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PubMedDate not supplied

Image-matching as a medical diagnostic support tool (DST) for brain diseases in children.

Imaging-matching is an important research area in imaging informatics. We have developed and evaluated a novel diagnostic support tool (DST) based on medical image matching using MR brain images. The approach consists of two steps, database generation and image matching. The database contains pre-diagnosed MR brain images. As the images are added to the database, they are registered to the 3D Talairach coordinate system. In addition, regions of interests (ROI) are generated, and image-processing techniques are used to extract relevant image parameters related to the brain and diseases from the ROIs and from the entire MR image. The second step is to retrieve relevant information from the database by performing image matching. In this step, the physician first submits a query image. The DST computes the similarity between the query image and each of the images in the database, and then presents the most similar images to the user. Since the database contains pre-diagnosed images, the retrieved cases tend to contain relevant diagnostic information. To evaluate the usefulness of the DST in a clinical setting, pediatric brain diseases were used. The database contains 2500 pediatric patients between ages 0 and 18 with brain Magnetic Resonance (MR) images of known brain lesions. A testbed was established at the Children's Hospital Los Angeles (CHLA) for acquiring MR images from the PACS server of patients with known lesions. These images were matched against those in the DST pediatric brain MR database. An expert pediatric neuroradiologist evaluated the matched results. We found that in most cases, the image-matching method was able to quickly retrieve images with relevant diagnostic content. The evaluation method and results are given.

Brain Diseases↗
PubMed1992

Protein sequence and mass spectrometric analyses of tau in the Alzheimer's disease brain.

Tau with unusually slow mobilities in sodium dodecyl sulfate-polyacrylamide gel electrophoresis was purified from the Sarkosyl-insoluble pellet of Alzheimer's disease brain homogenates. Such species of tau (PHF-tau) are considered to construct the framework of the sodium dodecyl sulfate-soluble form of paired helical filaments (PHF). Detailed comparison of peptide maps of PHF-tau and normal tau before and after dephosphorylation pointed to three anomalously eluted peaks which contained abnormally phosphorylated peptides, residues 191-225, 226-240, 260-267, and 386-438, according to the numbering of the longest tau isoform (Goedert, M., Spillantini, M. G., Jakes, R., Rutherford, D., and Crowther, R. A. (1989) Neuron 3, 519-526). Protein sequence and mass spectrometric analyses localized Thr-231 and Ser-235 as the abnormal phosphorylation sites and further indicated that each tau 1 site (residues 191-225) and the most carboxyl-terminal portion of the protein (residues 386-438) carries more than two abnormal phosphates. Ser-262 was also phosphorylated in a fraction of PHF-tau. Modifications other than phosphorylation, removal of the initiator methionine, and N alpha-acetylation at the amino terminus and deamidation at 2 asparaginyl residues were found in PHF-tau, but these modifications were also present in normal tau.

Alzheimer Disease↗
PubMed1988

Serum creatine kinase levels after succinylcholine in children with "muscle, eye and brain disease".

Four boys belonging to a group of children affected by a rare form of muscular dystrophy with eye and brain involvement, termed the "muscle, eye and brain disease" (MEB), were anaesthetized for various eye examinations and surgery. On some occasions succinylcholine was used during anaesthesia and the initially elevated serum creatine kinase (CK) values increased from a range of 122 to 1200 units.L-1 to a range of 4350 to 9690 units.L-1 22 hours after anaesthesia. CK values after anaesthesia without succinylcholine remained at the initially elevated levels. Rectal temperatures of the children were normal. These findings suggest that succinylcholine should be avoided in patients with MEB disease.

Anesthesia↗
PubMed2005

Expression of calsenilin in neurons and astrocytes in the Alzheimer's disease brain.

Calsenilin, a multifunctional Ca2+-binding protein, has been identified as an Alzheimer's disease-associated presenilin interactor. Here, we investigated the histochemical localization of calsenilin and its expression levels in the brains of sporadic Alzheimer's disease. Both messenger RNA and protein expression of calsenilin were observed in neurons of the cerebral cortex and hippocampus of control brains, and more intense staining was in Alzheimer's disease brains. Although calsenilin is primarily expressed in neurons, its immunoreactivity was also detected in reactive astrocytes of the Alzheimer's disease brains. In Alzheimer's disease brains, the caspase-derived fragment of calsenilin was only detected in cytosolic fraction. Our findings suggest that calsenilin overexpression in both neurons and reactive astrocytes may play an important role in apoptosis and in Alzheimer's disease pathology.

Aged↗
PubMed2001

The fluorescent Congo red derivative, (trans, trans)-1-bromo-2,5-bis-(3-hydroxycarbonyl-4-hydroxy)styrylbenzene (BSB), labels diverse beta-pleated sheet structures in postmortem human neurodegenerative disease brains.

A novel Congo red-derived fluorescent probe (trans, trans),-1-bromo-2,5-bis-(3-hydroxycarbonyl-4-hydroxy)styrylbenzene (BSB) that binds to amyloid plaques of postmortem Alzheimer's disease brains and in transgenic mouse brains in vivo was designed as a prototype imaging agent for Alzheimer's disease. In the current study, we used BSB to probe postmortem tissues from patients with various neurodegenerative diseases with diagnostic lesions characterized by fibrillar intra- or extracellular lesions and compared these results with standard histochemical dyes such as thioflavin S and immunohistochemical stains specific for the same lesions. These data show that BSB binds not only to extracellular amyloid beta protein, but also many intracellular lesions composed of abnormal tau and synuclein proteins and suggests that radioiodinated BSB derivatives or related ligands may be useful imaging agents to monitor diverse amyloids in vivo.

