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PubMed1985

Nutritional considerations in the patient with disabling brain disease.

Increased nutritional requirements are now recognized as the typical sequellae of head injury. Whether similar nutritional demands routinely accompany nontraumatic, disabling brain diseases is uncertain. Experience with patients suffering from head injury indicates that clinical criteria for differentiating the severity of neurological impairments categorize rather poorly the levels of nutritional need. Based on available data, "nutritional risk" can only be assigned to broad patient categories. Head-injured patients seem to be at nutritional risk and, by virtue of increased caloric and protein requirements, may benefit, in terms of reduced mortality, from early, intensive nutritional intervention. Because the nutritional risk cannot be established, the indications for aggressive nutritional support in the noninjured patient are even less clear than those for the trauma patient. Parenteral nutrition is often required to meet the goals of nutritional support because inadequacies in gastrointestinal function frequently mitigate successful enteral nutrition. Selective nutritional therapies involving the branched chain amino acids may reduce the attrition of the body cell mass seen in head injury patients. Furthermore, improvements in energy nutrient utilization in other than head-injured patients have been suggested when fat is provided in addition to glucose as a caloric source. When clinically feasible, enteral nutrition offers significant economic and physiological benefits over parenteral nutrition. In this regard, increasing attention has been focused on newer techniques of enteral access. These include percutaneous gastrostomies and nasally inserted small bore feeding tubes. The latter achieve duodenal intubation with a high success rate, and they offer the prospects of improved feeding tolerance and reduced tracheobronchial aspiration by allowing the administration of nutrients distal to the pylorus.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMedDate not supplied

The value of ophthalmoscopy in the diagnosis of arterial hypertension in patients with ischemic brain disease.

Beside dyslipoproteinemia, one of the key risk factors for the onset of brain atherosclerosis, as well as ischemic brain disease (IBD) is arterial hypertension. Significant number of patients is not aware of their hypertension, and a paradoxical blood pressure decrease can occur at the onset of IBD, due to the failure of autoregulation mechanisms. Likewise, valid anamnestic data can not frequently be obtained due to difficulties in communication with patients. Regarding these facts, our hypothesis was that ophthalmoscopy in patients with IBD had the greatest sensitivity in the diagnosis of hypertensive disease, its duration and severity. For that reason, the purpose of this study was to determine the significance of ocular fundus examination in those patients with IBD who were not aware of their hypertension, or the high blood pressure was not registered at the admission. Study comprised 140 IBD patients selected upon the following criteria: ophthalmoscopy was performed by the same ophthalmologist, and IBD was diagnosed according to clinical criteria and by brain computerized tomography. Results of the study demonstrated that 26 (18.6%) patients, although not aware of having hypertensive disease, had grade I hypertonic fundus, 14 (10%) had grade II, and 8 (5.5%) had grade III hypertonic fundus, which indicated the high sensitivity of ophthalmoscopy in the diagnosis of hypertensive disease, as well as its duration and severity. This is particularly important in patients with negative history of hypertension, and also suggests the significance of routine ophthalmoscopy in normotensive patients.

Aged↗
PubMed1997

Presenilin-1 immunoreactivity is localized intracellularly in Alzheimer's disease brain, but not detected in amyloid plaques.

The identification of the cellular and subcellular regions of the Alzheimer's disease brain to which the presenilin-1 (PS-1) protein localizes is expected to contribute to an understanding of its pathophysiological role. Toward this end, we have derived an affinity-purified antibody to a synthetic PS-1 peptide. In this report, we demonstrate that this antibody, called SW2, specifically recognizes full-length, 47-kDa PS-1 protein from rat primary cortical neurons, from a human neuronal cell line, and from human brain extracts on Western immunoblots. Immunohistochemical analysis of postmortem brain tissue from control and Alzheimer's disease patients using this SW2 antibody indicates an intracellular localization of PS-1 immunoreactivity with prominent perinuclear characteristics in neurons, with staining also detected in neuritic processes. Despite various treatments of the tissue sections, no PS-1 immunoreactivity was observed in neuritic plaques, the hallmark pathological lesions of Alzheimer's disease. In addition, confocal microscopic analysis of immunostained cultured primary neurons revealed a prominent perinuclear pattern of PS-1 immunoreactivity consistent with vesicular localization, as well as punctate staining in neuritic processes.

Alzheimer Disease↗
PubMed1998

[Analysis of abnormal findings observed on brain MRI T 2 weighted image in a system for the detection of asymptomatic brain disease in 1,200 cases].

