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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alzheimer's disease is a degenerative brain disorder with a progressive dementia which develops in middle or late life. The pathological findings of this disease are characterized by neurofibrillary tangles, senile plaques and cerebrovascular amyloidosis. However, cerebral hemorrhage caused by amyloid angiopathy rarely occurs. A 71-year-old woman, who had been suffering from an impairment of her cognitive ability for the past several months, suddenly developed a severe headache with vomiting and gait disturbance. Brain CT disclosed a hemorrhagic lesion in the right parieto-occipital region. In the following two years she had experienced two episodes of the similar subcortical hemorrhage which occurred in the right parietal lobe and bilateral parieto-occipital regions. She died at the age of 73. Histopathological examinations of the brain revealed a decreased number of neurons with diffuse distribution of senile plaques and neurofibrillary tangles in the neocortex and hippocampus. Severe cerebrovascular amyloid deposits were also seen. Immunostaining for amyloid was carried out using a monoclonal antibody to amyloid beta protein. The senile plaque and cerebrovascular amyloid was strongly immunoreactive to anti-beta protein antibody. Cerebral amyloid angiopathy is commonly seen in the brains with Alzheimer's disease and severe cerebrovascular degeneration secondary to heavy amyloid deposits may cause recurrent subcortical hemorrhages in the patients with this disorder.
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PMID:[An Alzheimer's disease case showing recurrent subcortical hemorrhage: an autopsy findings with immunohistochemical studies of cerebral amyloid deposits]. 280 20

The presence of amyloid P-component (AP) within cerebral amyloid deposits was investigated by means of biochemical and immunocytochemical methods. Immunoperoxidase on formalin-fixed, paraffin-embedded tissue sections from Alzheimer's Disease, Down's Syndrome, asymptomatic age-related cerebral amyloidosis, sporadic cerebral amyloid angiopathy, hereditary cerebral hemorrhage with amyloidosis-Icelandic type, and hereditary cerebral hemorrhage with amyloidosis-Dutch type revealed the presence of AP in the affected vessel walls in all cases, and in parenchymal deposits resembling neuritic plaques of Alzheimer's disease, sporadic cerebral amyloid angiopathy, and hereditary cerebral hemorrhage with amyloidosis-Dutch type. A short digestion of tissue sections with pepsin was required for immunodetection of AP in these latter structures. After extraction of leptomeningeal amyloid fibrils, AP was characterized by sodium dodecyl sulfate-polyacrylamide-gel electrophoresis, Western blot, gel chromatography, and partial amino acid sequencing. Our results indicate that: (a) AP from cerebral amyloidosis has similar biochemical properties and homologous amino terminal sequence to AP from systemic amyloidosis; (b) AP is associated to a variety of brain amyloid deposits regardless of their chemical nature. The presence of AP, a serum protein, within the brain parenchyma points to an impairment of the blood-brain barrier in these diseases.
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PMID:Isolation and characterization of amyloid P component from Alzheimer's disease and other types of cerebral amyloidosis. 296 74

We investigated amyloid deposition in the brain and other organs in 105 consecutive autopsy cases, aged 59 to 101 years. They consisted of two groups; 15 patients with dementia of Alzheimer type (DAT) and 90 patients without DAT. Amyloid deposition was found in 93% of all cases. The incidence of amyloid deposition increased with age. The number of organs affected with amyloid deposition in each case also increased with age. The incidence of amyloid deposition in each organ was as follows; 88% in pituitary gland, 66% in brain [amyloid of senile plaque (SP) (61%) and/or cerebral amyloid angiopathy (CAA) (56%)], 33% in pancreas, 3% in heart, and less in others. In immunohistochemical studies using the antisera to the various kinds of amyloid or related proteins, amyloid beta protein was demonstrated in brain amyloids including SP and CAA, but not in others. Cardiac amyloid was positive for prealbumin. Pituitary amyloid and CAA were positive for amyloid P-component. The incidence of brain amyloids in DAT were significantly higher than that in non-DAT. There was no significant difference in the incidence of pituitary and pancreatic amyloid between DAT and non-DAT. In the non-DAT patients, there were significant positive correlations in amyloid deposition between the brain and pituitary gland and between the brain and pancreas. Acceleration of amyloid deposition would be a process confined to the brain in the patients with DAT. The pathogenesis of the accelerated deposition of brain amyloids is discussed from the point of view of amyloidosis.
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PMID:Systemic amyloid deposition in old age and dementia of Alzheimer type: the relationship of brain amyloid to other amyloid. 306 4

The predominant protein of cerebrovascular and plaque core amyloid in Alzheimer's disease, Down's syndrome, hereditary hemorrhage with amyloidosis--Dutch type, sporadic cerebral amyloid angiopathy, and age-related amyloidosis is a unique polypeptide, called beta protein. The length of the plaque amyloid protein was reported to be 42-43 residues, but the complete length of the cerebral vascular amyloid is not known. To clarify this issue, amyloid fibrils from the leptomeninges of an Alzheimer's disease patient were isolated and the primary structure determined. The complete sequence of cerebrovascular beta-amyloid protein, although homologous to the plaque core amyloid protein previously reported, has 39 residues instead of 42. Amino terminal heterogeneity is present but minimal, and it is three residues shorter at the carboxy terminus. These differences are similar to those found in two cases of hereditary hemorrhage with amyloidosis--Dutch type. The differences between vascular and plaque beta-amyloid may reflect diverse processing of the beta protein precursor in the vessel wall and brain parenchyma due to tissue-specific endopeptidases.
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PMID:Differences between vascular and plaque core amyloid in Alzheimer's disease. 329 6

