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Martin Sjöbeck

Publications and source records attributed to Martin Sjöbeck.

10 recordsLinked to original sources
PubMed2006

Mapping the intracellular fraction of water by varying the gradient pulse length in q-space diffusion MRI.

Finite gradient pulse lengths are traditionally considered a nuisance in q-space diffusion NMR and MRI, since the simple Fourier relation between the acquired signal and the displacement probability is invalidated. Increasing the value of the pulse length leads to an apparently smaller value of the estimated compartment size. We propose that q-space data at different gradient pulse lengths, but with the same effective diffusion time, can be used to identify and quantify components with free or restricted diffusion from multiexponential echo decay curves obtained on cellular systems. The method is demonstrated with experiments on excised human brain white matter and a series of model systems with well-defined free, restricted, and combined free and restricted diffusion behavior. Time-resolved diffusion MRI experiments are used to map the spatial distribution of the intracellular fraction in a yeast cell suspension during sedimentation, and observe the disappearance of this fraction after a heat treatment.

Journal Article↗
PubMed2006

Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia.

BACKGROUND AND PURPOSE: Vascular dementia (VaD) has occasionally been associated with cerebral amyloid angiopathy (CAA), but the prevalence and significance of this counterintuitive relationship are poorly known. Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases. METHODS: We examined temporal and parietal regions of the cerebral cortex of 26 consecutive VaD cases from the Lund Longitudinal Dementia Study. We carried out immunohistochemistry and routine stainings, determined Apolipoprotein E (ApoE) genotypes, and obtained clinical characteristics on the studied group for retrospective analysis. RESULTS: CAA was marked in eight out of 26 cases, and correlated strongly with the presence of cortical microinfarcts, both in the temporal lobe and in the parietal lobe. Based on comparisons with eight age-matched VaD cases without CAA, the clinical records suggested that VaD cases with CAA as a group exhibited less pronounced neurological symptoms. A clear contribution of the ApoE genotype could not be identified. CONCLUSIONS: Based on a combination of the clinical and pathological data, we suggest that microinfarcts in the cerebral cortex associated with severe CAA may be the primary pathological substrate in a significant proportion of VaD cases. Future studies should be undertaken to confirm or dismiss the hypothesis that these cases exhibit a different symptom profile than VaD cases without CAA.

Aged, 80 and over↗
PubMed2006

White matter mapping in Alzheimer's disease: A neuropathological study.

White matter disease (WMD) with pervasive non-focal subtotal tissue loss is frequently seen in Alzheimer's disease (AD) upon neuropathological examination. Although WMD has varying effects on AD symptoms, accurate clinical detection is difficult due partly to scarcity of correlative structural imaging and histopathological studies. Neuropathological studies of WMD severity and distribution have been conducted earlier using semi-quantitative methods. A technique for quantifying WMD objectively in large white matter areas, based on optical density (OD) measurements on images of scanned whole-brain sections, was developed and was validated using conventional microscopic assessment. Altogether, 16 AD cases with concomitant WMD (AD-WMD) and 9 cases of AD without WMD (AD-only) were analysed. The OD values correlated significantly with the neuropathological severity of WMD and were significantly lower in AD-WMD than in AD-only in frontal, frontoparietal, temporal and parietal white matter but not in the occipital white matter, the frontal OD difference being greatest. Useful baseline information on WMD distribution in AD to relate to in vivo imaging results was obtained.

Aged↗
PubMed2006

Locus ceruleus degeneration is ubiquitous in Alzheimer's disease: possible implications for diagnosis and treatment.

Degeneration of the locus ceruleus (LC) and decreased cortical levels of norepinephrine are common findings in Alzheimer's disease (AD), but their significance is unknown. Because the noradrenergic system is accessible to pharmacological intervention, the role of LC degeneration and noradrenergic dysfunction in the pathogenesis and clinical manifestations of AD needs clarification. Hypothetically, loss of noradrenergic innervation could cause microvascular dysfunction and manifest as ischemia. The objectives of this study were to develop a scale for assessment of LC degeneration and to determine whether degeneration of the LC correlates quantitatively with either duration of clinical dementia, overall severity of AD pathology or with measures of ischemic non-focal white matter disease (WMD) in AD. This report is a pathological follow-up of a clinical longitudinal dementia study of 66 consecutive cases of AD without admixture of vascular dementia (VaD) from the Lund Longitudinal Dementia Study, neuropathologically diagnosed between 1990 and 1999. Ten cases of VaD were included for comparative purposes. No correlation between degree of LC degeneration and duration of dementia, AD or WMD severity was found. LC degeneration was significantly more severe in the AD group than in the VaD group. Even though LC degeneration was not associated with WMD or the severity of AD pathology in this AD material, we suggest that clinical studies on the consequences of noradrenergic dysfunction are warranted. Treatment augmenting noradrenergic signaling is available and safe. The marked difference in the level of LC degeneration between AD and VaD cases suggests that LC degeneration could be used as a diagnostic marker of AD.

Adrenergic Agonists↗
PubMed2005

Decreasing myelin density reflected increasing white matter pathology in Alzheimer's disease--a neuropathological study.

