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Biomedical subjects

E Englund

Publications and source records attributed to E Englund.

At least 37 records · Page 2Linked to original sources
PubMed1997

The apolipoprotein E epsilon4 allele frequency is normal in fronto-temporal dementia, but correlates with age at onset of disease.

The apolipoprotein (apoE) epsilon4 allele was studied in fronto-temporal dementia (FTD), a diagnostic category including the specific disorders Pick's disease and frontal lobe degeneration of non-Alzheimer type (FLD). These dementing diseases have neuronal and synaptic degeneration in common with Alzheimer's disease (AD), for which the presence of the apoE epsilon4 allele is a known risk factor, and lowers the age of onset of disease. Previous studies on the apoE epsilon4 allele frequency in FTD have been inconclusive. The structural hallmarks of AD, allegedly linked to apoE presentation, neuritic plaques (NP), primarily composed of aggregates of beta-amyloid, and neurofibrillary tangles (NFT), primarily composed of hyperphosphorylated tau, are lacking in FTD. However, tau-positive cytoskeletal pathology is found in Pick's disease, but not in FLD. Resolving whether the epsilon4 frequency is increased in FTD or not may thus give clues to the pathogenetic mechanism of apoE in AD. We therefore studied apoE alleles in a well characterized material of FTD patients. The epsilon4 allele frequency was similar in 25 patients with FTD (14.0%) as compared with 26 healthy controls (13.5%). A post-mortem neuropathological examination was performed in 10 cases (nine had FLD and one Pick's disease). Our finding of a normal epsilon4 allele frequency in our group of FTD, principally consisting of FLD cases, support hypotheses involving differential binding of apoE to beta-amyloid and/or tau, in the development of beta-amyloid deposition and NP formation and/or tau hyperphosphorylation and NFT formation, for the pathogenetic role of apoE in AD. The age at onset was significantly lower (P < 0.01) in FTD patients possessing the epsilon4 allele (48.7 +/- 8.0 years) than in patients not possessing this allele (58.9 +/- 7.6 years). We conclude that, although the apoE epsilon4 allele frequency is not increase in FTD, the epsilon4 allele is not an etiological factor, but may rather be an accelerating factor in the degenerative process of FTD, thereby resulting in an earlier presentation of the disorder in individuals predisposed to develop FTD.

Adult↗
PubMed1997

Radical endarterectomy of severely calcified ascending aorta prevents stroke during open-heart surgery.

In ten patients (7 women), mean age 73 years, with severely calcified ascending aorta, aortic valve and coronary artery disease were surgically treated after radical endarterectomy of the ascending aorta during cardiopulmonary bypass and with or without deep hypothermic total circulatory arrest. One patient died 10 days and one 11 months postoperatively of complications which neither directly nor indirectly could be attributed to the aortic endarterectomy. The eight surviving patients are doing well after follow-up averaging 16 months. CT scans 1 year postoperatively showed no aneurysmal dilation of the ascending aorta or aortic dissection distal to the endarterectomy site. Radical endarterectomy of calcified ascending aorta thus can be performed with relatively low mortality and stroke risk and may be considered in patients undergoing valve replacement and/or coronary artery bypass grafting.

Aged↗
PubMed1996

Fundamental pathological lesions in vascular dementia.

This review concerns the fundamental cerebral lesions in cases of vascular dementia. Extracerebral vascular alterations are dominated by atherosclerosis with or without thrombosis. In addition, occlusion of extracerebral arteries can be induced by thrombo-embolism and in rare cases by other vascular diseases, chiefly arteritis. Intracerebral microangiopathies are usually of arteriolosclerotic or hyalinotic types in which there is degeneration of smooth muscle cells of the media and deposition of components of extracellular matrix, chiefly collagens. Ageing, chronic hypertension, hyperlipidemias and diabetes are important factors inducing vascular lesions. The vascular lesions, often combined with systemic factors, may produce various ischemic and edematous alterations of the brain parenchyma. Occlusion and obliteration of arteries (macroangiopathy) are associated with large infarcts, whereas microangiopathy may cause lacunar infarcts and some forms of white matter degeneration. Cases of vascular dementia usually present many types of lesions in the brain parenchyma and its arterial supply. The extent and location of the injuries differ considerably from case to case. Location of the lesions, volume of destroyed tissue, multiplicity and bilateral occurrence are most important parameters underlying the clinical manifestations in vascular dementia. A strategic location of a small injury is in some cases of particular importance.

