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At least 109 records · Page 6Linked to original sources
PubMed1998

Lipid peroxides in the free radical pathophysiology of brain diseases.

1. Polyunsaturated fatty acids are essential for normal cell membrane functioning because many membrane properties, such as fluidity and permeability, are closely related to the presence of unsaturated and polyunsaturated side chains. Lipid peroxidation results in loss of membrane polyunsaturated fatty acids and oxidized phospholipids as polar species contributing to increased membrane rigidity. 2. Polyunsaturated fatty acids are released from membrane phospholipids by a number of enzymic mechanisms involving the receptor-mediated stimulation of phospholipase A2 and phospholipase C/diacylglycerol lipase pathways. 3. The overstimulation of excitatory amino acid (EAA) receptors stimulates the activities of lipases and phospholipases, and this stimulation produces changes in membrane phospholipid composition, permeability, and fluidity, thus decreasing the integrity of plasma membranes. 4. Alterations in properties of plasma membranes may be responsible for the degeneration of neurons seen in neurodegenerative diseases. Two major processes may be involved in neuronal injury caused by the overstimulation of EAA receptors. One is a large Ca2+ influx and the other is an accumulation of free radicals and lipid peroxides as a result of neural membrane phospholipid degradation. It is suggested that calcium and free radicals act in concert to induce neuronal injury in acute trauma (ischemia and spinal cord injury) and in neurodegenerative diseases.

Alzheimer Disease↗
PubMed2005

Beta-site APP cleaving enzyme 1 (BACE1) is increased in remaining neurons in Alzheimer's disease brains.

Alzheimer's disease (AD) is characterized by the extensive deposition of amyloid beta protein (Abeta) in the brain cortex. Abeta is produced from beta-amyloid precursor protein (APP) by beta-secretase and gamma-secretase. beta-Secretase has been identified as beta-site APP cleaving enzyme1 (BACE1). We produced rabbit polyclonal antibodies against the amino and the carboxyl terminals of BACE1. Using these antibodies, BACE1 was characterized in temporal lobe cortices by Western blotting and immunohistochemistry. Immunohistochemical studies employing anti-GFAP and anti-MAP2 antibodies as well as anti-BACE1 antibodies showed that BACE1 was expressed exclusively in neurons but not in glial cells. Brain samples were directly extracted by 0.5% SDS and analyzed by Western blotting and densitometer. Although the mean level of BACE1/mg protein in AD brains was not increased, the ratio of BACE1 to MAP2 or to NSE was significantly increased compared with that in control brains. Taken together, these findings suggest that those neurons that survive in AD brains might generate more BACE1 than normal neurons in control brains, indicating that increased BACE1 activity could be one of the causes of AD. This could justify the development of anti-BACE1 drugs for AD treatment.

Alzheimer Disease↗
PubMed1965

POLYOMA-LIKE VIRIONS IN HUMAN DEMYELINATING BRAIN DISEASE.

Specimens of brain tissue obtained at autopsy from three patients suffering from progressive multifocal leukoencephalopathy (PML) were examined by electron microscopy. In specimens from all three cases particles similar to those of the papova virus group were present, confirming previous observations. By the negative staining method it was possible to define the morphological characteristics of the particles more precisely and it was shown that they are structurally similar to virions of the polyoma-SV40-K type. The need is emphasized for obtaining fresh unfixed diseased tissue from persons suffering from PML in order that the biological properties of the particles can be investigated.

Autopsy↗
PubMed2002

Amyloid beta-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists.

Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid beta-peptide (Abeta), particularly the 42-amino acid peptide [Abeta(1-42)] and by extensive oxidative stress. Several sources of the oxidative stress and inflammatory cascades are likely, including that induced by advanced glycation end products, microglial activation, and by Abeta(1-42) and its sequelae. This review briefly examines each of these sources of oxidative stress and inflammation in AD brain and discusses their potential roles in the clinical progression of AD dementia.

Acute-Phase Reaction↗
PubMed2004

The splicing regulatory protein p18SRP is down-regulated in Alzheimer's disease brain.

Alzheimer's disease (AD) is the most common neurodegenerative disorder of aging, accounting for an estimated two-thirds of all cases of senile dementia. Using bioinformatics, the yeast two-hybrid-system, reverse transcription polymerase chain reaction, and fluorescence microscopy analysis, we demonstrate here that the new putative splicing regulatory protein p18SRP is a lysine-rich zinc finger domain-containing protein that interacts with the serine-arginine (SR)-rich splicing regulatory protein SRrp86. The additional finding of its down-regulation in the brain of AD subjects points to a possible pivotal role of p18SRP in the control of cellular survival.