Amyloid deposition is a prominent feature of a number of brain disorders, in which amyloid fibrils are found within blood vessel walls, the neuropil (neuritic plaques), neurons (neurofibrillary tangles). These include Alzheimer's disease (AD), AD changes associated with Down's syndrome, neurologically asymptomatic amyloidosis, Parkinson dementia of Guam, hereditary cerebral hemorrhage with amyloidosis of Icelandic origin (HCHWA-I), hereditary cerebral hemorrhage with amyloidosis of Dutch origin (HCHWA-D), and sporadic cerebral amyloid angiopathy (SCAA). Recently it was shown that the amyloid deposits in AD, Parkinson dementia of Guam, and HCHWA-D are formed by a similar 4-kd polypeptide called beta-protein. Because the nature of the amyloid deposits in other types of cerebral amyloidosis is not known, we have conducted immunocytochemical studies on brains from autopsy cases of AD, HCHWA-D, SCAA and neurologically asymptomatic elderly individuals. Brains from two subjects without neurologic involvement were used as controls. Sections from these specimens were incubated with rabbit polyclonal antibodies against 1) a synthetic peptide of 28 residues (anti-SP28), homologous to the NH2-terminal sequence of the beta-protein, 2) the main amyloid component of the HCHWA-I, a variant of cystatin C, and 3) purified fraction of neurofibrillary tangles. In all cases, anti-SP28 antibody specifically stained amyloid deposits in leptomeningeal and cortical vessels and neuritic plaques. These findings demonstrate that the amyloid deposits of SCAA and aged brains are composed of a protein antigenically similar to AD, HCHWA-D, and Parkinson dementia of Guam beta-protein, suggesting that all of these clinically and etiologically different morbid conditions are pathogenetically related. On this basis, they can be tentatively grouped as beta-protein deposition diseases. In addition, we found that HCHWA-D and SCAA vessels were mainly affected, while in AD parenchymal involvement predominates. These differences in the localization and extent of beta-protein deposits may account from the predominance of vascular complications in HCHWA-D and SCAA and of dementia in AD.
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PMID:Brain amyloid in normal aging and cerebral amyloid angiopathy is antigenically related to Alzheimer's disease beta-protein. 332 21

Neuropathological examination of 1400 successive autopsies in general and mental hospitals revealed that senile plaques and congophilic angiopathy are age related phenomena. There is, however, a remarkable difference between the two types of manifestation of senile amyloidosis. There was a significantly higher incidence of senile plaques in females. Moreover the increase of the incidence with age was also significantly higher in females. Congophilic angiopathy showed no predominance in females. In total 59% of males and 55% of females with senile plaques suffered from Senile Dementia of the Alzheimer Type (SDAT). SDAT appeared to be also an age related phenomenon characterized by a linear increase with age and a predominance in females.
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PMID:Age incidence of senile brain amyloidosis. 378 48

Senile cerebral amyloidosis has been investigated using immunoperoxidase and enzyme histochemical techniques in six unfixed brains. Our findings do not support the opinion that vascular and senile plaque amyloid are immunoglobulin-derived. In contrast with recent reports we did not detect prealbumin in senile plaques and congophilic angiopathy lesions. All senile plaques contain complement factors C1q, C3 and C4. The highest peroxidase activity was found in the amyloid nucleus but the corona also showed evident peroxidase activity.
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PMID:An immunohistochemical study on cerebral vascular and senile plaque amyloid in Alzheimer's dementia. 615 Dec 85

Histochemical methods were used to obtain information on the chemical constituents of brain amyloid in senile dementia of the Alzheimer type. The staining properties of brain amyloid (senile plaque and amyloid angiopathy) were compared with those of extraneural amyloidosis and endocrine amyloid. We found no histochemical differences between amyloid in senile plaques and in amyloid angiopathy. The content of aromatic amino acids was higher in amyloid of plaques and in amyloid angiopathy than in endocrine amyloid. Furthermore, we found persistent birefringence and affinity of brain amyloid for Congo red after exposure to potassium permanganate, suggesting that AA amyloid is not a major constituent of cerebral amyloid.
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PMID:Histochemical analysis of senile plaque amyloid and amyloid angiopathy. 615 16

A case of systemic amyloidosis associated with bronchiectasis is presented. At necropsy, contracted kidneys and centrilobular necrosis of the liver were observed. Systemic blood vessels had heavy deposition of amyloid, and the possibility of visceral ischemia and the development of contracted kidneys due to amyloid vascular disease as a pathogenetic relationship, was discussed against the background of a review of the literature.
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PMID:Amyloid vascular disease and contracted kidneys--report of a case with review of literature. 651 15

Ultrastructural studies of the brain in three cases of cerebral amyloid angiopathy demonstrated that the vascular amyloid in this disease is composed of fibrils identical to those in systemic amyloid disease, mixed with a large amount of vesicular debris. Amyloid appears to be derived from circulating protein and is depostied in areas of vascular basement membrane degeneration. The initiating degenerative change is thickening of basement membrane with accumulation of debris. Inflammation, when present, tends to accelerate amyloid deposition locally. Amyloid transport from the vascular wall into the brain parenchyma proceeds by overflow when perivascular astroglial end-feet are disarranged. Structures of perivascular amyloid plaques are similar to the neuritic (senile) plaques in Alzheimer's disease, which were used as control, except that the amyloid core of the plaques in Alzheimer's disease is not related to blood vessels.
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PMID:Ultrastructural features of cerebral amyloid angiopathy. 675


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