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)

Recognition that chronologic age is not per se a cause of dementia opens the way for a more active approach to Alzheimer-type dementias as a specific disease syndrome. "Alzheimerism" in many respects is to the cholinergic brain system what Parkinsonism is to the dopamineragic. Whether cell loss or choline acetyltransferase deficiency comes first is still unclear, as is the role of vasopressin. There is a real possibility that research might produce a palliative for ACh-based defects similar to the action of L-dopa in dopaminergic defects.
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PMID:Alzheimer's disease or "Alzheimerism"? 4 21

In a study of senile degenerative lesions-including Alzheimer's neurofibrillary changes, senile plaques and amyloid angiopathy-the hippocampal area of the brain was examined by thioflavine T fluorescence microscopy in 146 consecutive autopsy patients over the age of 49. The incidence and quantity of neurofibrillary changes and senile plaques rose with age, and an approximate positive correlation in quantity was noted among the three kinds of degenerative change. The quantity of neurofibrillary lesions and senile plaques was significantly different between the demented and non-demented patients, but not between the severely and less severly demented patients. The cause of dementia was studied retrospectively, based on the extent of morphologic changes in the brain, thus classifying dementia into three types: degenerative, vascular, and mixed. Clinically, the mixed type resembled the vascular type with regard to major neurologic signs, and there was some similarity to the degenerative type with regard to mental features.
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PMID:Senile degenerative brain lesions and dementia. 5 Mar 38

The visual cortical evoked response was studied in 19 patients suffering from a condition diagnosed as senile or presenile (type Alzheimer) dementia. When compared with a group of normal subjects used as reference group, the latencies of waves II through VI were increased or markedly increased in these patients, and the amplitudes of waves III and VI (and, less consistently, those of waves II and IV) were increased. This corroborates the sparse data on other types of dementia available in the literature.
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PMID:Visual evoked response in senile and presenile dementia. 5 64

More than 1400 necropsies performed on patients with either a nontraumatic cerebral hemorrhage (400 cases) or with dementia over the age of 55 (1010 cases), or both, have been reviewed. There were 15 cases in which a cerebral hemorrhage had occurred together with cerebral amyloid angiopathy all of whom had been demented. Eight of the 15 patients were hypertensive. The 7 non-hypertensives showing only the amyloid change included two cases of "atypical" Alzheimer's disease with acute neurological features, and 5 cases of senile dementia (aged 72 to 78 years) coupled with focal neurological disorders. In the hypertensive patients, aged 67 to 86 years, with a progressive dementing syndrome and acute neurological signs, multiple ball-like hemorrhages (7 cases) and/or cerebral hematomas (3 cases) were associated with a combination of amyloid and hyalinar (hypertensive) angiopathy, often affecting segments of the same pial and cortical vessels. From these data and recent reports on lethal cerebral hemorrhage occurring spontaneously or after neurosurgical procedures in demented old people, cerebral amyloid angiopathy, which is not necessarily associated with systemic amyloidosis or severe (pre)senile cerebral degeneration, may be considered a rare but important cause of cerebral hemorrhage in the aged. The "vascular" type of presenile dementia, occasionally complicated by focal cerebrovascular lesions or bleeds, is considered a variant of Alzheimer's disease. The mechanism leading to formation of cerebral amyloid is unknown.
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PMID:Cerebrovascular amyloidosis with cerebral hemorrhage. 6 54

Choline acetyltransferase activity (presynaptic cholinergic system) and high affinity binding of cholinergic antagonists (postsynaptic cholinergic system) were measured in brain tissue removed after death from both mentally normal and demented old people. Muscarinic receptor binding sites in frontal cortex decreased with advancing years only in old people without appreciable morphological evidence of senile degeration. Preliminary data for temporal lobe suggested that also in Pick's disease the density of receptor binding sites is reduced. The markers are not significantly reduced in cases of mixed senile and vascular dementia. However, in non-vascular senile dementia of the Alzheimer type, there were indications that the presynaptic marker is selectively depleted. Therefore, centrally acting anticholinesterases might be beneficial, particularly in the early stages of the disease.
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PMID:Neocortical cholinergic neurons in elderly people. 6 73

Extensive biochemical analysis of whole temporal lobe from cases of dementia and controls suggests that Alzheimer's disease is a primary degenerative nerve-cell disorder and not the result of accelerated ageing. There is selective loss of neocortical cholinergic neurones. Transmitter systems apart from the cholinergic system appears to be affected, but to a lesser extent, and there are no significant changes in the caudate nucleus. The change in cholinergic neurones has been confirmed in biopsy samples.
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PMID:Accelerated ageing or selective neuronal loss as an important cause of dementia? 8 62

Progressive electroencephalographic disorganization and decreased voltage amplitude in the late components of the averaged visual evoked potentials were recorded in the last two years of life of a patient with Down disease and Alzheimer degeneration. Taken together with quantitative histopathologic findings, the electrophysiologic alterations are interpreted in terms of recent evidence from an experimental animal model of dementia. Neurons with neurofibrillary degeneration become electrically inactive and contribute to the loss of voltage generators associated with neuron death in Alzheimer disease. Loss of voltage generators may result in disfacillitation and disinhibition of surviving neurons, thus causing the loss of normal rhythms.
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PMID:Alzheimer degeneration in Down syndrome. Electrophysiologic alterations and histopathologic findings. 12 52

The abnormal aggregates of fibrillar material found in neurons in Alzheimer's disease, senile dementia, the Guam Parkinsonism-Dementia complex, Down's syndrome, and postencephalitic Parkinsonism were studied by means of tilt-stage electron microscopy and with X-ray images of scale models of a bifilar helix. The model fulfills the structural criteria established by electron microscopy. These studies showed that the "twisted tubule" which makes up the neurofibrillary tangle in many pathological situations is a bifilar helix made up of 130 A filaments.
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PMID:Neurofibrillary tangles of paired helical filaments. 12 41

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

Reductions in 2 neurotransmitter synthesizing enzymes in brain, glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT), have been found in dementias of different origins, including senile dementia (Alzheimer type). Significant reductions in cerebral GAD have also been found in depression (unipolar). The GAD reductions did not generally appear to be localised in any specific region of the brain examined. However, the reduction of CAT in the hippocampus, relative to reductions in other areas examined, was substantially greater in the brains with Alzheimer-type changes. GAD and CAT activities in normal brains were examined for the effects of some variable factors inherent in necropsy biochemical measurements. These factors included: (i) age; (ii) agonal status; (iii) time of death, and (iv) delay in tissue sampling; and GAD was found to be significantly influenced by (ii), (iii) and (iv) and CAT by (i), (iii) and (iv). None of these factors accounted for the total alterations in the enzyme activities of the mentally abnormal brains. The results indicate that reductions in cerebral GAD require to be interpreted with caution in view of the sensitivity of this enzyme to premortem status but that reductions in cerebral CAT may be a more reliable index of pathological change in senile (Alzheimer-type) dementia.
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PMID:Neurotransmitter enzyme abnormalities in senile dementia. Choline acetyltransferase and glutamic acid decarboxylase activities in necropsy brain tissue. 14 89


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