Aged↗
PubMed1990

White matter changes in dementia of Alzheimer's type: the difference in vulnerability between cell compartments.

Structural white matter changes were found to be common in dementia of Alzheimer's type. A neuropathological investigation was undertaken in order to characterize and quantify these white matter changes. The tissue changes were compared with those in white matter in normal control cases and in complete white matter infarcts. Our results support the hypothesis that the white matter lesion seen in dementia of Alzheimer's type is due to incomplete infarction involving both axons and myelin and is a result of mild ischaemia. In mild ischaemia, the myelin compartment appears to be the most vulnerable. We have termed the lesion selective incomplete white matter infarction.

Aged↗
PubMed1988

White matter changes in dementia of Alzheimer's type. Biochemical and neuropathological correlates.

A correlative neuropathological-biochemical study was undertaken in order to characterize the selective incomplete white matter infarctions (SIWI) frequently found in dementia of Alzheimer's type. The brain tissue analysed represented white matter with incomplete infarction, complete infarcts and with histologically normal tissue, in cases with dementia, mainly of Alzheimer and multi-infarct type, in nondemented subjects with cerebral infarcts and in age-matched control cases. The biochemical results verify the existence of the white matter changes and agree on their regional distribution as they appear in the morphological analyses. The increasing severity of SIWI as assessed histologically was reflected in a proportional reduction of several biochemically quantified white matter components. The histological difference between incomplete and complete infarction was also expressed biochemically. Incomplete white matter infarction with and without associated complete infarcts were biochemically similar. The aetiological significance of the loss of different white matter components is discussed. The biochemical data support the concept of SIWI as being an independent white matter disorder of cerebrovascular, hypoperfusional/hypoxic origin.

Aged↗
PubMed1987

Frontal lobe degeneration of non-Alzheimer type. IV. White matter changes.

The cerebral white matter in 16 cases of frontal lobe non-Alzheimer degeneration with dementia (FLD), four cases of Pick's disease and five age-matched controls was studied microscopically. All cases of dementia had white matter alterations, consisting of gliosis and loss of myelin, with a regional spread of changes that roughly corresponded with that of the cortical degeneration. The white matter changes were less severe than the cortical alterations, although the relative degree of severity between grey and white matter pathology varied from case to case. The white matter changes were in some respects similar in FLD and Pick's disease. They differed from those of other organic dementias. In FLD, they seem to be part of the histopathologic picture and to be secondary to the cortical degeneration.

Aged↗
PubMed1987

Correlations between histopathologic white matter changes and proton MR relaxation times in dementia.

Our previous studies have shown that incomplete white matter infarctions are common in senile dementia of the Alzheimer type. To visualize and interpret these changes on magnetic resonance imaging (MRI), knowledge of MR relaxation times associated with this histopathology is important. The proton MR relaxation times T1 and T2 were determined in vitro for 3 groups of specimens. Fifty specimens of normal and incompletely infarcted white matter from 21 patients with senile dementia and 38 normal and pathologic white matter specimens from 19 elderly cases with infarcts were analyzed. The specimens were evaluated for infarct type, grade of incomplete infarction, and the proportion of old complete or incomplete infarction versus normal tissue in each sample. The incomplete infarct had longer relaxation times than normal white matter, with prolongation of T1 and T2 being proportional to the severity of the tissue changes. Old complete infarcts had longer relaxation times than both normal white matter and incomplete infarctions. These differences in relaxation times, reflecting various degrees of tissue damage, are important for the interpretation of MR images in vivo. Visualization of incomplete infarctions is essential for an in vivo diagnosis of these frequent and sometimes extensive changes.

Alzheimer Disease↗
PubMed1986

A white matter disorder in dementia of the Alzheimer type: a pathoanatomical study.