Aged↗
PubMed2002

PACSIN 1 interacts with huntingtin and is absent from synaptic varicosities in presymptomatic Huntington's disease brains.

Huntington's disease (HD) is caused by a pathological expansion of a CAG repeat in the first exon of the gene coding for huntingtin, resulting in an abnormally long polyglutamine stretch. Despite its widespread expression, mutant huntingtin leads to selective neuronal loss in the striatum and cortex. Here we report that the neurospecific phosphoprotein PACSIN 1, which has been implicated as playing a central role in synaptic vesicle recycling, interacts with huntingtin via its C-terminal SH3 domain. Moreover, two other isoforms, PACSIN 2 and 3, which show a wider tissue distribution including the brain, do not interact with huntingtin despite a highly conserved SH3 domain. Furthermore, this interaction is repeat-length-dependent and is enhanced with mutant huntingtin, possibly causing the sequestration of PACSIN 1. Normally, PACSIN 1 is located along neurites and within synaptic boutons, but in HD patient neurons, there is a progressive loss of PACSIN 1 immunostaining in synaptic varicosities, beginning in presymptomatic and early-stage HD. Further, PACSIN 1 immunostaining of HD patient tissue reveals a more cytoplasmic distribution of the protein, with particular concentration in the perinuclear region coincident with mutant huntingtin. Thus, the specific interaction of huntingtin with the neuronal PACSIN isoform, PACSIN 1, and its altered intracellular distribution in pathological tissue, together with the observed differences in the binding behavior, suggest a role for PACSIN 1 during early stages of the selective neuropathology of HD.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

[Proton magnetic resonance spectroscopy in the diagnosis of brain diseases].

The role and position of proton magnetic resonance spectroscopy have been studied in diagnosis of brain diseases. 114 patients with various diseases of the brain have been examined (multiple sclerosis--41, insults of different etiology--17, encephalopathy--12, AIDS infection--23, epilepsy--12, reduction of the intellectual ability of various etiology--9). MR tomography and 1HMR Spectroscopy have been done with Magnetom "Vision", 1.5 T (Siemens) in the CRIRR, St. Petersburg. To get a proton magnetic-resonance specter, SVS_STEAM, SVS_STEAM-20 and SVS_SE-135 sequences have been used with the following parameters: TR 5000 ms, TE 10, 20 and 135 ms respectively, number of acquisitions--100. Typical changes of metabolities in every group have been revealed. The performed examinations have shown that proton magnetic resonance spectroscopy enables to widen our know-ledge about the nature of pathologic changes, that grow with different diseases of the brain.

Adolescent↗
PubMedDate not supplied

Calcium precipitation in acute and chronic brain diseases.

In rat brain, calcification associated with excitotoxicity has been proposed to play a protective role, whereas in human brain, nonartherosclerotic calcification is present in several pathological conditions without any clear significance. To determine if calcification can be viewed as a protective step of calcium homeostasis during chronic and acute neuronal suffering, cerebral cortex and hippocampus of patients with Alzheimer's disease, vascular dementia and neonatal hypoxia-ischemia were investigated. To investigate the human specificity, these two areas were also studied in dogs with established cognitive deficits. In all groups, calcium precipitates were observed in the cerebral parenchyma associated with neuronal damage. The cerebral cortex presented a higher degree of calcification than the hippocampus. The neonatal hypoxia-ischemia group was characterised by a higher degree of calcification, whereas the groups with lowest calcification were the Alzheimer's patients and dogs. As shown by X-ray microanalysis, in the precipitates, calcium is mainly associated with phosphorus in a form that resembles hydroxyapatites. Thus, intracellular calcium concentration associated with neuronal suffering may reduce the energy extrusion. We propose that, to help overcome excitotoxicity, calcium precipitation acts in CNS of vertebrates as a new compartment of the calcium homeostasis in which free cytoplasmic calcium ions are inactivated by phosphate ones.

Acute Disease↗
PubMed1992

A histochemical study of iron, transferrin, and ferritin in Alzheimer's diseased brains.

