Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BRAIN DISEASE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1994

Delusional misidentification: an exemplary symptom illustrating an interaction between organic brain disease and psychological processes.

Delusional misidentification provides us with an excellent example of how it is necessary to take both organic brain disease and psychological processes into account when describing the development of mental symptoms. A model of delusional misidentification is proposed which was developed in an attempt to explain this interaction. The model is based on the events that occur during preconscious processing of perceptions. It predicts an inverse relationship between the presence of organic brain disease and the presence of paranoid delusions. This was tested using a retrospective analysis of case reports. A graded and inverse relationship between the degree of organic disturbance and the presence of paranoid delusions preceding the delusional misidentification was found. A satisfactory model of delusional misidentification syndromes must be able to acknowledge the way these two forces are able to interact.

Adult↗
PubMed1996

Effects of freezing storage time on the density of muscarinic receptors in the human postmortem brain: an autoradiographic study in control and Alzheimer's disease brain tissues.

The effect of sex, age (range = 41-84 years), postmortem delay (range = 1-71 h) and freezing storage time (FST) (range = 8-75 months) at -25 degrees C on the density of muscarinic receptors (MR) was examined in tissue sections of several representative areas of 41 postmortem brains from adult patients who had died from non-neurological disorders using [3H]N-methylscopolamine as a ligand. Neither age, sex nor postmortem delay determined significant changes in the density of MR in frontal and entorhinal cortex, hippocampus and striatum. By contrast, FST significantly decreased the densities of MR in frontal and entorhinal cortex, pyramidal layer of CA1 and CA3 fields at the hippocampus and over caudate nucleus. This reduction in MR densities did not reach statistical significance, for any region, when FST was less than 39 months. Although there was a tendency towards a decrease, no significant changes were observed in putamen and over hippocampal dentate gyrus. FST (range = 11-78 months) also significantly decreased the densities of MR in the same regions of postmortem brains from 18 patients who had died with a clinico-pathological diagnosis of Alzheimer's disease (AD). Even though there was a general tendency towards a decrease (between 7% in the caudate and 30% in the dentate gyrus at the hippocampus), no significant differences could be seen in MR densities between control and AD cases, except in the hilus in the dentate gyrus (P < 0.022), when brains were matched for FST. From the present results it is clear that control and diseased brains must also be matched for FST as well as for other factors such as sex, age and postmortem delay. It is possible that differences in FST could in part account for the variability of the reported results measuring MR in control and AD brains. At least for MR, FST shorter than three years would seem to be acceptable when performing this kind of studies.

Adult↗
PubMed2001

Brain metabolism and brain disease: is metabolic deficiency the proximate cause of Alzheimer dementia?

The potential of impairments in oxidative/energy metabolism to cause diseases of the brain had been proposed even before the major pathways of oxidative/energy metabolism were described. Deficiencies associated with disease are known in all the pathways of oxidative/energy metabolism and are associated with some of the most common disorders of the nervous system, including Alzheimer's disease (AD) and Parkinson's disease. A common mechanism in these conditions appears to be a downward mitochondrial spiral, involving abnormalities in energy metabolism, calcium metabolism, and free radicals (reactive oxygen and nitrogen species). In AD, the spiral appears to interact with abnormalities in the metabolism of the Alzheimer amyloid precursor protein (APP) and its Abeta fragment. Several lines of evidence indicate that the mitochondrial spiral may be a proximate cause of the clinical disabilities in AD. Decreases in cerebral metabolic rate (CMR) characteristically occur in AD and in other dementias. Inducing decreases in CMR leads to clinical disabilities characteristically associated with AD and with analogous problems in experimental animals. Treatments directed toward normalizing CMR appear to help at least some patients. Further studies of this possibility and of treatments designed to ameliorate the mitochondrial spiral may prove useful for treating AD and perhaps some other dementing disorders.

Alzheimer Disease↗
PubMed1997

Parvalbumin-immunoreactive neurons in the hippocampal formation of Alzheimer's diseased brain.