In cases of Alzheimer's presenile and senile dementia, Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT), respectively, we have observed, in addition to the gray matter degeneration, a lesion that has the character of an incomplete infarction confined to the white matter. It is encountered in 60% of both groups, with mild changes in two thirds and moderate or severe changes in one third. It involves the deep white matter symmetrically, tapering off toward the cortex. It is characterized by partial loss of myelin, axons, and oligodendroglial cells; mild reactive astrocytic gliosis; and sparsely distributed macrophages as well as stenosis resulting from hyaline fibrosis of arterioles and smaller vessels. No complete or cavitating infarctions and no hypertensive vascular changes were observed. The white matter changes are thought to be due to hypoperfusion of the concerned white matter territories since, in addition to the white matter hyaline vascular stenosis, these cases show signs of cardiovascular disease, usually with hypotension. The white matter disorder also occurs independent of the gray matter process of AD and SDAT and may be seen as the sole brain lesion in non-AD subjects. Its occurrence is thus neither regularly related to the severity nor to the regional appearance and accentuation of the cortical Alzheimer process and is thus not likely to be just the result of a wallerian degeneration. Histologically it is similar in several respects to Binswanger's disease, although with some distinct differences. It is thus related to the cerebrovascular group of disorders in addition to AD and SDAT. In view of its frequency and severity, this white matter lesion is important to define, to diagnose, and ultimately to prevent or cure.

Aged↗
PubMed1986

Brain changes in dementia of Alzheimer's type relevant to new imaging diagnostic methods.

The aim of the article is to correlate grey and white matter changes and their topography to the results of modern methods for brain imaging such as CT, rCBF, PET, SPECT and NMR in Alzheimer's type of dementia. The findings are based on the study of a large material investigated thoroughly patho-anatomically. The findings are correlated with psychiatric and neurophysiologic follow-up studies. The degenerative grey matter process shows a regionally varying accent according to a pattern which is consistent and typical for the disease. This corresponds to metabolic changes on rCBF, PET and SPECT and thereby becomes of diagnostic value. This pattern is largely symmetric. Metabolic asymmetries have however been reported on PET scans. In this context individual variations of the topographic degenerative brain pattern and normal anatomical brain asymmetries are of interest. The white matter however also frequently shows changes, in particular loss of myelin and axons and a mild gliosis, slight in 1/3 of the cases and severe in an additional 1/3. These changes cause a decrease of density in the centrum semiovale correlating to lipid depletion. They may also influence the ventricular shape and size, of interest in CT or NMR studies. Also here variations in ventricular shape, normal and such due to pathological processes unrelated to the Alzheimer disease, may cause confusion, regarding degree of atrophy and even type of brain process. Such factors should be considered in the interpretation of non-invasive brain studies.

Aging↗
PubMed1981

Regional pattern of degeneration in Alzheimer's disease: neuronal loss and histopathological grading.

The various structural components of the cortical degeneration of Alzheimer's disease were defined and graded. The severity of the degenerative process was thus mapped in different cortical areas where neuronal numbers and cortical width were also measured and compared with controls. Contrary to the general opinion that the degenerative process is rather uniformly diffuse, though accentuated in the medial temporal and frontal cortex, we found a consistent and more elaborate pattern with clearcut regional differences. Thus the degeneration involved, besides basal medial temporal limbic areas, the posterior cingulate gyrus and superior parietal lobule particularly, with somewhat less marked changes in the inferior parietal lobule and inferior temporal gyri. The sensorimotor, calcarine and anterior cingulate areas of the cortex were notably spared until very late stages. This regionally variable severity of the degeneration was also paralleled by a regionally varying reduction in neuronal numbers and cortical width, and agrees with our previously published results of a regional pattern which closely correlates with clinical parameters, including symptom pattern and regional cerebral blood flow alterations.

Aged↗
PubMedDate not supplied

Diagnostic value of electron microscopy in a case of juvenile neuronal ceroid lipofuscinosis.

Neuronal ceroid lipofuscinoses (NCLs) represent a large group of inherited neurodegenerative disorders characterized by an abnormal accumulation of lipopigment in neuronal and extraneuronal cells. The authors present a case of juvenile neuronal ceroid lipofuscinosis in a 7-year-old boy. Ultrastructural examination of a skin biopsy disclosed deposits of curvilinear profiles and fingerprint-like structures in epithelial cells of sweat glands, endothelial cells, peripheral nerve endings, and fibroblasts. These findings allowed specific confirmation of the assumed diagnosis of juvenile neuronal ceroid lipofuscinosis. Due to the genotypic and phenotypic variability within the group of NCLs, the clinical investigation may be long and complicated. With the NCL disorders in mind, an accurate diagnosis based on ultrastructural examination of a skin biopsy may shorten this investigation, thus benefitting the patient.

