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

We have used the end-specific monoclonal antibodies to amyloid beta-protein (A beta), BC05 and BA27, to investigate the molecular characteristics of the cored or stellate type of amyloid plaque that is sometimes present, along with the more common diffuse type of plaque, in the cerebellar cortex in (usually younger) cases of Alzheimer's disease. In five such cases of Alzheimer's disease the (many) cored plaques were strongly BA27, but less strongly BC05, immunopositive, indicating the presence of (much) A beta 40 and A beta 42(43), respectively. Diffuse plaques were only BC05 positive, except on rare occasions where a litter BA27 reactivity was present. Cerebellar cored plaques, like the diffuse plaques, were not associated with tau or astrocytic (glial fibrillary acid protein) immunoreactivity, though in contrast to cerebellar diffuse plaques, but like the cored plaques in the cerebral cortex, microglial cells were usually present. The cause of this form of A beta deposition in the cerebellum is not known. Although congophilic angiopathy was severe in two patients, this was only mild in the other. Similar plaques were also seen in the cerebellum of most, but not all, of five other younger patients with chromosome 14-linked Alzheimer's disease and again, although congophilic angiopathy was severe in one such case with many cored plaques, this was not so in the others. At present the relationship (if any) between this pathological change and the possession of the chromosome 14 mutation of Alzheimer's disease or the occurrence of congophilic angiopathy remains uncertain.
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PMID:Atypical amyloid (A beta) deposition in the cerebellum in Alzheimer's disease: an immunohistochemical study using end-specific A beta monoclonal antibodies. 878 65

Alzheimer disease, like other common chronic diseases, likely has genetic and environmental risk factors. Prevention of arteriosclerotic vascular disease has occurred based on efforts to reduce risk factors demonstrated in epidemiologic and more basic science research. At present, there are no known risk factors for Alzheimer disease which could form the basis of a preventive strategy. To make progress in the prevention of Alzheimer disease, new findings from epidemiology and basic science will be needed. The current state of the art of epidemiologic studies of dementia is well enough developed to test credible hypotheses. The availability of reliable biomarkers along with cooperative efforts between molecular biologists and clinical epidemiologists should allow us to pursue promising fields in clinical research.
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PMID:Prevention of Alzheimer disease: a perspective based on successes in the prevention of other chronic diseases. 887 81

The prevention of dementia is of critical importance. The increasing population of high-risk older individuals will result in an increasing prevalence of dementia. Primary prevention of dementia and Alzheimer disease can take either a public health or high-risk preventive medicine approach. At the present time, there is little evidence to support a specific primary public health approach such as a specific nutrient. The possible association of vascular disease with dementia may offer the best preventive high-risk approach. The identification of individuals with clinical and subclinical vascular disease is possible. There is a very high prevalence of subclinical cerebral infarction in older individuals. Specific treatments can prevent clinical disease such as stroke and coronary heart disease. Whether therapies will prevent some dementia can be determined.
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PMID:Potential prevention of Alzheimer disease and dementia. 887 82

Senile plaques were found in the cerebral cortices of three very aged cats (more than 18 years old). The plaques consisted of a coarse assembly of silver staining-positive materials, and was morphologically different from the well-known classical, primitive, and diffuse plaques. Congophilic amyloid angiopathy was observed in a few cortical arterioles of the oldest cat (20 years old). The senile plaques and a few cortical blood vessels were immunopositive for amyloid beta-protein (A beta). A beta-positive materials were also sparsely distributed in the cortical neuropil but did not form senile plaques there. These findings should help to clarify the development of senile plaques and the early stage of A beta deposition.
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PMID:Senile plaques in very aged cats. 892 23

Since the PAD gene (also called promoter of Alzheimer's disease amyloid A4 precursor gene or amyloid beta-protein precursor promoter) has two AP-1 consensus sequences, and members of the Fos and Jun families are the major components of the transcription factor activator protein-1 (AP-1), we have investigated the localization of c-Fos and c-Jun immunoreactivity and its relationship to beta-amyloid deposition in the brains of patients with Alzheimer's disease and amyloid angiopathy. c-Jun, but not c-Fos, immunoreactivity is observed in the muscular layer of meningeal and cerebral blood vessels with amyloid angiopathy, and in the soma of glial cells and cellular processes of unknown origin surrounding beta-amyloid deposits in the brain. These results show that c-Jun may participate in the cascade of events leading to increased beta-APP (beta-amyloid precursor protein) production and beta-amyloid deposition in the brains of patients with Alzheimer's disease and amyloid angiopathy.
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PMID:Amyloid deposition is associated with c-Jun expression in Alzheimer's disease and amyloid angiopathy. 900 42

Seizures and epilepsy in the elderly are an important and increasingly common clinical problem. Major known causes include cerebrovascular disease, brain tumor, degenerative disorders such as Alzheimer disease and cerebral amyloid angiopathy, and toxic-metabolic syndromes such as nonketotic hyperglycemia, postcardiac arrest, and drug-induced seizures. Recognition of seizures may be complicated by relatively unique clinical presentations and differential diagnosis. Nonconvulsive status epilepticus may present as recurrent episodes of confusion. The electroencephalogram is less useful than in the pediatric age group, but has a role in the evaluation of a first seizure and may rarely show characteristic patterns, such as poststroke periodic lateralized epileptiform discharges. Convulsive status, especially that associated with drug toxicity, is associated with increased mortality in the elderly. Pharmacological treatment is complicated by age-related changes in pharmacokinetics and pharmacodynamics and drug-drug and drug-disease interactions. Some of the new antiepileptic drugs may offer advantages for use in the elderly. Oxcarbazepine has fewer drug interactions than carbamazepine, and gabapentin has one, a reduction of felbamate renal elimination. Vigabatrin causes little cognitive dysfunction, while drugs that reduce excitatory amino acid neurotransmission, such as lamotrigine and felbamate, have potentially protective effects in patients with ischemic cerebrovascular disease. The use of barbiturates, primidone, the benzodiazepine clobazam, and the calcium blockers flunarizine and cinnarizine should preferably be avoided in the elderly.
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PMID:Seizures and epilepsy in the elderly. 943 89