The number and topographic distribution of immunocytochemically stained parvalbumin interneurons was determined in the hippocampal formation of control and Alzheimer's diseased brain. In control hippocampus, parvalbumin interneurons were aspiny and pleomorphic, with extensive dendritic arbors. In dentate gyrus, parvalbumin cells, as well as a dense plexus of fibers and puncta, were associated with the granule cell layer. A few cells also occupied the molecular layer. In strata oriens and pyramidale of CA1-CA3 subfields, parvalbumin neurons gave rise to dendrites that extended into adjacent strata. Densely stained puncta and beaded fibers occupied stratum pyramidale, with less dense staining in adjacent strata oriens and radiatum. Virtually no parvalbumin profiles were observed in stratum lacunosum-moleculare or the alveus. Numerous polymorphic parvalbumin neurons and a dense plexus of fibers and puncta characterized the deep layer of the subiculum and the lamina principalis externa of the presubiculum. In Alzheimer's diseased hippocampus, there was an approximate 60% decrease in the number of parvalbumin interneurons in the dentate gyrus/CA4 subfield (P<0.01) and subfields CA1-CA2 (P<0.01). In contrast, parvalbumin neurons did not statistically decline in subfields CA3, subiculum or presubiculum in Alzheimer's diseased brains relative to controls. Concurrent staining with Thioflavin-S histochemistry did not reveal degenerative changes within parvalbumin-stained profiles. These findings reveal that parvalbumin interneurons within specific hippocampal subfields are selectively vulnerable in Alzheimer's disease. This vulnerability may be related to their differential connectivity, e.g., those regions connectionally related to the cerebral cortex (dentate gyrus and CA1) are more vulnerable than those regions connectionally related to subcortical loci (subiculum and presubiculum).

Adult↗
PubMed2000

[Clinico-neurologic aspects of acute inflammatory brain diseases].

Despite the progress, which has been made in diagnosis and therapy of encephalitis and bacterial meningitis, these acute inflammatory diseases of the brain still display a certain amount of morbidity and mortality. History, physical examination, analysis of serum and cerebrospinal fluid and radiological examination are the mainstay for the diagnosis of these diseases. With respect to the acute inflammatory diseases of the brain computed tomography and magnetic resonance imaging fulfill three purposes: 1. They can be used to clarify the diagnosis and to rule out other diseases. 2. They can identify the focus from which a bacterial meningitis can evolve. 3. Complications like edema, cerebral vasculitis, septic sinus thrombosis, hydrocephalus or abscess can be visualized. If the diagnosis is made early, the possible complications are recognized in good time and the appropriate therapy is started immediately, then morbidity and mortality can be kept at a minimum.

Brain↗
PubMed1989

Mutated and hypermutated genes of persistent measles viruses which caused lethal human brain diseases.

Persistent measles viruses (MVs) causing lethal human brain diseases are defective, and the structure of several mutated matrix genes has been elucidated previously. The present study of four persistent MVs revealed a high number of differences from a consensus sequence also in other genes. Amino acid changes accumulated in the carboxyl terminus of the nucleocapsid protein and in the amino terminus of the phosphoprotein, but did not significantly alter these products, which are implicated in viral replication and transcription. The contrary is true for the envelope glycoproteins: In three of four cases, mutations caused partial deletion of the short intracellular domain of the fusion protein, most likely compromising efficient viral budding. Moreover, in the hemagglutinin gene of a strain showing strongly reduced hemadsorption, 20 clustered A to G mutations, resulting in 16 amino acid changes, were detected. This hypermutation might be due to unwinding modification of a part of the MV RNA genome accidentally present in a double-stranded form. Finally, we classified four lytic and seven persistent MV strains on the basis of their sequences. Surprisingly, the four lytic viruses considered belong to the same class. The persistent viruses form more loosely defined groups, which all differ from the vaccine strain Edmonston.

Amino Acid Sequence↗
PubMed1981

Cognitive dysfunction in schizophrenia, affective disorder and organic brain disease.

