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)

Cerebrospinal fluid gamma-aminobutyric acid (CSF GABA) was analyzed in 151 patients who underwent evaluation for central nervous system disease. CSF GABA was not detected in 19 of these patients, who had no evidence of neurologic disease and who served as controls. GABA was most frequently detected in patients with cerebrovascular disease, and was detected only in Parkinson's syndrome of atherosclerotic origin and dementia of multi-infarct type. CSF GABA was not detected in Alzheimer's disease or Huntington's disease. Patients with grand mal seizures exhibited CSF GABA elevation within 24 hours of the ictus. In patients with multiple sclerosis GABA detection was related to the presence or exacerbation of spinal cord lesions. Further study is necessary to evaluate the significance of elevated CSF GABA in central nervous system disease.
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PMID:Cerebrospinal fluid gamma-aminobutyric acid in neurologic disease. 13 99

A group of diseases of the brain characterized by dementia have been discussed. The pathologic features of each were described and illustrated. It seems that, in summary, several points merit emphasis. First of all, as more people survive to the seventh, eighth, and ninth decades, the most common dementia, senile Alzheimer's disease, will become a more significant public health problem. Second, while at the present time there is no successful therapy available, there are some glimmerings of hope on the horizon. The discovery of the agent of Creutzfeldt-Jakob disease seems to have placed us on the fringe of a whole new series of advances. A novel type of disease agent awaits characterization and definition, and there are hints that similar agents could be responsible for the development of the degenerative diseases, perhaps in conjunction with environmental toxins and in the medium of a permissive genetic background. In the case of Huntington's chorea, it seems reasonable that a pharmacologic agent could be found to control the symptoms such as L-dopa therapy has done for patients with Parkinson's disease. It may develop, however, that such an agent will control the choreiform movements but will not influence the dementing condition.
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PMID:Pathology of dementia. 16 30

A systematic study of the central and peripheral nervous systems in 3 cases of Parkinson's disease has demonstrated that Lewy bodies are present in 27 nuclei. Of these 20 nuclei (12 pigmented and 8 unpigmented) are involved in 2 or all 3 cases. It is noticed that the distribution of Lewy bodies in Parkinson's disease described here corresponds surprisingly well to that of monoamine (dopamine, noradrenaline and serotonin) cell bodies demonstrated in rats by the histochemical fluorescence method. This correlation is similar to that of Alzheimer's neurofibillary changes in postencephalitic Parkinsonism as described by Ishii. Inasmuch as these viewpoints are also in agreement with preciously reported biochemical data on Parkinsonism, it is suggested that Parkinsonism (idiopathic and postencephalitic) should represent a system degeneration of monoamine neuron systems.
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PMID:Parkinson's disease: distribution of Lewy bodies and monoamine neuron system. 17 63

Large numbers of Lewy bodies in the substantia nigra were found in a case of Alzheimer's disease. Parkinsonian symptoms were not recognized. The patient appears to be an example of an association recognized by Woodard but not yet understood. The case is discussed in the context of reported relationships between Parkinson's disease or "Lewy body disease" and dementia, on the one hand, and reports linking various forms of psychoses with an unusually high incidence of Lewy bodies, on the other.
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PMID:Lewy bodies in the presence of Alzheimer's disease. 21 17

Five cases of age range 62-72 years with progressive dementia and muscular rigidity are reported and discussed from the clinicopathologic point of view. The neuropathology of these cases was characterized by the widespread occurrence of Lewy bodies (LB) in the CNS as well as the presence of senile changes. The presence of numerous LB in the cerebral cortex and basal ganglia was especially characteristic, although their distribution pattern in the diencephalon and brain stem was identical to that found in paralysis agitans. On the other hand, the presence of senile changes in the cerebral cortex was almost identical to the neuropathology of senile dementia or Alzheimer's disease. Nosologically, the present cases may represent either a combination of atypical paralysis agitans with senile dementia and Alzheimer's disease, or a new disease.
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PMID:Dementia-Parkinsonism syndrome with numerous Lewy bodies and senile plaques in cerebral cortex. 22 31

