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At least 433 records · Page 24Linked to original sources
PubMed1995

Cytochrome c oxidase in Alzheimer's disease brain: purification and characterization.

Cytochrome c oxidase (COX) is deficient in both peripheral tissue and brain of Alzheimer's disease (AD) patients and may be of pathogenic significance in AD. We purified COX from AD brains (n = 3) and control brains (n = 3) and characterized the enzyme kinetically and spectrally. Purified AD brain COX displayed anomalous kinetic behavior compared with control brain COX in that the low Km binding site was kinetically unidentifiable. For purposes of comparison, we purified COX from a standard beef heart preparation and found normal kinetic behavior. AD brain COX may be structurally abnormal and may make an important contribution to the bioenergetic defect seen in AD.

Aged↗
PubMed1981

Depressive syndromes in middle age and organic brain disease.

41 patients with a depressive syndrome in middle age (mean age 55 years) were investigated. 19 of them had purely monopolar depressive syndromes without any organic features; 22 patients had a depressive syndrome associated with an organic brain disease (11 vascular, 11 primary degenerative disease). In all patients psychiatric and neurological investigations, a WAIS test, an EEG and a computer tomography were performed. The clinical findings were significantly different in both groups of depression but there was still a considerable overlap of symptoms. The EEG was inconclusive, the psychological test (WAIS) and the computer tomography showed the clearest separation between the organic and the nonorganic depressions leaving only 10% of inconclusive findings. Therefore, it may be concluded that the differential diagnosis of organic or nonorganic depressive syndrome in middle age cannot be made on the basis of one investigation on its own but on the combined results of clinical, functional, and morphological examinations.

Cerebrovascular Circulation↗
PubMed2004

At issue: will the term brain disease reduce stigma and promote parity for mental illnesses?

The author questions both the scientific evidence and potential effect of the current trend to change the language used to describe certain serious mental illnesses (schizophrenia, schizoaffective disorder, or bipolar affective disorder) to "brain diseases." It is argued that changing nomenclature will not be effective in reducing stigma unless the treatment and financial circumstances of the seriously mentally ill are improved. Finally, it is suggested that we need to expand our understanding and treatment of "physical illnesses" to encompass the social and psychological dimensions, not narrow our view of psychiatric illnesses.

Bipolar Disorder↗
PubMed1986

Propranolol treatment of assaultive patients with organic brain disease. A double-blind crossover, placebo-controlled study.

A double-blind, placebo-controlled crossover study was conducted to examine the effects of long-acting propranolol in the treatment of violent behavior associated with organic brain disease in 10 patients whose symptoms had proved refractory to various conventional medications. Long-acting propranolol treatment was associated with reductions of assaultive behavior without apparent sedative effects. Cautions are noted regarding potential undesirable side effects which may necessitate careful patient monitoring during treatment.

Adult↗
PubMedDate not supplied

KP-1 is a marker for extraneuronal neurofibrillary tangles and senile plaques in Alzheimer diseased brains.

KP-1 immunostaining with microwave pretreatment in formalin-fixed, paraffin-embedded sections enhanced its immunoreactivity revealing extraneuronal neurofibrillary tangles (NFTs) called ghost tangles, senile plaques (SPs) and perivascular deposits as well as microglial labelling in Alzheimer-diseased brains. KP-1 stained cored and uncored SPs, granules within the SPs, perivascular beta-amyloid protein (beta AP) and star-like beta AP deposits in cortical layer I, which was confirmed in comparison to silver-impregnated structures in the Reusche-stained or Gallyas-Schiff-stained sections. On double immunostaining with KP-1 and ubiquitin, ghost tangles were labelled by KP-1 and intraneuronal NFTs were positive for ubiquitin. A few KP-1-positive granules deposits different from amyloid core were found within the SPs and the outer margin of amyloid cores of SPs were stained by KP-1. KP-1-positive microglia were attached to the ubiquitin-positive intraneuronal NFTs. Microglia were more numerously labelled by CR3/43 than by KP-1, and CR3/43-positive microglia were found to be preferentially attached to SPs. As KP-1 recognizes lysosome-associated antigen CD68, similarities between KP-1 positivity and Reusche-stained structures suggested that lysosomal activity was associated with beta AP deposits and ghost tangles were involved in lysosome-associated processes. It is speculated that lysosomes play a role in the process of ghost tangle formation and in beta AP deposits leading to SP formation.

