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Query: UMLS:C0002395 (Alzheimer's disease)
110,584 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence and forms of cerebral amyloid angiopathy were studied in 15 cases of Alzheimer's disease using Congo red staining and polarization. Thirteen cases showed slight to severe involvement; two contained no amyloid vascular degeneration. There was a correlation between the presence of amyloid-rich plaques and cerebral amyloid angiopathy (especially the plaque-like angiopathy) but no correlation with "amyloid-poor" senile plaques or Alzheimer's neurofibrillary degeneration.
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PMID:The incidence of cerebral amyloid angiopathy in Alzheimer's disease. 4 97

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

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

Clinical and neuropathological findings of a 63-year-old male and a 25-year-old female with Down's syndrome are presented. Neuropathological examination of the older patient revealed intense features of Alzheimer's disease or senile dementia, including congophilic angiopathy and extensive mineral deposits in the globus pallidus and in the white matter of the cerebellum. In the hippocampus of the younger patient, plaque-like bodies and a few neurofibrillary tangles were found. From a survey of the cases hitherto reported in the literature it appears that among patients over 50 years of age it is common to encounter pathological features typical of Alzheimer's disease or senile dementia, that plaque-like bodies may occur in the second decade, neurofibrillary tangles in the third decade and a congophilic angiopathy in the fourth decade. The congophilic angiopathy is a frequent finding. Due to their high frequency, calcium or calciumlike deposits are regarded as important histopathological substrates of Down's syndrome. The clinical symptomatology of the long-surviving patients with Down's syndrome is that of a non-characteristic brain aging process and differs from that of the typical Alzheimer's disease. Organic dementia is not regularly found. Altogether, the anatomical findings in adult patients with Down's syndrome indicate a premature aging of the brain, which becomes more significant and widespread with increasing age.
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PMID:[Cerebral degeneration in Down's syndrome]. 15 70

The historical events in the evolution of Alzheimer's disease are reviewed, including the initial description by Alois Alzheimer and the subsequent controversy regarding the nosological specificity of this entity. The similarity of senile dementia and Alzheimer's disease is emphasized. The basis for the modern concept of Alzheimer's disease as premature or accelerated aging is included in the review. The pathological correlates of the major categories of adult dementia have been described. The traditional criteria of neurofibrillary tangles and senile plaques have been re-evaluated using the current insight into these changes afforded by electron microscopy and biochemistry. The significance of amyloid has been described because it occurs within the senile plaque and also as the essential component of congophilic angiopathy. The new information regarding neuronal cell counts and the loss of choline acetyltransferase has been evaluated in terms of an indication of a pathogenic mechanism of Alzheimer's disease. The current understanding of normal pressure hydrocephalus, Creutzfeldt-Jakob disease, and multi-infarct dementia has been described. Brain biopsy in dementia has been described as having diagnostic, research, pathogenic, and prognostic value. The precautions involving the performance and handling of the biopsy have been stressed, particularly because these procedures involve conditions of possible slow virus etiology. The polemic for Alzheimer's disease as aging or slow virus infection has been summarized. At this time a consideration seems justified that Alzheimer's disease is an age-related, slow virus disease due to a hitherto unknown immune defect. Aging as an etiological agent must be clarified before Alzheimer's disease, in any form, can be considered to be an inevitable consequence of longevity.
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PMID:Adult dementia: history, biopsy, pathology. 37 82

Blood vessels with amyloid angiopathy and senile plaques in the cortices of the brains with Alzheimer's disease and senile dementia were observed by means of a scanning electron microscope. the results obtained were as follows: The blood vessels with amyloid angiopathy were surrounded by solid substances. The senile plaques consisted of rough solid substances, contained degenerated cell processes, and almost all plaques existed around the degenerated capillaries with amyloid angiopathy. From the above described findings, we suggest that the senile plaque has an extremely cose relationship to the capillary which had undergone amyloid angiopathy.
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PMID:Observations of amyloid angiopathy and senile plaques by the scanning electron microscope. 50 98

