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At least 127 records · Page 7Linked to original sources
PubMed1999

[Functional MRI: brain plasticity, brain disease and functional recovery].

Brain plasticity may be defined as long-term alteration in behavior related activity of distributed neural systems. Functional imaging, and particularly functional MRI, allows to investigate the mechanisms underlying brain plasticity. Two aspects may be distinguished: one is learning in healthy subjects; the other is functional reorganization following or associated with acute or chronic brain injury. Because functional MRI is totally non invasive, it appears well suited to follow such reorganization over time. This theme will be developed in the following text.

Brain Diseases↗
PubMed2000

Role of phospholipase A(2) on the variations of the choline signal intensity observed by 1H magnetic resonance spectroscopy in brain diseases.

Phospholipase A(2) catalyzes the hydrolysis of membrane glycerophospholipids leading to the production of metabolites observable by both 1H and 31P magnetic resonance spectroscopy. The signal of choline-containing compounds (Cho) observed by 1H magnetic resonance spectroscopy is constituted of metabolites of phosphatidylcholine, especially phosphocholine (PCho) and glycerophosphocholine (GPCho). The phosphomonoester (PME) and phosphodiester (PDE) signals observed by 31P magnetic resonance spectroscopy are, respectively, precursors and catabolites of phospholipids. A large number of brain diseases have been reported to cause variations in the intensity of the Cho, PME and PDE signals. Changes in the activity of phospholipase A(2) have been measured in many brain diseases. In this review, the relationships between the results of 1H and 31P magnetic resonance spectroscopy and the phospholipase A(2) assays are analyzed. In many brain diseases, the variation in the Cho signal intensity can be correlated with a stimulation or inhibition of the phospholipase A(2) activity.

Animals↗
PubMed2001

[Cerebrogenic cardiac arrhythmia in patients with organic brain diseases of nonvascular genesis].

Cardiological examination covered 115 patients (79 males and 36 females aged 16-44 years) with organic brain pathology of nonvascular genesis: epilepsy (n = 51), sequelae of closed craniocerebral trauma (n = 37) or cerebral inflammation (n = 27). The control group consisted of 15 healthy subjects. It was found that patients with brain diseases have a variety of cardiac rhythm and conduction disturbances which occur much more often than in the control group (p < 0.01). Cardiac arrhythmia was encountered most often in epileptics and patients with complications of closed craniocerebral trauma (96.1% and 70.3%, respectively). Rates of cardiac arrhythmia and conduction disorders in patients with brain diseases correlated with frequency of epileptic fits and severity of organic alterations in the brain. The pattern of rhythmic and conduction disorders was formed according to dysfunction of suprasegmentary vegetative centers with prevalent activation of the sympathetic or parasympathetic autonomic nervous system. Cardiac arrhythmia and related negative feelings deteriorate "quality of life" in patients with brain pathology that's why it is necessary to detect and treat them early.

Adolescent↗
PubMed1997

Retinoic acid synthesis in normal and Alzheimer diseased brain and human neural cells.

Retinoids play fundamental roles in CNS development, but their distribution, metabolism, and function within the mature human CNS are unknown. In these studies, extracts of autopsy tissues recovered from histopathologically confirmed control and Alzheimer diseased brains were tested for their ability to synthesize retinoic acid. Retinaldehyde dehydrogenase (RLDH), the enzyme that forms retinoic acid from retinaldehyde, was present in hippocampus, frontal cortex, and parietal cortex. The RLDH activity of hippocampus and parietal cortex from Alzheimer diseased brains was 1.5- to 2-fold higher (p < 0.05) compared to the controls. In contrast, the RLDH activity of frontal cortex was the same for both Alzheimer diseased and control groups. A cultured human glioblastoma (U251) and neuroblastoma (LA-N-5) cell line synthesized retinoic acid from retinaldehyde or retinol, suggesting that a variety of neural cell types possess this activity. LA-N-5 cells grown in vitamin A-depleted medium had higher (p < 0.05) RLDH activity (0.35 +/- 0.04 nmol/mg/h) than LA-N-5 cells grown in vitamin A-replete media (0.15 +/- 0.02 nmol/mg/h). This difference was lost when retinol was added back to the medium, confirming that a reduction in vitamin A supply can induce RLDH activity in neural cells. However, this feedback mechanism does not appear to explain the higher RLDH activity of Alzheimer diseased hippocampus and parietal cortex, because the overall vitamin A status as indicated by serum retinol and carotenoid levels and by hippocampal retinoid content was similar for the Alzheimer diseased and control groups. These studies establish the presence of retinoids and RLDH activity in human brain tissues, and indicate that retinoic acid synthesis is modulated in some regions of Alzheimer diseased brain.

