Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty brains from patients prospectively studied in a geriatric hospital (Charles Richet Study) were examined pathologically. The patients were senile (mean age: 85) and demented and had been clinically diagnosed as senile dementia of Alzheimer type (SDAT), vascular or multi-infarct dementia (VD), mixed dementia (MD). The whole brain was studied after formalin fixation and coronal sections. The senile changes were quantified in 6 neocortical areas, hippocampus and amygdala and subcortical structures after staining by thioflavine--S and Bodian's method. The other vascular and degenerative lesions were semiquantitatively studied. Three groups of patients were identified after microscopic examination: 1. SDAT (n = 27), 2. VD (n = 6), 3. MD (n = 15), 2 patients had no significant pathological correlate for dementia. Comparison of thioflavine S and Bodian's method in 30 cases showed the former to be more sensitive for the identification of senile plaques. In SDAT, 13/27 brains lacked neurofibrillary tangles in the neocortex. Amyloid angiopathy was observed in 78% of the brains but lacked in 5/6 cases affected by pure VD. Significant lesions of the substantia nigra were observed in 13 cases with typical features of Parkinson's disease in 2 cases. The locus coeruleus was affected mainly in SDAT cases (20/27) and in some cases of VD or MD (6/21). The raphe nuclei showed neuronal loss in 18% of the cases, mostly SDAT. In this series of cases, neocortical neurofibrillary tangles could be lacking in SDAT. Amyloid angiopathy was almost always present in SDAT and MD. Subcortical structures involved in cholinergic, noradrenergic and serotoninergic innervation of the cortex were more severely impaired in SDAT and MD than in VD. Mixed dementia was frequent in these very old demented patients. Clinical and pathological criteria are needed to identify this group of patients.
 ...
PMID:[Neuropathologic study of 50 cases of senile dementia]. 207 18

In a prospective longitudinal study with death as the end point in 17 middle-aged patients with Down's syndrome, dementia was clinically diagnosed in 15 patients, by means of careful observations in daily circumstances. Autopsies were performed in 10 cases: 8 demented patients and 2 nondemented patients. Neuropathologically, Alzheimer-type abnormalities were demonstrated in 9 patients, both demented and nondemented, and combined Alzheimer-type abnormalities with infarctions were demonstrated in 1 patient. In the 14 demented patients who did not show evidence of cerebrovascular or systemic vascular disease, dementia had an early onset and was rapidly progressive (mean age at onset, 51.3 years in the moderately retarded patients and 52.6 years in the severely retarded patients; mean duration of symptoms, respectively, 4.9 and 5.2 years). Cognitive and behavioral decline corresponded to symptoms of dementia of the Alzheimer's type in patients without Down's syndrome, but often were not recognized early. In the present group of patients, there was a remarkably high incidence of gait and speech deterioration. Also, the incidence of epileptic seizures and myoclonus was about eightfold, as compared with dementia of the Alzheimer's type in patients without Down's syndrome.
 ...
PMID:The natural history of dementia in Down's syndrome. 213 13

Arteriolosclerotic leucoencephalopathy in the elderly (ALE) is characterized by white matter lesions associated with atherosclerosis and arteriolosclerosis. Mild lesions are focal and probably represent early status cribosus or incomplete lacunar infarcts. Moderate and severe lesions are diffuse areas of demyelination in the centrum semiovale in which lacunar infarcts are seldom observed. The incidence of ALE in a consecutive necropsy series of 50 cases (mean age 62.6 +/- 13.1 years) was 52%, it was rare in the fourth and fifth decades but increased thereafter to reach a prevalence of 100% at the age of 80 years. Mild lesions occurred in 19 patients and lesions were moderate or severe in 7 (14%). The mean age was higher in this group (74.7 +/- 7.6 years) than in patients with white matter changes as a whole. Dementia occurred only in 3 patients with moderate or severe ALE. These data suggest that (a) ALE is common in old age and is probably the cause of leuko-araiosis in most CT scans in the elderly; (b) ALE may be asymptomatic; (c) the severity of white matter changes may be not related to the severity of neurological deficits; and (d) multiple lacunar infarcts or associated degenerative diseases (i.e., Alzheimer's disease) may be the main cause of dementia in patients with ALE. White matter lesions in ALE, Binswanger's disease, transition areas in multi-infarct encephalopathy (MIE) and Alzheimer's disease (AD) are similar in morphology and are probably the result of a subacute hypoperfusion/hypoxic process. Increased arterial blood pressure is a frequent risk factor in ALE, Binswanger's disease and MIE, whereas congophilic angiopathy of the meningeal and cortical vessels, in addition to mild or moderate arteriolar hyalinosis in the white matter, may play a role in the pathogenesis of incomplete infarctation of the white matter in patients with AD.
 ...
PMID:Arteriolosclerotic leucoencephalopathy in the elderly and its relation to white matter lesions in Binswanger's disease, multi-infarct encephalopathy and Alzheimer's disease. 223 Aug 30