Aged↗
PubMed2000

Detection of complement alternative pathway mRNA and proteins in the Alzheimer's disease brain.

Previous research on complement activation in the Alzheimer's disease (AD) brain has focused almost exclusively on the classical complement pathway. The alternative pathway represents another important arm for complement activation, converging with the classical cascade at the C5 cleavage step. Here, we show that mRNA for a critical alternative pathway component, factor B, is present in AD frontal cortex and that the factor D cleaved split products of factor B, Bb and Ba, are significantly increased, indicating alternative pathway activation. By contrast, the two major inhibitors of alternative pathway activation, factor H and factor I, are present at the level of mRNA and protein but are not significantly upregulated. Immunohistochemical analysis reveals significant positive staining in AD sections for all three components. Taken together with previous reports demonstrating alternative pathway activation by amyloid beta peptide, these findings suggest that conditions conducive to chronic alternative pathway activation may exist in the AD brain.

Aged↗
PubMed2006

Thrombin and prothrombin are expressed by neurons and glial cells and accumulate in neurofibrillary tangles in Alzheimer disease brain.

Thrombin is a serine protease that is generated by proteolytic cleavage of its precursor, prothrombin. We previously showed that thrombin proteolyses the microtubule-associated protein tau and that phosphorylation of tau inhibits this process. To characterize further the role of thrombin in the brain, we investigated prothrombin and thrombin expression in cultured brain cells and in brains of control, Alzheimer disease (AD) and parkinsonism-dementia complex of Guam (PDCG). We show by reverse transcriptase-polymerase chain reaction that prothrombin mRNA is expressed in brain tissues, neuroblastoma cells, and cultured human astrocytes, oligodendrocytes, and microglial cells. We also show by immunohistochemistry that the proteins prothrombin and thrombin are present in brain using specific monoclonal and polyclonal antibodies for both proteins. All antibodies stained residual serum in blood vessels, as well as normal pyramidal neurons and their processes, and some astrocytes. Additionally, in AD and PDCG cases, all antibodies stained extra- and intracellular neurofibrillary tangles (NFTs), senile plaques, and reactive microglial cells. The ubiquitous expression of prothrombin and thrombin in brain cells suggests that thrombin plays an important physiological role in normal brain. The accumulation of thrombin and prothrombin in NFTs supports the hypothesis that thrombin may be involved in tau proteolysis and that failure to metabolize tau may lead to its aggregation in neurodegenerative diseases.

Aged↗
PubMed1985

Regional mitochondrial respiratory activity in Huntington's disease brain.

This study investigated mitochondrial respiratory activity in Huntington's disease (HD) brain. Mitochondrial membranes from caudate and cortex of HD and non-HD autopsied brains were assayed for succinate oxidation, cytochrome oxidase activity, and cytochromes b, cc1, and aa3. There was a significant decrease in HD caudate mitochondrial respiration, cytochrome oxidase activity, and cytochrome aa3, whereas cytochromes b and cc1 were normal. These findings are consistent with the hypothesis that mitochondrial dysfunction may contribute to the localized hypometabolism and progressive atrophy of the HD caudate.

Brain↗
PubMed2006

[Advance refusal of treatment in case of loss of autonomy due to persistent brain disease].

A short overview is given of the current debate on ethics and legal clarification of the range and binding force of so-called living wills demanding interruption of treatment in case of loss of autonomy due to persistent or progressive brain disease. Using the examples of dementia and persistent vegetative states - conditions with growing significance for psychiatrists - the binding force of living wills is examined for cases in which the irreversibility and extent of consciousness loss cannot be predicted with certainty. The range of living wills' authority appears also unclear. Legal proposals for limiting them to disease conditions near death are confronted by other proposals that reject such limitations. Added to this is the medical uncertainty of assessing the criterion nearness to death in irreversible and life-limiting diseases. The patient's right of self-determination, confirmed by high court decisions, to refuse in advance treatments that are life-prolonging but require consent is opposed to the medical obligation to save life and act in the patient's best interest. Moral dilemmas caused by this situation on the part of physicians, carepersons, and relatives or others, particularly authorized persons, should be solved by an exhaustive discussion with all persons who are involved in such decisions, and in a way that comes as near as possible to the patients living will.