We used the Wechsler Adult Intelligence Scale (WAIS) to study a sample of patients with affective disorder (N = 52), schizophrenia (N = 17) and organic brain disease (N = 8). Schizophrenic patients had lower verbal, performance and full-scale IQs than patients with affective disorder, but were no different from those with organic brain disease. An individual WAIS subscale analysis showed that, compared with affectives, schizophrenics had relatively poorer performance on language than non-language tasks. These differences were independent of age, sex, handedness, educational level or drug administration and are consistent with a variety of studies demonstrating significant cerebral dysfunction in carefully diagnosed schizophrenic patients.

Adult↗
PubMed2004

Deficiency of the Mre11 DNA repair complex in Alzheimer's disease brains.

The hallmarks of Alzheimer's disease (AD) brains are deposition of Abeta plaques, appearance of neurofibrillary tangles, and extensive loss of neuronal cells. While Abeta plaques and neurofibrillary tangles play a significant role in the pathogenic dysfunction of neurons, factors that accelerate the neurodegenerating process remain to be defined. One set of factors examined in this study is the Mre11 protein complex, composed of Rad50, Mre11 and Nbs1. This protein complex plays an essential role in cellular responses to DNA damage, such as initiating cell cycle checkpoints and repairing damaged DNA. A defect in any component of this protein complex is detrimental to cells. Recently, several groups have observed abnormal cell cycle regulation and/or accumulated DNA damage in AD neurons. These pathological alterations could conceivably be caused or exacerbated by any compromise in the Mre11 complex. In this study, we compared the levels of the Mre11 complex proteins in brain samples from AD and age-matched non-dementia controls. We show for the first time that the Mre11 complex proteins are present in neurons of the adult human cortex and cerebellum. These proteins were found substantially reduced in the neurons of AD cortex. Our finding suggests that the loss of the Mre11 complex may be associated with the pathogenesis of AD.

Acid Anhydride Hydrolases↗
PubMed2006

[Alcohol brain disease: systematization of metalcohol psychoses].

Based on the own clinical observations, the author analyzes pathogenetic hypotheses and contemporary typology of metalcohol psychoses, proposes a concept of alcohol brain disease, including typical and atypical forms. It is suggested that typical forms rest on specific neurometabolic disturbances while the constitutional predisposition plays a main role in the forming of atypical variants. The principles of effective treatment of alcohol brain disease are considered.

Disease Progression↗
PubMed1997

The expression of mRNA for a kappa opioid receptor in the substantia nigra of Parkinson's disease brain.

We molecularly cloned the kappa opioid receptor from a human substantia nigra cDNA library. When expressed in HEK293 cells, the cloned receptor had similar pharmacological characteristics to the rat kappa opioid receptor. Northern blot analysis showed the presence of a single transcript of about 6 kb in size for mRNA prepared from the substantia nigra. Using in situ hybridization histochemistry, we studied the expression of this receptor in postmortem human brains from control and Parkinson's disease subjects. Kappa opioid receptor mRNA was present in melanized (possibly dopaminergic) neurons of the substantia nigra and the nucleus paranigralis. On the other hand, Parkinson's disease brains had markedly fewer melanized neurons, as expected, and correspondingly very low or background levels of mRNA for the kappa opioid receptor. However, in some cases, remaining melanized neurons still expressed the receptor mRNA. From these results we suggest that dopaminergic neurons in the human substantia nigra and the nucleus paranigralis synthesize kappa opioid receptors and express them in their perikarya and their terminal regions. The kappa opioid receptor expressed in the melanized neurons may play a role in the normal function of dopaminergic systems and possibly in the etiology of Parkinson's disease.

Aged↗
PubMed1962

Procaine (novocain) treatment of patients with senile and arteriosclerotic brain disease.

Of 32 patients (13 men and 19 women) with a mean age of 81.1 years committed to a mental hospital for senile or arteriosclerotic psychoses, 11 received 2% procaine hydrochloride according to Aslan's method, for an average of 13 months, 11 for 6 months, and 10 normal saline. Of 20 patients, with a mean age of 72 years, who attended the geriatric psychiatric clinic of a general hospital, 10 were treated with procaine hydrochloride and 10 with normal saline for six months. Procaine hydrochloride applied for six or 12 months did not appreciably alter the symptomatology and course of senile and arteriosclerotic brain disease. It did not improve the senile amnestic syndrome or neurological symptomatology, when present. The general mood and level of activity improved temporarily. It was also temporarily helpful in alleviating depressive symptoms in patients suffering from arteriosclerotic brain disease.