Alzheimer Disease↗
PubMed1976

Visual localization in patients with unilateral brain disease.

The accuracy of localization of briefly exposed single dots and pairs of dots was assessed in patients with lesions of the left and right hemispheres and in control patients without history or evidence of brain disease. A remarkably high frequency of impaired performance was found in the patients with right hemisphere lesions. The performance of the patients with left hemisphere lesions was comparable with that of the control patients. Visual field defect was associated with defective localization in the right hemisphere group but not in the left hemisphere group. Aphasic disorder and age were not related to performance level. The relationship of the findings to those of previous studies of visual localization in patients with unilateral brain disease is discussed.

Adult↗
PubMed1999

Tau protein in normal and Alzheimer's disease brain.

In 1975, Weingarten and colleagues isolated a protein factor that was able to induce microtubule formation. They called this factor tau (t). Some ten years later a new era of research on this microtubule-associated protein was launched when several groups almost simultaneously discovered that tau was the predominant protein component of the paired helical filaments (PHFs) and neurofibrillary tangles (NFTs) which are characteristic pathological lesions of the Alzheimer's disease brain. Subsequent findings that PHF-tau isolated from Alzheimer's disease brain was phosphorylated to a greater extent than non-PHF tau, led to extensive investigation into the posttranslational modifications (mainly phosphorylation) of tau in normal and Alzheimer's disease brain. The present review highlights the literature concerning the normal functioning and processing of tau protein, and examines the evidence for the involvement of the abnormal posttranslational processing of tau in the pathology of Alzheimer's disease. Finally, speculation as to the relationship between abnormal processing of tau, other subcellular abnormalities seen in Alzheimer's disease, and the pathological causes of the disease are discussed.

Journal Article↗
PubMed1978

Chronic brain disease: an overview.

The author discusses the current state of clinical and pathological knowledge regarding chronic brain disease, focusing particularly on the dementias. His review of clinical studies deals with diagnostic issues and methods, etiology, and treatment. More basic research on brain alterations with aging, their relation to clinical manifestations of dementia, and studies of specific disorders are also reviewed. These disorders have been receiving increasing attention from psychiatrists, who are becoming more aware of the importance of organic cerebral factors in their patients' complaints. The need to understand the chronic brain diseases and their appropriate diagnosis and treatment will continue to grow as the proportion of older individuals in our society increases.

Aging↗
PubMed1997

Aggregation of beta-amyloid peptide is promoted by membrane phospholipid metabolites elevated in Alzheimer's disease brain.

Increased amounts of beta-amyloid (A beta) peptide deposits are found in Alzheimer's disease brain. These amyloid deposits have been implicated in the pathophysiology of this common dementing illness. A beta peptides have been shown to be toxic to neurons in cell culture, and this toxicity is critically dependent on the aggregation of the peptide into cross-beta-pleated sheet fibrils. Also, in vivo and postmortem NMR studies have shown changes in certain brain membrane phospholipid metabolites in normal aging and more extensive alterations in patients with Alzheimer's disease. The finding that membrane phospholipids affect the aggregation of A beta suggests that the abnormalities in membrane metabolism found in Alzheimer's disease could affect the deposition of A beta in vivo. Therefore, we examined the effect of membrane phospholipid metabolites that are altered in Alzheimer's disease brain on the aggregation of A beta(1-40) using a light scattering method. Certain metabolites (glycerophosphocholine, glycerophosphoethanolamine, and alpha-glycerophosphate) augment the aggregation of A beta. Other membrane phospholipid metabolites (phosphocholine, phosphoethanolamine, and inositol-1-phosphate) have no effect. We conclude that increased membrane phospholipid metabolite concentrations may play a role in the deposition of A beta seen in normal aging and the even greater deposition of A beta observed in Alzheimer's disease.