Biopsy↗
PubMedDate not supplied

Vascular dementia: the role of cerebral infarcts.

Although vascular dementia (VaD) is the second most frequent cause of dementia after Alzheimer disease (AD), the concept remains controversial in terms of delineation. The objective of this review is to investigate, from available literature, the role of cerebral infarcts in the pathogenesis of VaD and to identify areas of interest that need further evaluation and research. The incidence of new onset dementia is increased after stroke. Stroke subtypes, total volume of cerebral infarction and functional tissue loss, and location of the lesions are probably the major determinants of VaD. Any cause of stroke can lead to VaD. In some circumstances the causal relation between stroke and dementia is clear: (1) in young patients who are unlikely to have associated Alzheimer pathology; (2) when the cognitive functioning was normal before stroke, impaired immediately after, and does not worsen over time; (3) when the lesions are located in strategic areas; and (4) when a well-defined vasculopathy known to cause dementia is proven. However, several issues remain unsolved in VaD: lack of specificity of the diagnostic criteria; influence of white matter changes and associated Alzheimer pathology; influence of preexisting cognitive status; possibility of having VaD without stroke and the clinical relevance of silent infarcts to VaD; and best therapeutic strategy to be used to prevent VaD and to prevent stroke in patients with VaD. These questions form the basis for proposals for future research.

Cerebral Infarction↗
PubMedDate not supplied

Reduced number of caudate nucleus dopamine uptake sites in vascular dementia.

The dopamine (DA) uptake sites in the caudate nucleus were studied in patients with vascular dementia (VAD) and in a control group using the presynaptic DA uptake site marker [3H][2beta-carbomethoxy-3beta-(4-fluorophenyl) tropane] as radioligand. There was a significant decrease in the number of DA uptake sites in the VAD group, while the binding affinity was unchanged. The present results indicate that in the patients investigated, the cerebrovascular disease process involves dopaminergic neuron terminals in the caudate nucleus. Our findings are discussed in relation to the reductions in number of DA uptake sites that have previously been revealed in Alzheimer's and Parkinson's diseases.

Aged↗
PubMedDate not supplied

Magnetic resonance imaging and histopathology in dementia, clinically of frontotemporal type.

The magnetic resonance imaging (MRI) and computed tomography findings in 28 patients with the clinical diagnosis of frontotemporal dementia (FTD) were compared with the findings in a control group of 76 individuals without dementia or stroke. A pattern of frontal and temporal atrophy with predominantly frontal white matter changes was found in the FTD patients, and this was significantly different from the radiological findings in the control group. Six of the FTD patients have undergone autopsy. Histopathological evaluation showed a primary cortical degenerative disease (frontal lobe degeneration of non-Alzheimer type) in 3 of them, and primary white matter disorder, mainly frontal, of basically ischemic type (selective incomplete white matter infarction) in 3 of them. MRI could be a helpful tool to support the clinical diagnosis FTD, especially in young patients. MRI may also be helpful for the differentiation of a primary neurodegenerative from a mainly ischemic-vascular type of dementia.

Adult↗
PubMedDate not supplied

Alzheimer's disease and the cerebellum: a morphologic study on neuronal and glial changes.

Structural manifestations of Alzheimer's disease (AD) including neuronal loss were investigated in 12 cases of AD and in 10 healthy age-matched controls, with focus on the cerebellum. Linear Purkinje cell (PC) density was measured in the vermis and cerebellar hemispheres. Neurons were also counted in the inferior olivary nucleus. In vermis of the AD cases, the mean PC number was significantly lower (p = 0.019) than in the controls. The neurons in the inferior olive were similarly fewer, though not significantly (p = 0.13). Molecular layer gliosis and atrophy in the vermis was clearly severer in AD than in the controls. Features typical of cerebral Alzheimer encephalopathy (plaques, tangles and microvacuolization) were inconspicious. The structural cerebellar changes in the AD cases were thus neuronal loss, atrophy and gliosis, judged to represent the disease process, and with a main involvement in the vermis. This may be reflected in some of the symptoms and signs seen in AD, signs that are generally overlooked or judged to be of noncerebellar origin.

Aged↗