BACKGROUND: White matter disease (WMD) is frequently seen in Alzheimer's disease (AD) at neuropathological examination. It is defined as a subtotal tissue loss with a reduction of myelin, axons and oligodendrocytes as well as astrocytosis. Studies quantitatively defining the myelin loss in AD are scarce. The aim was to develop a method that could provide numerical values of myelin density in AD. The purpose was to compare the myelin contents in increasing grades of pathology of WMD, with age and cortical AD pathology as well as in different regions of the brain in AD. MATERIAL AND METHODS: Sixteen cases with AD and concomitant WMD were investigated with an in-house developed image analysis technique to determine the myelin attenuation with optical density (OD) in frontoparietal, parietal, temporal and occipital white matter on whole brain coronal sections stained for myelin with Luxol Fast Blue (LFB). The OD values in LFB were compared grouped according to Haematoxylin/Eosin (HE) evaluated mild, moderate and severe WMD or normal tissue. The OD values were also correlated with age and cortical AD pathology and compared between the different studied white matter regions. RESULTS: Increasing severity of WMD was associated with a statistically significant OD reduction. No correlation was seen between age and OD or overall cortical AD pathology. The OD values were significantly lower in frontoparietal-compared to occipital white matter. CONCLUSIONS: Myelin loss in AD with WMD is a marked morphologic component of the disease and it is possible to determine the reduction objectively in neuropathological specimens with quantitative measures. This may be of use for clinical diagnostics including brain imaging.

Age Factors↗
PubMed2005

Long-term follow-up in depressed patients treated with electroconvulsive therapy.

DESIGN: Our aim was to study the long-term effects of electroconvulsive therapy (ECT) in depression. A total of 55 patients were followed-up 20 to 24 years after an ECT series; 13 patients were still alive, and 10 agreed to participate in the study. All 55 patients had been investigated with clinical and neuropsychological assessment and with neurophysiological measurements and with regional cerebral blood flow (rCBF) and EEG before the first ECT, 6 months later, and after approximately 1 year. These investigations were repeated in the 10 patients. RESULTS: Before the original ECT series, all patients had suffered from severe mood disorder. At follow-up, the 10 patients showed no clear signs of mood disorder or cognitive impairment. There was a slightly subnormal performance in working memory and in verbal as well as visual episodic memory on all 3 occasions after the ECT series. The rCBF measurement showed a significant average CBF decrease from the first to the last measurement. There was, moreover, a significant rCBF decrease in frontal areas at the last measurement compared with the 3 previous assessments. CONCLUSION: All ten patients followed-up 20 to 24 years after an ECT series were mentally healthy and thus besides a moderate visual memory dysfunction, no severe side effects were observed with clinical and neuroimaging techniques.

Adult↗
PubMed2004

Severe cerebral amyloid angiopathy characterizes an underestimated variant of vascular dementia.

Cerebral amyloid angiopathy (CAA) is a frequent finding on neuropathological examination of patients with Alzheimer's disease (AD). A recent study from our laboratory showed that CAA also frequently occurred in vascular dementia with additional mild Alzheimer encephalopathy (VaD-ae, i.e. Alzheimer pathology that does not fulfill criteria for AD). Because CAA is associated with cerebral hemorrhages and infarctions, it is of significant interest to confirm or dismiss the hypothesis that CAA contributes clinically in the many patients that present with VaD-ae. Therefore, we examined entire temporal lobes of 11 VaD-ae cases and 11 age-matched AD cases with Abeta immunohistochemistry. Six of 11 VaD-ae cases had severe CAA, more extensive than in any AD case. There was a trend toward more cortical infarctions in this group, indicating that CAA in VaD may be of clinical importance and an underestimated cause of dementia.

Aged↗
PubMed2004

MRI with diffusion tensor imaging post-mortem at 3.0 T in a patient with frontotemporal dementia.

The formalin-fixed brain of a patient with clinically diagnosed frontotemporal dementia (FTD) was examined post-mortem using magnetic resonance imaging (MRI) with diffusion tensor imaging (DTI) at 3.0 T. Frontotemporal atrophy as well as bilateral frontal white matter abnormalities were seen. The white matter changes were slightly more extensive on DTI than on conventional MRI. Correlation with histopathology of the corresponding regions revealed typical frontal lobe degeneration of non-Alzheimer type, with mild frontotemporal degeneration in the outer cortical layers and a moderate frontal white matter gliosis with demyelination. Post-mortem MRI/DTI with histopathologic correlation will enhance our understanding of the basis of white matter changes observed in dementia patients and may improve the in vivo MRI/DTI diagnostic assessment in FTD.

Aged↗
PubMed2003

Brain tissue microarrays in dementia research: white matter microvascular pathology in Alzheimer's disease.

Tissue microarrays (TMA) consist of up to 1000 cylindrical tissue cores from different donor paraffin blocks relocated into one recipient block, allowing for efficient histopathological studies by fluorescence in situ hybridization, RNA in situ hybridization or immunohistochemistry. On the background of the increasing interest of the TMA technique in cancer research and the suggestion of its application also in studies of non-neoplastic intracranial disorders, the technique was applied to pathologic white matter in AD brains. Eight cases with AD and concomitant white matter pathology were neuropathologically diagnosed on whole brain coronal slides. The TMA technique was used to grade severity of white matter pathology and to quantify small vessels with traditional staining and immunohistochemical markers. These measurements were compared with the whole brain neuropathological assessment. The technique produced good results with preserved tissue structures as confirmed by the whole brain evaluation. Severity of white matter pathology evaluated on the TMA cores correlated negatively with small vessel quantities, and statistically significant differences in vessel quantities paralleled different grades of white matter pathology. It is concluded that the TMA technique could be further utilized in studies of dementing disorders, and may have its advantages in large, clinically well-characterized materials (e.g. in quantitative mapping of white matter changes).

Aged↗