Adult↗
PubMed2002

Multi-chemical networking profile of the living human brain: potential relevance to molecular studies of cognition and behavior in normal and diseased brain.

Anatomical, electrophysiological and functional neuroimaging studies show that the human brain is a complex network, where cortico-cortical and thalamo-cortical connections are organized in a specific pattern giving rise to brain function. In our recent studies we found that chemical connectivity between brain regions might be changed in different conditions (e.g. aging, chronic pain, cognitive interference). The elucidation of properties of the human brain multi-chemical networking profile is the subject of this study. In vivo proton magnetic resonance spectroscopy was used to determine relative concentrations of multiple chemicals (N-Acetyl aspartate, choline, glutamate, glutamine, GABA, inositol, glucose, and lactate in relation to creatine/phosphocreatine complex) in 6 brain regions: thalamus, and cingulate, insula, sensorimotor, orbital frontal, and dorsolateral prefrontal cortices. The properties of the brain multi-chemical networking profile within and across the studied regions were examined using correlation analysis. Strong positive correlations were seen between chemicals within brain regions. Negative correlations were primarily seen across brain regions. The cortical connectivity for both neurotransmitters (GABA and glutamate) was stronger than for the other chemicals, and was stronger than for the same neurotransmitters in the thalamus. Factor analysis indicated that the natural clustering of regional chemical concentrations is by brain region and not by chemicals. These findings support the idea for the existence of a specific pattern of multi-chemical networking profile in the brain where the major excitatory and inhibitory neurotransmitters in neocortex perform a regulatory function.

Adult↗
PubMed1986

Peptides derived from prodynorphin are decreased in basal ganglia of Huntington's disease brains.

The contents of methionine-enkephalin-Arg-Gly-Leu, dynorphin A, dynorphin B and alpha-neoendorphin have been measured in both control and Huntington's disease brains obtained postmortem. All 4 peptides were significantly reduced in the caudate nucleus and putamen of Huntington's disease compared with the control group. No differences were observed in frontal cortex or hypothalamus. Immunocytochemistry showed a marked depletion of dynorphin-like immunoreactivity in Huntington's disease substantia nigra.

Basal Ganglia↗
PubMed2003

Neuregulin-1 and erbB4 immunoreactivity is associated with neuritic plaques in Alzheimer disease brain and in a transgenic model of Alzheimer disease.

Neuregulin-1 (NRG-1) regulates developmental neuronal survival and synaptogenesis, astrocytic differentiation, and microglial activation. Given these NRG-1 actions, we hypothesized that the synaptic loss, gliosis, inflammation, and neuronal death occurring in Alzheimer disease (AD) is associated with altered expression of NRG-1 and its receptors (the erbB2, erbB3, and erbB4 membrane tyrosine kinases). We examined the expression and distribution of NRG-1 and the erbB kinases in the hippocampus of AD patients and cognitively normal controls and in transgenic mice that coexpress AD-associated mutations of the beta amyloid precursor protein (APP(K670N,M671L)) and presenilin-1 (PS1(M146L)). In the hippocampi of both control humans and wild type mice, NRG-1 and the 3 erbB receptors are expressed in distinct cellular compartments of hippocampal neurons. All 4 molecules are associated with neuronal cell bodies, but only NRG-1, erbB2, and erbB4 are present in synapse-rich regions. In AD and in the doubly transgenic mouse, erbB4 is expressed by reactive astrocytes and microglia surrounding neuritic plaques. In AD brains, microglia and, to a lesser extent, dystrophic neurites, also upregulate NRG-1 in neuritic plaques, suggesting that autocrine and/or paracrine interactions regulate NRG-1 action within these lesions. NRG-1 and erbB4, as well as erbB2, are similarly associated with neuritic plaques in the doubly transgenic mice. Thus, in AD the hippocampal distribution of NRG-1 and erbB4 is altered. The similarities between the alterations in the expression of NRG-1 and its receptors in human AD and in APP(K670N;M671L)/PS1(M146L) mutant mice suggests that this animal model may be very informative in deciphering the potential role of these molecules in AD.

Aged↗
PubMed2003

Expression and distribution of carboxypeptidase B in the hippocampal subregions of normal and Alzheimer's disease brain.

Earlier neurochemical studies suggested that human brain carboxypeptidase B may play a significant role in the degradation of amyloid-beta1-42 in the brain. Using an immimohistochemical technique we report here on the neuronal expression and distribution of this enzyme in the segments (CA1a, CA1b and CA1c) of the CA1 subfield and in area CA4 of the hippocampus in normal and Alzheimer's disease brain samples. Its distribution was compared with the appearance of neurofibrillary tangles in the same brain sample. For immunohistochemical localization of carboxypeptidase B, a specific C14-module antibody was applied, together with the Gallyas silver impregnation technique for the demonstration of neurofibrillary tangles. The results revealed that, in the control samples, most of the immunoreactivity appeared in segment CA1a in the pyramidal cells, less in segment CA1b and least in segment CA1c. In the Alzheimer's disease samples, there was no particular immunostaining in the neurons, but, a large number of silver-impregnated degenerated neurons appeared. The results support the suggestion that carboxypeptidase B may play a significant role in elimination of the intracellular accumulation and toxicity of amyloid-beta in the human brain and thereby protect the neurons from degeneration.

Aged↗