Four different approaches to Alzheimer disease changes have been successively applied, and allowed a permanent feed forward-feed back enrichment of knowledge: morphologists described neurofibrillary tangles, senile plaques, amyloid angiopathy; with the help of immunohistochemical and biochemical techniques, they recognised A beta- and tau-associated pathologies; this, in turn, allowed more precise analysis of the lesions, and permitted recognising new ones such as neuropil threads; molecular genetics and molecular biology provided new insights, allowing the discovery of additional pathologic proteins, the relevance of which to physiology and pathology of the nervous system has now to be settled down. The increasingly intricate complex of lesions of Alzheimer syndrome is reviewed. A more comprehensive understanding is urgently needed for initiating efficient therapeutic researches. It will require together continuing a multidisciplinary approach, and a renewal of research in neuropathology.
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PMID:[Alzheimer's disease lesions: from morphology to cell biology]. 910 51

We studied the morphological and immunohistochemical characteristics of subpial amyloid plaques (SAPs), which were found particularly in the cerebellum of an Alzheimer's disease (AD) patient, and compared them to the senile plaques (SPs) and amyloid angiopathy in AD cerebrum. The case presented herein exhibited a variety of amyloid deposition including SAPs and amyloid angiopathy. SAPs were visualized most intensely with antibodies to amyloid-beta protein (A beta), compared with the conventional staining methods including silver impregnation techniques. The most unique feature of the SAPs consisted in their morphology and location, which was between the pia mater and brain parenchyma, occasionally bulging outside the brain surface. Immunostaining with monoclonal antibodies against the carboxyl termini of A beta showed that SAPs were invariably positive for A beta 42/43, two-thirds of which were associated with A beta 40. Ultrastructurally SAPs appeared either fibrillar or amorphous and were separated originally from the brain parenchyma by sheets of glia limitans. The chronological relationships in the evolution of the SAPs are discussed with relevance to their morphology and location.
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PMID:Subpial amyloid plaques in the cerebellum in a case of Alzheimer's disease. 913 93

Hereditary cerebral hemorrhage with amyloidosis-Dutch type is caused by a mutation at codon 693 of the beta amyloid precursor protein gene. The disease is clinically characterized by strokes and dementia. In addition to cerebral plaques, cerebral amyloid angiopathy is the pathological hallmark. We investigated the correlation between radiological (white matter hyperintensities and focal lesions on magnetic resonance images) and pathological lesions (cerebrovascular amyloid angiopathy and plaques) and the apolipoprotein E genotype in patients with the disease. Twenty-five patients were studied using magnetic resonance imaging, and brain tissue from 8 patients was studied histopathologically. Neither the white matter hyperintensity scores nor the number of focal lesions on magnetic resonance images were associated with the presence of an epsilon4 allele. Nor was a correlation found between the number and type of plaques and the apolipoprotein E genotype. All patients had severe amyloid angiopathy in all cortical areas investigated. This study showed that the apolipoprotein E genotype does not modulate amyloid-related structural lesions in hereditary cerebral hemorrhage with amyloidosis of the Dutch type.
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PMID:Dutch hereditary cerebral amyloid angiopathy: structural lesions and apolipoprotein E genotype. 915 36

Familial Alzheimer's disease (FAD) tends to present with more prominent neurological symptoms including cerebellar signs than sporadic Alzheimer's disease (SAD). In order to elucidate the pathological differences in the cerebellum, which may be associated with the cerebellar symptoms, we have investigated morphometrically beta-amyloid deposits, atrocytosis, Purkinje cells and dentate neurons in the cerebellum of 10 FAD patients including two cases with the beta-amyloid precursor protein (APP) gene mutation (APP717 Val-->Ile), 10 SAD patients and 10 non-demented age-matched controls. The regions examined included the molecular, Purkinje cell and granular cell layers, the cerebellar white matter and the dentate nucleus. Purkinje cell density in FAD was significantly lower than in SAD. There were no significant differences in the density of dentate neurons among the three groups. The density of astrocytes in FAD was significantly greater than that in SAD in the granular cell and Purkinje cell layers and in the white matter. There were no significant differences in the amount and subtypes of beta-amyloid deposits (extracellular, vascular and perivascular) between FAD and SAD in all the regions investigated. In two cases with the APP mutation, both Purkinje cell loss and beta-amyloid deposition in the cerebellum were greater than the mean for FAD and SAD cases. Astrocytosis in the mutation cases was not greater than the mean for FAD cases except for the dentate nucleus in one case. Extracellular beta-amyloid deposits were not seen in any of the control cases although amyloid angiopathy was observed in one case. This study demonstrates for the first time that Purkinje cell loss and reactive astrocytosis of the cerebellum in FAD are more severe than in SAD, but that beta-amyloid deposition in the cerebellum in both FAD and SAD are similar. The more prominent neurological signs observed in FAD may be explained by more severe neurodegeneration than are found in sporadic cases.
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PMID:Cerebellar pathology in sporadic and familial Alzheimer's disease including APP 717 (Val-->Ile) mutation cases: a morphometric investigation. 917 27


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