Advance Directives↗
PubMed1976

Carotid-vertebral artery blood transit time: results in healthy subjects and patients with schizophrenia and brain disease.

Estimation of blood transit time in the neck and the extension of this into the head was made by a method of electrical impedance, over a wide age range, in 159 healthy subjects, 160 schizophrenic patients, and 199 patients with organic brain disease. In each case, the distance between the electrocardiogram and the next succeeding pulse-volume impedance wave was measured and averaged over 30 serial wave forms. Chronological age proved a significant variable, transit times lengthening progressively with the age, but only for measurements extending into the head. Sex and hemispheric laterality played no significant role. With age held constant, mean transit times into the head were significantly prolonged in both groups of patients as compared with controls. No significant differences were found however between means of psychiatric andneurological patients. It is suggested that these results reinforce the organic etiology of schizophrenia.

Adolescent↗
PubMed1986

Therapeutic effects of pindolol on behavioral disturbances associated with organic brain disease: a double-blind study.

A double-blind, placebo-controlled crossover study was conducted to examine the effects of pindolol for the treatment of 11 patients with impulsive, explosive behaviors and other emotional-behavioral abnormalities as a consequence of brain disease or injury. Pindolol treatment was associated with significant therapeutic benefits without sedation and without the use-limiting side effects that occur with propranolol.

Adult↗
PubMedDate not supplied

Quantitative 1H and 31P MRS of PCA extracts of postmortem Alzheimer's disease brain.

Several previous studies have shown metabolic abnormalities in perchloric acid extracts of postmortem Alzheimer's disease (AD) brain by both proton (1H) and phosphorus-31 (31P) magnetic resonance spectroscopy (MRS). In all of these studies the results were expressed in relative terms, in units of mol percent. The results of this study, expressed in the absolute units of mumol/g wet weight, verify the previous 1H and 31P MRS studies. Absolute increases were found for myo-inositol, aspartate, L-glutamate, alanine, phosphocholine, and the phosphodiesters,. Absolute decreases were found for phosphoethanolamine and N-acetyl-l-aspartate. Many of these changes also were observed in non-AD dementia brain extracts, but changes in myo-inositol, inositol-l-phosphate, aspartate, and L-glutamate appeared to be more specific for AD in extracts of many brain areas. These results suggest that compounds related to membrane degradation and excitatory neuro-transmission increase in Alzheimer's disease while compounds related to neuronal integrity and inhibitory neurotransmission are decreased.

Aged↗
PubMed1994

Proteolysis of A beta peptide from Alzheimer disease brain by gelatinase A.

It has been recently reported that the 72 kDa proteolytic enzyme gelatinase A/type IV collagenase/matrix metalloproteinase 2 (MMP2) hydrolyzed the Lys 16-Leu 17 peptide bond of a synthetic decapeptide (YEVHHQKLVFF) representing the soluble A beta sequence of amino acid residues 10-20. Our aim was to test if this enzyme could also degrade the insoluble 40-42 residues long A beta peptides purified from Alzheimer Disease brain. Our results indicate that MMP2 hydrolyzes A beta 1-40 and A beta 1-42 peptides at Lys 16-Leu 17, at Leu 34-Met 35, and Met 35-Val 36 peptide bonds. These results suggest that MMP2 has the ability of degrading A beta of AD in vitro. If this hydrolysis also occurs in the brain's extracellular matrix, the enzymatic action of gelatinase a could prevent the generation of amyloidogenic A beta 1-40(42).

Alzheimer Disease↗
PubMed1993

Regional specificity of membrane instability in Alzheimer's disease brain.

We report an inherent tendency towards the destabilisation of cellular membranes in Alzheimer's disease (AD) brain. This tendency is a natural consequence of abnormal membrane lipid composition, which has previously been documented in AD. Membrane destabilisation may contribute to AD pathogenesis in its own right and may also facilitate amyloid beta-protein deposition, which is potentially neurotoxic. The instability was found to co-localise selectively with areas of neurodegeneration in AD brain, thereby possibly accounting for the focal pathology observed in this disorder.

Aged↗