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.
Aktuelle Gerontol 1979 Sep
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.
J Am Geriatr Soc 1975 Sep
PMID:Senile degenerative brain lesions and dementia. 5 Mar 38

The laboratory transmission to animals of an apparently degenerative disease of the nervous system, Creutzfeldt-Jakob disease (CJD), is now well established. Important questions arising from this observation are the possibility of natural transmission or infectivity and the existence of other similarly transmissible diseases. Epidemiological studies have revealed some possible clusters of CJD and also an association with previous craniotomy, but there is no definite evidence of natural infection. A few instances have been reported of experimental CJD in animals following inoculation with material from Alzheimer's disease, but apart from this there is so far no evidence of transmission of any other form of degenerative nervous disease.
Postgrad Med J 1978 Sep
PMID:Creutzfeldt--Jakob disease. 10 82

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.
Arch Neurol 1975 Sep
PMID:Alzheimer degeneration in Down syndrome. Electrophysiologic alterations and histopathologic findings. 12 52

Spatial dysgnosia may occur in patients with various forms of brain disease, including tumors, vascular accidents, Alzheimer's disease, multiple sclerosis, and developmental aberrations. Patients with lesion in the nondominant hemisphere, particularly at the junction of the occipito-temporoparietal regions, may manifest predominantly visuospatial dysgnosia--a loss of the sense of "whereness" in the relation of himself to his environment and in the relation of objects to each other. Visuospatial disturbances caused by lesions in the dominant hemisphere may be masked by other gnostic symptoms. Patients with more extensive lesions, especially those involving similar areas in both hemispheres, may also exhibit other cognitive disturbances associated with vision.
Am J Ophthalmol 1979 Sep
PMID:Visuospatial dysgnosia. 22 55

Brain monoamine concentrations were determined post mortem in 19 patients with dementia of Alzheimer type. Samples were taken from 10 parts of the brain and compared with an age-matched control group. There were lower mean concentrations of dopamine in the demented group of patients in seven regions of the brain, and two of these were at a significant level. There were also significantly lower concentrations of homovanillic acid in the nucleus caudatus and in the putamen. The means of the concentrations of noradrenaline were also lower, and in the putamen and the cortex gyrus frontalis significant differnces were observed. The 5-hydroxytryptamine concentrations were slightly lower in the demented group but the differences did not reach significance. The degree of intellectual deterioration was negatively correlated with the noradrenaline concentrations in the hypothalamus and the cortex gyrus cinguli.
Br J Psychiatry 1979 Sep
PMID:Changes in the brain catecholamines in patients with dementia of Alzheimer type. 48 47

Chromatin samples were prepared from forty human brains. Chromatin was separated into a heavy heterochromatin fraction and two euchromatin fractions: intermediate euchromatin and light euchromatin. Employing a bacterial RNA polymerase as probe, only the euchromatin fractions were capable of RNA synthesis. In Control human brains, in brains of patients with dialysis dementia and in brains of elderly individuals without or with dementia of a type other than Alzheimer's disease, the euchromatin fractions accounted for about 75 per cent of the total DNA. In contrast, in brains of patients with advanced senile dementia or presenile dementia of the Alzheimer type, a wide range of euchromatin content was encountered with an average value of 55 per cent. Heterochromatization occurred in both neuron and glia enriched fractions suggesting that a major alteration in protein metabolism occurs in Alzheimer's disease.
Brain 1979 Sep
PMID:Altered chromatin conformation in Alzheimer's disease. 49 1

Because there is evidence that central cholinergic mechanisms are depleted in dementia, we studied the effects of central cholinergic augmentation on the memory of 5 patients with Alzheimer disease. Patients received placebo, lecithin, physostigmine, or lecithin plus physostigmine in a double-blind study using titrated doses of the acetylcholinesterase inhibitor physostigmine. Memory was evaluated with alternate forms of the selective reminding procedure. Compared with lecithin alone, the combination of physostigmine and lecithin consistently enhanced memory storage and retrieval; physostigmine without lecithin produced no memory facilitation. The strategy of combining a cholinergic agonist and precursor holds promise, although a larger clinical trial is needed.
Ann Neurol 1979 Sep
PMID:Effects of physostigmine and lecithin on memory in Alzheimer disease. 53 19

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.
Neurology 1979 Sep
PMID:Dementia in Parkinson disease: a neuropathologic study. 57 1

The brains of 3 adult subjects suffering from normotensive hydrocephalus have been examined pathologically. The diagnosis of normotensive hydrocephalus was based on clinical symptoms, pneumoencephalography and isotope cisternography, in 1 case integrated with the results of the constant-infusion manometric test. Part of the neuropathological findings were common to the 3 patients: leptomeningeal non-obstructive fibrosis, ventricular ependymal disruption, subependymal glial reaction, periventricular demyelination and spongiosis. Other neuropathological abnormalities were peculiar to each patient: leptomeningeal signs of previous subarachnoid haemorrhage; arteriosclerosis and multiple brain cystic infarcts; Alzheimer's plaques in the gray matter. The possible pathogenetic significance of the neuropathological findings summarized above in relation to the development of normotensive hydrocephalus is discussed.
J Neurol Sci 1977 Sep
PMID:Anatomo-clinical correlations in normotensive hydrocephalus. Reports on three cases. 91 28


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