Angiopathie bei Alzheimerscher Krankheit

Gerhard, L.; Bergener, M; S, Homayun

doi:10.1007/bf00316721

Cited by 15 publications

(6 citation statements)

References 13 publications

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“…These changes were identified as corresponding to those described in patients from a family with presenile dementia and spastic paraparesis by Worster-Drought et al (1940;1944) of probable autosomal dominant inheritance. Similar families were recorded by van Bogaert et al (1940) and Luers (1947), and the subject has been reviewed by Gerhard et al (1972).…”

supporting

confidence: 74%

Genetic factors in amyloidosis.

Thomas¹

1975

Journal of Medical Genetics

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supporting

confidence: 74%

Genetic factors in amyloidosis.

Thomas¹

1975

Journal of Medical Genetics

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“…Jellinger (9) stated that this change in the vessels occurred in a high proportion of the AA cases in patients with hypertension. On the other hand, Ulrich et al (14) and Gerhard et al (15) reported AA patients with a history of or a familial disposition toward rheumatic diseases without hypertension, who showed prominent “Verdoppelung” of the blood vessels. However, it has not been established that hypertension or rheumatic disease plays an accelerating role in the formation of such types of vascular change resulting in infarction.…”

Section: Discussionmentioning

confidence: 99%

“…The pathogenesis and pathomechanism of AA are not known, but some relationship with rheumatic disease has been suggested (14–16), namely, a specific immune disorder in the background. Rosenthal (17) found an increased serum amyloidlike substance (SAA) in the aged, especially in patients over the age of 80.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Amyloid Angiopathy in the Elderly

Tomonaga

1981

J American Geriatrics Society

146

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In this study an attempt was made to determine the relationship between cerebral amyloid angiopathy (AA) and other cerebrovascular lesions in the aged. The brains of 128 autopsy patients over 60 years of age were examined by both light and electron microscopy. The frequency of cerebral AA increased with age and was 58 percent in patients over the age of 90. The change was observed more often in women than in men. In 7 cases of severe AA, the temporal or occipital cortex was the most common site. Most cases of AA were complicated by the formation of senile plaques in the cortex. Electron microscopic examination revealed amyloid fibrils deposited in clusters in the media and adventitia of the vessels, destroying their structure. Some blood vessels on the surface of the cortex showed hyalinosis, angionecrosis, duplication of the wall, or fibrotic occlusion. AA is sometimes a cause of cerebral bleeding. Five cases of massive cerebral bleeding were found among patients aged 90 or older, including a temporal hematoma in a 92-year-old woman which was believed to be due to the marked AA noted in the temporal lobes. Small cortical infarctions were common in the temporal lobes.

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“…The high incidence of CAA in Alzheimer's dis ease has been stressed by others 7 -,2 -l3 - 17 and one recent study 18 has suggested that specific psychiatric sympto matology may be associated with the presence of CAA, a premise we find difficult to accept. Some authors have considered CAA to be an atypical "vas cular" form of Alzheimer's disease, 19 but others feel CAA is a distinct entity entirely separate from the latter. 20 Mountjoy et al 7 compared CAA in 15 patients with senile dementia of the Alzheimer type with 30 patients who had normal mentation and died with a variety of medical conditions.…”

Section: Discussionmentioning

confidence: 99%

Cerebral amyloid angiopathy: incidence and complications in the aging brain. II. The distribution of amyloid vascular changes.

Vinters¹,

Gilbert²

1983

Stroke

449

274

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SUMMARY Ten histologic sections were sampled from similar cortical regions in each of 84 autopsy brains removed from patients aged 60 to 97 years. The sections were stained by the Congo-red method and examined under polarized light for the presence of cortical {parenchymal) cerebral amyloid angiopathy (CAA). Some degree of CAA was found in 36% of all brains examined, with a higher proportion of patients affected in each successive decade of life. Angiopathy was seen most frequently and was of greater severity in the parietal and occipital gray matter. Overall, it was often a patchy and asymmetric lesion. There was sparing of subcortical white matter and the hippocampi. CAA was most severe in cases of Alzheimer's disease, but occurred in the absence of this condition. Stroke Vol 14, No 6, 1983THE CLINICAL AND PATHOLOGIC FEATURES of cerebral hemorrhages related to cerebral amyloid angiopathy (CAA) in eleven patients are reported. 1To try and understand the pathogenetic mechanism in these cases we have asked: How common is CAA in the aging human population, and what is the cerebral cortical topography of amyloid vascular change?Previous studies 2 " 7 addressed but incompletely an swered these questions. A survey of the cerebral corti cal distribution of CAA as a function of age in a large unselected autopsy population has not previously been available. Material and MethodsThe survey was carried out on 84 post-mortem brain examinations in patients over 60 years of age, irrespec tive of the clinical diagnosis, taken from consecutive complete necropsies carried out in a large general hos pital. However, none of the 11 patients described pre viously 1 were included in this topographic survey. The age of the patients at death ranged from 61 to 97 years. The total number of brains examined in each age cate gory was as follows: 60-69 years -21, 70-79 years -28, 80-89 years -28, and over 90 years -7. The brains were fixed routinely for one to two weeks, after which time 1 cm coronal slices of the cerebral hemi spheres were cut. In addition to routine blocks taken for neuropathologic diagnosis, 10 extra tissue blocks of similar size were taken from each brain and submit ted for Congo-red staining, method of Stokes and Trichey. 8 These 10 blocks were taken from the same re gions in each brain ( fig. 1) and were sectioned to include leptomeninges (when possible), cortex and subcortical white matter from the right and left superi or frontal lobe, right and left superior temporal gyrus, right and left parietal lobe, right and left medial occipi tal lobe, and both hippocampi at the coronal level of the lateral geniculate nuclei. All these sections were then examined with and without polarized light, and individual vessels within the brain that demonstrated any Congo positive material with apple-green birefrin gence in their walls were scored as amyloid-containing blood vessels. The relative severity of CAA in a given section was assessed as follows. If one or two vessels were posi tive, the involvement was scored as 1 + ; if thr...

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Angiopathie bei Alzheimerscher Krankheit

Cited by 15 publications

References 13 publications

Genetic factors in amyloidosis.

Genetic factors in amyloidosis.

Cerebral Amyloid Angiopathy in the Elderly

Cerebral amyloid angiopathy: incidence and complications in the aging brain. II. The distribution of amyloid vascular changes.

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