 patients with dementia. In patients with DAT, rCMRgl showed marked decrease in the associated areas in the temporo-parietal lobes, and it was relatively preserved in the primary cortices such as sensory, motor and visual areas. Frontal lobes were also involved in patients with advanced disease. In Pick disease, the frontal lobes were severely impaired. Multi-infarct dementia, Parkinson dementia and supranuclear palsy showed diffuse or multiple involvement throughout the entire brain. Correlation with rCMRgl and clinical severity was found in DAT patients. In conclusion, F-18 FDG PET is clinically useful in the differential diagnosis and grading of dementias.
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PMID:[F-18 FDG PET in dementia]. 260 Oct 95

Immunohistological and biochemical studies were initiated to determine whether or not neural membrane components were associated with degenerative changes characteristic of Alzheimer's disease (AD). Monoclonal antibody A2B5, developed against embryonic chick retinal cells and previously shown to react with neural surface gangliosides, was applied to formalin-fixed sections of control and AD brain tissue. Frontal cortex and hippocampus of AD cases exhibited high levels of A2B5 immunoreactivity within those neurons undergoing neurofibrillary degeneration. Neuritic processes associated with senile plaques were also highly reactive with the A2B5 antibody. The amount of gangliosides and their pattern after HPTLC were the same in control and AD cases. However, the unexpected observation was made that the A2B5 antibody reacted with human brain sulfatides in addition to the expected reactivity with minor gangliosides. The average level of sulfatides in AD brain was significantly higher than in normal controls. The data support the involvement of one or more membrane components with neurodegeneration in the Alzheimer brain.
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PMID:Monoclonal antibody to embryonic CNS antigen A2B5 provides evidence for the involvement of membrane components at sites of Alzheimer degeneration and detects sulfatides as well as gangliosides. 266 46

Frontal and temporal sections of 4 normal human brains and 3 brains from patients with a diagnosis of Alzheimer-type dementia (ATD) were stained with Vicia villosa lectin conjugated to biotin to localize glycoproteins containing terminal N-acetylgalactosamine. These lectin binding sites were localized at the surface of a population of non-pyramidal interneurones. Examination of the co-existence of calbindin D28K or parvalbumin (PVA) with the lectin-binding material revealed that in the human cerebral cortex the lectin labelled only the PVA-immunoreactive neurones. Cell counts of the number of lectin-staining cells revealed that these cells are lost in ATD. The few remaining lectin-staining cells in ATD are shrunken and showed reduced expression of the lectin-staining material.
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PMID:Vicia villosa lectin-positive neurones in human cerebral cortex. Loss in Alzheimer-type dementia. 279 Apr 70

Frontal and temporal cortical tissue from the brains of elderly cases of Down's syndrome was used to make preparations of neuronal cell bodies containing senile plaque cores. Polarisation microscopy revealed normal "classical" plaque cores, and also a high proportion of unusual "amorphous" plaque cores which we have not seen in Alzheimer's disease. These two forms were easily distinguished by electron microscopy. This suggests that late Down's syndrome may not be an exact model for Alzheimer's disease.
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PMID:Isolated senile plaque cores in Alzheimer's disease and Down's syndrome show differences in morphology. 294 73

Results from measurements of regional cerebral blood flow (rCBF) by 133Xe inhalation are presented for neuropathologically proven cases of frontal lobe degeneration of non-Alzheimer type, Pick's disease, Alzheimer's and Creutzfeldt-Jakob's diseases with frontal predominance and one case of bilateral thalamic infarction. The pathological and neuropsychiatric findings in these cases were described in the preceding articles. rCBF-data were available in nine patients with the diagnosis of frontal lobe degeneration of non-Alzheimer type and in all four patients with Pick's disease. All 13 patients showed a pathologic flow pattern with focally reduced values in frontal, especially pre-frontal, areas of both hemispheres. The most pronounced focal pathology was seen in the Pick group. Post-central areas were typically better preserved. Two cases of Alzheimer's disease with frontal accentuation had, in addition to low frontal values, also a parietal focal reduction. Frontal flows were also reduced in two cases of Creutzfeldt-Jakob's disease while the hypofrontality fluctuated from one study to another in the case of thalamic infarcts. The extent and localization of cerebral dysfunction in patients with organic dementing disorders, including those affecting the frontal lobes, can thus be described by means of rCBF measurements. Previous studies have shown about 90% accuracy of diagnosis by rCBF compared to diagnosis at autopsy. The possibility for exact localization of the dysfunction has recently been improved by the development of a high-resolution system (254 detectors). Results from the first recordings with this system are presented.
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PMID:Frontal lobe degeneration of non-Alzheimer type. III. Regional cerebral blood flow. 368 55

Receiver operating characteristic (ROC) curves were used to quantitatively assess the ability of individual detectors in a 32-detector 133Xe inhalation system to discriminate between two populations over the range of regional cerebral blood flow (rCBF) values. These populations were clinically evaluated as normal (age 63.1 +/- 13.1, n = 23) and presumed Alzheimer's disease (age 72.7 +/- 7.0, n = 82). Summary statistics showed that for homologous detectors the average value of blood flow in the normal group was greater than the flow value in the group of subjects with Alzheimer's disease. Conclusions drawn from single values of flow or mean hemispheric flow can lead to erroneous conclusions about hemisphere asymmetries. However, the dynamic relationship between the correct identifications (true positives) compared with incorrect identifications (false positives) of Alzheimer's disease at each detector varies over the range of blood flow values, and quantitative characterization of this relationship in terms of an ROC curve provides more insight into the structure of the data. Detectors approximating the speech, auditory and association cortex were most effective in discriminating between groups. Frontal detectors were marginally useful diagnostically.
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PMID:Receiver operating characteristic analysis of regional cerebral blood flow in Alzheimer's disease. 403 42


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