Alzheimer Disease↗
PubMed2004

At issue: Stop the stigma: call mental illness a brain disease.

Educating the public that mental illness is a brain disease is a popular strategy for combating mental illness stigma. Evidence suggests that while such an approach reduces blame for mental illness, it may unintentionally exacerbate other components of stigma, particularly the benevolence and dangerousness stigmas. Conversely, psychosocial explanations have proven promising, yet they ignore the growing evidence regarding genetic and biological factors. We propose a balanced approach that combats the various myths about mental illness with factual information.

Biomedical Research↗
PubMed1983

Head injury unmasking other brain diseases.

Sixteen patients previously free of neurological complaints sustained minor head injuries and subsequently presented acutely with a wide range of unexpected, serious brain diseases. These included brain tumours, berry aneurysms, arteriovenous malformations and brain abscess. The possible, responsible mechanisms include direct mechanical trauma to the asymptomatic brain lesion, hydrocephalus and brain oedema. This unusual complication of head injury should be suspected when a florid neurological syndrome follows a minor head injury. CAT scanning usually identifies the responsible disease. Because of its therapeutic implications, this complication deserves recognition in the differential diagnosis and management of head injuries.

Brain Diseases↗
PubMed1993

[Brain injury and brain disease. Need and importance of early rehabilitation].

Early rehabilitation means rehabilitation which begins during the treatment for acute illness or trauma, immediately after the management of life-threatening conditions and stabilization of vital functions. Early rehabilitation is intended to make extensive use of the regenerative capacities of the brain and prepare effortless transition to further training programs. The necessity of early rehabilitation after severe brain injury or vascular brain disease is now recognized. However the means available now, i.e. trained staff, equipment and buildings, are insufficient. In order to estimate the resources needed the epidemiology of head and brain injury and vascular brain disease in Germany was analyzed by Infratest Gesundheitsforschung, Munich. The study was initiated and supported by the Kuratorium ZNS. The data concerning the years spanning 1987 to 1989 and the emerging conclusions will be presented. Also, important and meanwhile accepted suggestions for the founding and equipment of rehabilitative care units will be discussed.

Brain Damage, Chronic↗
PubMed2002

Presence of hydroxysteroid dehydrogenase type 10 in amyloid plaques (APs) of Hsiao's APP-Sw transgenic mouse brains, but absence in APs of Alzheimer's disease brains.

This immunocytochemical study using two anti-amyloid beta-protein (Abeta) monoclonal antibodies, 4G8 and 6E10, revealed the presence of Abeta in both amyloid plaques (APs) and blood vessels of brains of Hsiao's APP-Sw transgenic mice (also known as Tg2576) and human Alzheimer's disease (AD) brains. Further study using both monoclonal (5F3) and polyclonal (R-228) antibodies to hydroxysteroid dehydrogenase type 10 (HSD-10) [formerly called SCHAD (short-chain L-3-hydroxyacyl-CoA dehydrogenase); also called ERAB (endoplasmic-reticulum-associated amyloid beta-peptide-binding protein)] indicated that HSD-10 was present in the APs of Tg2576 mice but was absent or immunocytochemically undetectable in the APs of AD brains. Our observations also revealed that HSD-10 was present in the blood vessels of both Tg2576 mice and AD brains. Immunogold electron microscopy also indicated that HSD-10 was present in the amyloid fibers (AFs), mitochondria, nuclear heterochromatin, and nucleolus of Tg2576 mouse brains but was absent in APs of AD brains. These results suggest that the human APP gene transferred to mice may induce overexpression of HSD-10 in mouse APs and in various other cellular components of mouse brains. It is also possible that the human APP gene responsible for HSD-10 deposition in APs of these Tg2576 mice brains is different from that of AD brains. Alternatively, the HSD-10 gene and APP gene may function independently in AD brains. Despite these differences, the Tg2576 mouse, as shown in this study, is a proper animal model for the study of AD and also for the investigation of HSD-10.

3-Hydroxyacyl CoA Dehydrogenases↗