An inquiry was made into the physical and behavioural problems presented by patients admitted to hospital because of dementia. 81 patients were studied over a period of 3 years, and a comparison was made between the 38 with idiopathic (Alzheimer's) dementia, and the others, most of whom suffered from focal cerebral arteriosclerosis or Parkinson's disease with dementia. The average age was between 70 and 80 years, and the hospital stay averaged 18-28 months. Nursing difficulties ranged from immobility of the patients on the one hand to wandering on the other, especially in the Alzheimer's group. Behaviour disturbances, shouting, incontinence and degenerate habits were found in a high proportion and the incidence of fractures reached 15%. Vascular incidents as complications or causes of death were relatively uncommon; in those who died, the cause was usually infection. The mainstays of treatment were tranquillising drugs, used only when necessary, and in minimal quantities, simple occupational activity, and an awareness by the staff of the high morbidity to which these patients were prone.
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PMID:The physical and behavioural complex of dementia. 40 46

Thirty-four autopsy cases conforming to the standard neuropathologic criteria of Parkinson disease were sex- and age-matched with controls who had died of infarct or trauma. All brains were reviewed for changes compatible with Alzheimer disease, and available clinical data were retrospectively reviewed. Nineteen (56 percent) of the Parkinson cases had shown some degree of dementia. The average parkinsonian brain weight was 1281 gm; it was 1365 gm for the controls (p less than 0.02). Plaques, neurofibrillary tangles, granulovacuolar degeneration, and cortical cell loss were present in all but one of the parkinsonian brains; these pathologic changes were present in fewer controls and to a lesser degree. The higher incidence of dementia in patients with Parkinson disease may be explained by the simultaneous presence of Alzheimer disease.
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PMID:Dementia in Parkinson disease: a neuropathologic study. 57 1

Based on a suspected pathological relationship of autoimmunity in Alzheimer's disease (AD), antibodies to myelin basic protein (MBP) were investigated in the sera of AD patients, healthy controls and disease controls. As detected by the protein-immunoblotting technique at a screening serum dilution of 1:400, sera from 16 of 18 (89%) AD patients were positive for antibodies to MBP. In contrast, sera from only 7 of 90 controls (healthy adults and elderlies, Parkinson's disease patients, mentally-retarded children and Down's syndrome patients) showed a positive reaction. This approximately 11-times higher incidence of antibodies to MBP in AD patients was statistically significant (P < or = 0.0001) and may indicate an autoimmune process in the pathophysiology of the disease.
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PMID:Immunoblot detection of antibodies to myelin basic protein in Alzheimer's disease patients. 128 91

Delirium is commonly defined as a transient organic brain syndrome characterized by concurrent disorders of attention, perception, thinking, memory, psychomotor behavior, and the sleep-wake cycle. One of the difficulties in studying delirium is that symptoms tend to fluctuate over the course of the day. Pre-existing organic brain disease appears to be a significant risk factor for the development of delirium, and numerous studies have shown a high rate of delirium in patients with cerebrovascular disease, Parkinson's disease, and Alzheimer's disease. The cognitive deficits associated with delirium have not been widely studied in a systematic, quantitative fashion. Following resolution of the frank delirium, documented cognitive deficits can be observed, and may persist in a diluted form for a period of months. Residual cognitive deficits may be due to a minimal and persistent confusion or to an underlying brain disorder.
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PMID:Cognitive deficits in delirium: assessment over time. 129 18

A4 protein (beta-protein, beta-amyloid) deposits were identified with silver stains in postmortem brainstem sections from 13 patients with Alzheimer disease (AD), 6 patients with mixed Alzheimer disease and Parkinson disease (AD-PD), 5 disease controls, and 2 elderly controls. A rostro-caudal gradient of A4 was found in patients with AD and AD-PD, such that A4 was most prevalent in the midbrain and least prevalent in the medulla. The brainstem of the controls contained little or no A4. The midbrain tectum and tegmentum contained the greatest densities of A4, but the red nucleus and substantia nigra pars reticulata were largely spared. This distribution of A4 suggests that A4 deposition is a function of synaptic connectivity rather than passive diffusion from vascular sources.
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PMID:Distribution of amyloid in the brainstem of patients with Alzheimer disease. 130 Apr 98


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