Aged↗
PubMed1994

Short note: possible role of macrophage metabolic products including quinolinic acid and neopterin in the pathogenesis of inflammatory brain diseases.

It is hypothesized that macrophage metabolic products, including the possible neurotoxic NMDA receptor agonist quinolinic acid, and neopterin, may play a role in the pathogenesis of inflammatory brain diseases. It is suggested that the production of neopterin may have physiological roles, including to inhibit folate synthesis in intracellular pathogenic microorganisms and to inhibit viral nucleic acid synthesis. The possible role of excess neopterin production during chronic infection in the pathogenesis of inflammatory brain diseases is discussed.

Biopterins↗
PubMed2003

Demonstration of puromycin-sensitive alanyl aminopeptidase in Alzheimer disease brain.

Puromycin-sensitive alanyl aminopeptidase (PSA, EC 3.4.11.14) is a member of the ubiquitous aminopeptidase family, which cleaves N-terminal amino acids from proteins. PSA is suggested to function as a trimming protease in the MHC class I pathway, which is activated in brains of Alzheimer disease (AD). We examined the immunohistochemical localization of PSA in brains of AD and control cases using a rabbit anti-PSA. In the control cases, the antiserum revealed staining in a few glial cells and blood vessels. In AD brain, however, intensely stained cells were found richly in the cerebral cortex. Double immunofluorescence studies confirmed that PSA-positive cells were reactive microglia. Such PSA-positive reactive microglia tended to locate in and around senile plaques and were sometimes observed to associate with neurons containing neurofibillary tangles. The present result indicates that reactive microglia express PSA-immunoreactive molecules, probably in association with the pathological conditions of AD.

Alzheimer Disease↗
PubMed1993

Morphological and biochemical analyses of amyloid plaque core proteins purified from Alzheimer disease brain tissue.

Amyloid plaque cores were purified from Alzheimer disease brain tissue. Plaque core proteins were solubilized in formic acid which upon dialysis against guanidinium hydrochloride (GuHCl) partitioned into soluble (approximately 15%) and insoluble (approximately 85%) components. The GuHCl-soluble fraction contained beta-amyloid1-40, whereas the GuHCl-insoluble fraction was fractionated into six components by size exclusion HPLC: S1 (> 200 kDa), S2 (200 kDa), S3 (45 kDa), S4 (15 kDa), S5 (10 kDa), and S6 (5 kDa). Removal of the GuHCl reconstituted 10-nm filaments composed of two intertwined 5-nm strands. Fractions S5 and S6 also yielded filamentous structures when treated similarly, whereas fractions S1-S4 yielded amorphous aggregates. Chemical analysis identified S4-S6 as multimeric and monomeric beta-amyloid. Immunochemical analyses revealed alpha 1-antichymotrypsin and non-beta-amyloid segments of the beta-amyloid precursor protein within fractions S1 and S2. Several saccharide components were identified within plaque core protein preparations by fluorescence and electron microscopy, as seen with fluorescein isothiocyanate- and colloidal gold-conjugated lectins. We have shown previously that this plaque core protein complex is more toxic to neuronal cultures than beta-amyloid. The non-beta-amyloid components likely mediate this additional toxicity, imposing a significant influence on the pathophysiology of Alzheimer disease.

Aged↗
PubMed1989

Altered gene expression in Alzheimer's disease brain tissue.

We review the evidence for altered gene expression in Alzheimer's disease brain and identify alternative molecular approaches for isolating additional novel markers. One marker, pADHC-9, was isolated from a human hippocampal cDNA library by differential screening with AD and control cDNA probes. This clone hybridizes to a 2 Kb RNA which is increased 2 fold in AD hippocampus. The deduced amino acid sequence of pADHC-9 codes for a 52 kDAL protein similar to a testicular sulfated glycoprotein secreted by rat Sertoli cells. The normal function of this protein in brain and whether that function is altered in Alzheimer's disease is unknown.

Alzheimer Disease↗