Cerebral amyloid angiopathy can present as lobar intracerebral hemorrhage in an elderly person, presumably due to increased fragility of the vessels affected by amyloid deposition. For this reason, patients presenting with intracerebral hemorrhage and suspected of having cerebral amyloid angiopathy have often been treated nonsurgically. Since 1983 we have evaluated 11 patients with cerebral amyloid angiopathy (nine women and two men, mean age 73 years) who have undergone either intracerebral hematoma evacuation or brain biopsy. Nine of the 11 patients presented with intracerebral hemorrhage, which was unilobar in three patients and multilobar in six and involved the parietal lobes seven times, the frontal lobes four times, the temporal lobes four times, and the occipital lobes twice. These nine patients underwent hematoma removal, with no cases of abnormal intraoperative bleeding or recurrent hemorrhage. Six patients improved neurologically, and two were unchanged after hematoma evacuation; the remaining patient had a fatal cardiopulmonary arrest during the immediate postoperative period. During follow-up in seven patients (median 11 months, range 1 week to 74 months) none experienced a recurrent intracerebral hemorrhage and four continued to improve. Two of the 11 patients had cerebral amyloid angiopathy diagnosed by brain biopsy as part of an evaluation for dementia, also without surgical complications. This series suggests that patients with cerebral amyloid angiopathy may safely undergo operative procedures, and patients presenting with intracerebral hemorrhage may show neurologic improvement following evacuation of the hematoma.
 ...
PMID:Surgical experience with cerebral amyloid angiopathy. 223 47

The clinical history and magnetic resonance imaging (MRI) findings are presented of 7 patients with hereditary cerebral haemorrhage with amyloidosis--Dutch type (HCHWA-D). The diagnosis was based on clinical and genealogical data, was confirmed in 3 patients at autopsy and in 2 others by biopsy. Focal neurological signs, and at least some degree of global cognitive deterioration, were observed in all patients, with unequivocal dementia in 4. MRI showed haemorrhages and areas of gliosis and, to a variable extent, hyperintensity of the white matter in T2-weighted images. Neuropathological examination revealed a large recent haemorrhage together with residual lesions from previous haemorrhages or infarcts in all patients examined. The white matter lesions, present on MRI, turned out to be areas of 'incomplete infarction' with demyelination. It is concluded that (hereditary) amyloid angiopathy can lead to strokes, but also to subcortical ischaemic encephalopathy. Amyloid angiopathy should therefore be considered in the differential diagnosis of white matter lesions, found on CT or MRI, especially when patients present with a cerebral haemorrhage. The relationship between HCHWA-D and Alzheimer's disease, another disease with cerebral amyloid deposition and diffuse white matter involvement, is discussed.
 ...
PMID:Hereditary cerebral haemorrhage with amyloidosis--Dutch type. Magnetic resonance imaging findings in 7 cases. 224 95

An 88-year-old mentally normal woman (Blessed test score = 27) had very large amounts (397/mm2) of deposits stained by anti-beta A4 serum in the first temporal gyrus. Senile plaques and neurofibrillary tangles were lacking on sections stained with the Bodian's silver method, with anti-tau and anti-paired helical filament (anti-PHF) antibodies. The following beta A4 deposits were found in decreasing order of frequency: diffuse (64.8%), stellate (24.4%), primitive (10.2%), classic (0.6%) plaques. Compact plaques were not observed. Diffuse deposits predominated in layers I, III and IV. On the contrary, the rare classic plaques were located in layers II and III. No amyloid angiopathy was seen with Congo red stain although beta A 4 deposits were seen in vessel walls with immunocytochemistry. These data indicate that severe diffuse beta A4 deposits in the neocortex do not induce dementia. They suggest that the development of senile plaques composed of beta A4 amyloid and of degenerating neurites is not related solely to the density of the diffuse beta A4 deposits. Nor does it depend on the regional susceptibility of the nervous tissue since beta A4 deposits were seen in highly vulnerable cortical areas. Some other, as yet unknown, factors seem necessary. In addition, determination of beta A4 level in the neocortex is not sufficient for the diagnosis of dementia of Alzheimer type.
 ...
PMID:Large amounts of neocortical beta A4 deposits without neuritic plaques nor tangles in a psychometrically assessed, non-demented person. 225 57

