ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Clinical and neuropathological similarities between Alzheimer disease and the transmissible spongiform encephalopathies have sparked intensive investigation of the role of nearly every arm of the immune system in the etiology and pathogenesis of Alzheimer disease. These endeavors have yielded intriguing results but no clear-cut answers. Studies of humoral and cellular immune function in patients with dementia of the Alzheimer type (DAT), immunohistochemical examinations of Alzheimer brain tissue and HLA typing of both sporadic and familial DAT are reviewed. Sporadic DAT appears to be associated with the complement allotype C4B2 in the major histocompatibility complex, which is linked very closely to HLA. Mechanisms for the role of complement in the pathogenesis of DAT are postulated.

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

This preliminary study was undertaken to investigate the effect of dietary silicon and aluminum on levels of these elements in brain. Two ages of rats, 22 day and 10 month, were assigned to 1 of 4 diets: 1) low silicon; 2) low silicon plus aluminum; 3) silicon supplemented; and 4) silicon supplemented plus aluminum. Rats were 23 and 28 months old upon termination of the experiment. Twelve brain regions were analyzed for silicon and aluminum. Regional variations in silicon, which were independent of dietary silicon supplementation, suggest that silicon may be an essential element in brain. Aluminum supplementation decreased the silicon content in selected brain regions, including those thought to be involved in Alzheimer disease. A relationship has been established between silicon, aluminum and age. In 23-month rats, aluminum supplementation did not increase brain aluminum content. By contrast, in 28-month rats, aluminum supplementation of the low silicon diet increased brain aluminum content in most regions. No increase occurred in silicon supplemented groups of the same age. Dietary silicon supplementation thus appeared to be protective against aluminum accumulation in aging brain.

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Recent investigations revealed that the physical properties of both central andperipheral cell membranes are changed in dementia of the Alzheimer Type (DAT). Weattempted to ascertain whether this effect is specific for DAT by studying the polarization ofdiphenylhexatriene (DPH) fluorescence (an indicator of membrane “microviscosity”) in themembranes of platelets isolated from DAT patients, patients with multi-infarct dementiaand healthy controls. The 3 groups were matched as closely as possible for age and sexdistributions. Platelet phospholipid composition was also examined in an attempt to identifythe chemical basis of the membrane change(s)These studies revealed that DPH fluorescence polarization is significantly reduced in plate-lets from DAT patients, but not in patients with multi-infarct dementia, compared withcontrols. Analysis of the phospholipid composition of platelets from the 3 groups of subjectsdid not find any significant differences which might explain the change in membrane properties.

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Although relatives' retrospective reports are often used in characterizing the onset and progression of symptoms in dementia of the Alzheimer type (DAT), little is known about the accuracy of these accounts. The primary purpose of this paper is to summarize preliminary data obtained from relatives in an ongoing family study of DAT. Preliminary findings suggest there is rough reliability to relatives' recall of the progression of symptoms over time. This observation is discussed in relation to literature from other areas (e.g. child development, psychopathology) where the reliability of relatives' retrospection has been more thoroughly examined.

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0893-0341    

出版商:OVID    

年代:1987

数据来源: OVID