In three cases of cerebral amyloid angiopathy there was also a chronic cerebral vasculitis characterized by segmental fibrinoid necrosis, chronic adventitial inflammatory infiltrates, obliterative "endarteritis" and hyaline arteriolar change, resembling rheumatoid vasculitis. Two of these cases had rheumatoid arthritis, and one had unspecified "arthritis" at the onset of dementia. Both vasculitis and amyloidosis involved the leptomeningeal and cerebral cortical vessels. In the two autopsy-verified cases, the vascular disease was limited to the brain. In the third case, only a brain biopsy was available. Amyloid-containing neuritic plaques were present in the cerebral cortex in all three cases, but they were abundant only in one, which also showed numerous Alzheimer tangles.
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PMID:Cerebral amyloid angiopathy: possible relationship to rheumatoid vasculitis. 57 77

A 58-year-old normotensive woman died 24 hours after a stroke. Two months earlier, she had a transient neurological episode consistent with cerebrovascular insufficiency. Necropsy demonstrated a massive recent hemorrhage in the right occipital lobe associated with severe cerebral amyloid angiopathy (CAA). The cerebral cortex showed interstitial and perivascular neuritic plaques but no Alzheimer's tangles. There was no family history of CAA. A review of the literature indicated that only ten cases of such hemorrhage caused by nonfamilial CAA have been reported. Massive intracerebral hemorrhage seems to be more common in patients with familial Icelandic forms of CAA.
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PMID:Fatal massive intracerebral hemorrhage complicating cerebral amyloid angiopathy. 63 62

Senile dementia of the Alzheimer type is becoming one of the most common of the malignant diseases as our society ages. Currently, research has identified several pathophysiological changes, including the bihelical filament and the loss of the enzyme choline acetyltransferase from the cortex. Although genetic factors play some role in this disease, the important environmental risk factors have not yet been identified and there is, at present, no specific treatment. The second most common cause of dementia, cerebrovascular disease, produces dementia only when there is destruction of brain tissue, as in individuals who have multiple strokes or who have hypertensive vascular disease leading to multiple lacunae. In both multi-infarct dementia and in the lacunar state, hypertension appears to play a greater role than it does in other forms of vascular disease. Many of the other causes of dementia, including normal pressure hydrocephalus, CNS infections or tumors, metabolic disorders produced by thiamine or vitamin B12 deficiency or thyroid dysfunction, are often reversible. Every patient, whatever the age, with a developing dementia deserves a thorough workup to identify these treatable disorders.
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PMID:Dementias. 75 96

Primary cerebrovascular amyloidosis resulting in significant cerebral parenchymal damage was encountered in 23 autopsied cases at the Mayo Clinic over the past 10 years. Patients were 60 to 97 years old and both sexes were equally represented. Large- and medium-sized leptomeningeal and cortical arteries showed the characteristic pattern of medial and intimal involvement, with luminal stenosis. The walls of smaller arteries were often diffusely infiltrated, with fibrinoid degeneration and miliary aneurysm formation. The amyloid nature of the infiltrate was confirmed by electron microscopic examination in all cases. All cases showed varying numbers of perivascular or independent senile plaques in the cerebral cortex. Alzheimer's neurofibrillary tangles were absent or were limited to the hippocampal region in all but two cases. Multiple, small cortical infarcts and hemorrhages were regularly present. Larger hemorrhage was present in nine cases. Of nine patients with terminal massive cerebral hemorrhage, only two were hypertensive. Six patients had had progressive dementia; four had had single episodes of vascular events and seven, multiple episodes; and four had had both dementia and vascular episodes. Primary cerebral amyloid angiopathy should be regarded as an important cause of mental deterioration and fatal cerebrovascular accidents in the elderly.
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PMID:Clinicopathologic studies of primary cerebral amyloid angiopathy. 75 33


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