Using modified Bielschowsky method, we studied neuropathologically 159 aged subjects autopsied during the period from 1976 to 1988, of which we found 19 cases (average age at death: 82.6 ys) with numerous diffuse plaques in the frontal and temporal neocortex and no severe senile changes in H1-H3 of Ammon's horn (dp group). Amyloid angiopathy had been excluded and one case was excluded because of considerable cerebrovascular lesions. The dp group was divided into 8 demented (average age at death: 86.0 ys) and 10 nondemented patients (average age at death: 79.7 ys). We compared the number, type, and ratio of types of senile plaques in the frontal cortex, temporal cortex, and putamen of the demented and nondemented groups, and obtained the following results: (1) Eight (14%) of the 59 nondemented and 8 (40%) of the 20 demented cases in which no severe senile changes in the neocortex and hippocampus had been detected by Bodian stain showed numerous diffuse plaques in the neocortex when the modified Bielschowsky method was used. (2) The ratio of classic and primitive plaques to diffuse plaques in the frontal cortex was the same in both groups, but the nondemented group had exclusively diffuse plaques in the temporal cortex. (3) In the putamen 2 nondemented cases (20%) and 6 demented cases (75%) had exclusively diffuse plaques. We considered that classic and primitive plaques are more closely related to dementia than are diffuse plaques in the temporal lobe in cases without severe senile changes in the hippocampus.
 ...
PMID:[Cases of numerous diffuse plaques in the neocortex but without severe senile changes in the hippocampus]. 227 58

To aid in the prospective study of Binswanger's disease, a poorly understood form of vascular dementia, a standardised criteria for its antemortem diagnosis was proposed. These criteria include dementia, bilateral radiological abnormalities on computed tomography (CT) or magnetic resonance imaging (MRI), and at least two of the following three clinical findings: A) a vascular risk factor or evidence of systemic vascular disease; B) evidence of focal cerebrovascular disease; and C) evidence of "subcortical" cerebral dysfunction. These criteria were validated in two ways. First, by retrospectively applying them to a series of 30 demented patients with various pathological diagnoses. Second, by prospectively applying them to a series of 184 patients with clinically typical Alzheimer's disease. The sensitivity and specificity of the criteria appear adequate for use in clinical research.
 ...
PMID:Clinical diagnosis of Binswanger's disease. 178 35

Alzheimer's disease is a frequent cause of dementia in the elderly. The prevalence and incidence increase with aging. It is hypothesised that the age related decline in liver size and lysosomal function results in decreased clearance as well as decreased or altered proteolysis of the Alzheimer precursor protein, and results in the deposition of A4 protein in cerebral blood vessels and brain with congophilic angiopathy and senile/amyloid plaque formation.
 ...
PMID:Hepatic aging as an etiological factor in the development of Alzheimer's disease. 229 79

Clinical and computed tomographic findings in 24 patients with hereditary cerebral hemorrhage with amyloidosis-Dutch type were reviewed. The common initial symptoms were headache and vomiting. Computed tomographic scans showed 50 hypodense and 49 hyperdense cortical lesions and in 20 patients the scans also showed generalized white matter hypodensity. Impairment of consciousness was related to the size of the hemorrhagic lesion. Dementia, seen in 11 patients, was related to the duration of the disease and the number of focal lesions on the computed tomographic scans, but not to the presence of white matter hypodensity. It is concluded that in hereditary cerebral hemorrhage with amyloidosis-Dutch type, lobar hemorrhages account predominantly for the acute clinical syndromes. The hemorrhages often have an irregular shape and are responsible for progression of the symptoms after an acute onset. Furthermore, cerebral amyloid angiopathy leads to a generalized abnormality of the white matter, probably due to chronic hypoperfusion.
 ...
PMID:Hereditary cerebral hemorrhage with amyloidosis-Dutch type. Clinical and computed tomographic analysis of 24 cases. 234 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>