Immunohistochemical and histochemical staining were performed on Alzheimer's diseased brain tissue obtained at autopsy. The iron-regulatory proteins transferrin and ferritin as well as iron are, in general, found predominantly in oligodendrocytes similar to that previously reported for normal brain tissue. However, in the vicinity of senile plaques, the staining pattern is altered for both proteins and iron. Transferrin is homogenously distributed around the senile plaques and is apparently extracellular. In addition, transferrin is found in astrocytes in the cerebral cortical white matter of the Alzheimer's tissue rather than its normal distribution in oligodendrocytes. A robust ferritin immunoreaction accompanies senile plaques and many blood vessels in the Alzheimer's brain tissue. Although many ferritin-positive oligodendrocytes are present in the Alzheimer's tissue, most of the ferritin-containing cells associated with senile plaques and blood vessels are microglia. Iron can also be demonstrated in the senile plaques. The iron reaction product is observed both diffusely in proximity of the plaques and in cells associated with the plaques. These data strongly suggest a disruption in brain iron homeostasis in Alzheimer's disease as demonstrated by alterations in the normal cellular distribution of iron and the proteins responsible for iron regulation. These data will contribute to understanding both the potential for oxidative damage and the potential for metal neurotoxicity in Alzheimer's disease.

Alzheimer Disease↗
PubMed2000

Visual syndromes as the presenting feature of degenerative brain disease.

The symptoms of a degenerative brain disease are dictated by its topography. Visuo-spatial impairment may be a severe and early feature of degenerative dementia. Visual symptoms in such patients are broadly divisible into dorsal and ventral visual syndromes, which result from a degenerative focus in occipito-parietal and occipito-temporal visual association cortices, respectively. The dorsal visual syndrome includes asimultanagnosia and Balint's syndrome. The ventral visual syndrome includes alexia and visual agnosia (prosopagnosia). Less often, hemineglect or visual field defects result. When Alzheimer's disease and Creutzfeldt-Jakob disease present in this way there is a topographic shift of neurodegenerative changes to posteriorly situated cortices. Patients with corticobasal ganglionic degeneration often develop symptomatic involvement of contiguous sensorimotor cortices causing mixed perceptual-motor syndromes. Even in patients with more typical patterns of dementia, the degree of visuo-spatial impairment may hinder driving skills, and the issue of driving should be addressed early in the clinical course.

Cerebral Cortex↗
PubMed2006

[Brain diseases and modern-day society].

Brain diseases represent one of the largest strains in the developed societies of the modem world. The major lost is in the indirect expenses caused by psychical disorders. Psychiatric diseases start frequently in childhood, affect from the life lasting view one half of the population and frequently result in disablement. Administrative of the World Health Organization and of European Union consider these problems highly important and require emancipation of psychically disabled, including the financial support for the care. Only 4% of the National Budget is directed to that sector in Czech Republic, which is the second lowest share (after Slovakia).

Czech Republic↗
PubMed1992

Hyponatraemia in acute brain disease.

Hyponatraemia (HN) can result from a wide range of mechanisms, and therapy must be individualized. Two theories of the origin of HN in acute brain disease have prevailed. The first is the cerebral salt wasting syndrome (CSWS), where excessive natriuresis caused by some unknown cerebral natriuretic factor lowers the total sodium pool of the body and hence the plasma concentration. The second theory is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), where an increase in total body water is caused by unphysiological secretion of ADH, lowering the concentration of sodium in the plasma. A third possibility is 'sodium shift', i.e. a displacement of sodium from the extracellular to the intracellular space with a simultaneous movement of potassium in the opposite direction. The morbidity and mortality associated with HN only arise in cases where the rate of development of HN was 0.5 mmol h-1 or more. Symptoms respond promptly when the HN is quickly corrected with furosemide and 3% sodium chloride.

Acute Disease↗
PubMed1995

Immunocytochemical characterization of glial fibrillary tangles in Alzheimer's disease brain.

Neurofibrillary tangle is a major cytoskeletal pathology in Alzheimer's disease brains, and has been considered to develop exclusively in neuronal cells. We examined brains with Alzheimer's disease and observed argyrophilic fibrillary tangles not only in cortical neurons but also in subcortical glial cells in the frontal and temporal white matter. The tangles in glial cells were immunolabeled by antibodies against tau and ubiquitin, and double immunocytochemistry analyzed by confocal laser scanning microscopy demonstrated that the cytoplasms of tangle-bearing glia were labeled by antibodies against transferrin and 2'3'-cyclic nucleotide 3'-phosphohydrolase. Ultrastructurally, they were made up of bundles of straight filaments 16 nm in diameter and constricted filaments. These results indicate that fibrillary tangles resembling neurofibrillary tangles may develop in oligodendrocytes in brains with Alzheimer's disease and are distinguishable from glial cytoplasmic inclusions observed in multiple system atrophy brains. We referred to them as glial fibrillary tangles. Glial fibrillary tangles commonly occurred in this disease condition, and glial cells might be involved under the pathological processes similar to neuronal cells.

Aged↗