In this study we described the significance of asymptomatic cerebral infarction (ACI) and periventricular hyperintensity (PVH) observed on brain MRI in a system for detection of asymptomatic brain disease with 1,200 cases. The risk factors (RF), population in each age bracket of ACI and PVH, among groups with hypertension (HTG) and without RF (no-RFG), were investigated. The RF of ACI were hypertension (HT), diabetes mellitus (DM), and aging. Without DM, those are common RF of PVH. The population of PVH and ACI with PVH increased with aging in no -RFG. On the other hand, only the population of ACI with PVH increased with aging in HTG. The rate of these abnormal findings in HTG was significantly higher than that in no-RFG. In addition, HT accelerated the occurrence of these findings by 10-20 years. When patients were over 60 years old, ACI increased rapidly. Accordingly, we concluded that (1) PVH and ACI had a common background. (2) Long term follow up concerning the incidence of ACI in the group with only PVH was necessary. (3) It was desirable that treatment for RF should be effected before the age of sixty.

Adolescent↗
PubMedDate not supplied

Comparison of fluid-attenuated inversion recovery and T2-weighted magnetic resonance images in dogs and cats with suspected brain disease.

To compare fluid-attenuated inversion recovery (FLAIR) and T2-weighted magnetic resonance (MR) imaging in small animal patients with suspected brain disease, paired sets of FLAIR and T2-weighted MR images of 116 dogs and cats were reviewed separately without any patient information. Images were rated as normal or abnormal using a five-point scale, and the distribution, signal intensity, and anatomic location of abnormalities were recorded. In 60 animals, both FLAIR and T2-weighted images were normal. In 50 animals, the same abnormalities were identified in both FLAIR and T2-weighted images. Overall, very good agreement was found between FLAIR and T2-weighted MR images (kappa = 0.88). FLAIR images had abnormalities that were not recognized in the corresponding T2-weighted images in six of 116 examinations (5%). In four of these, the abnormalities in FLAIR images were thought to represent pathology, including granulomatous meningoencephalitis in one dog, postictal edema in one dog, and undiagnosed lesions in two dogs. In the remaining two examinations, the abnormalities in FLAIR images were probably artifacts. No examples were found of intracranial abnormalities in T2-weighted images that were not visible in FLAIR images. In this study, acquiring FLAIR images in addition to T2-weighted images resulted in detection of otherwise occult abnormalities in relatively few patients.

Animals↗
PubMed1997

Monoclonal antibodies to a 100-kd protein reveal abundant A beta-negative plaques throughout gray matter of Alzheimer's disease brains.

Here we describe the initial characterization of a 100-kd protein recognized by four new monoclonal antibodies that reveal abundant and unique plaque-like lesions throughout gray matter of Alzheimer's disease brains. This 100-kd protein and these new plaque-like lesions were identified by four monoclonal antibodies raised to immunogens extracted from Alzheimer's disease neurofibrillary abnormalities. However, these antibodies did not recognize hyperphosphorylated tau in Western blots or neurofibrillary lesions by immunohistochemistry. As all of these antibodies displayed similar properties, one, AMY117, was used to characterize the new plaque-like lesions in detail. These studies demonstrated that AMY117-positive plaques were not visualized by amyloid stains and never co-localized with A beta deposits, although AMY117-positive and A beta-positive lesions frequently occurred in the same cortical and subcortical gray matter regions. Abundant AMY117-positive plaques were found in the brains of all 32 sporadic Alzheimer's disease patients and all 6 elderly Down's syndrome subjects. Although AMY117-positive plaques also were seen in the brains of nondemented patients with numerous A beta deposits. AMY117-positive plaques were rare or absent in the brains of other elderly controls and patients with other neurodegenerative or neuropsychiatric disorders. We conclude that the AMY117-positive plaques described here for the first time are major lesions of the Alzheimer's disease brain. Thus, it will be important to elucidate the role played by the 100-kd protein and the AMY117 plaques in the etiology and pathogenesis of Alzheimer's disease.

Aged↗
PubMed1999

Expression of the dihydropyrimidinase related protein 2 (DRP-2) in Down syndrome and Alzheimer's disease brain is downregulated at the mRNA and dysregulated at the protein level.

Deteriorated migration, axonal pathfinding and wiring of the brain is a main neuropathological feature of Down Syndrome (DS). Information on the underlying mechanisms is still limited, although basic functions of a series of growth factors, cell adhesion molecules, guidance factors and chemoattractants for brain histogenesis have been reported. We used proteomics to detect differences in protein expression between control, DS and Alzheimer's disease brains: In five individual brain regions of 9 individuals of each group we performed two dimensional electrophoresis with MALDI--identification of proteins and determined mRNA levels of DRP-2. Significantly decreased mRNA levels of DRP-2 in four brain regions of patients with DS but not with AD as compared to controls were detected. 2D electrophoresis revealed variable expression of DRP-2 proteins, which showed a high heterogeneity per se. Dysregulation of DRP-2 was found in brains of patients with DS and AD presenting with an inconsistent pattern, which in turn may reflect the inconsistent neuropathological findings in patients with DS and AD. The decrease of mRNA DRP-2 steady state levels in DS along with deteriorated protein expression of this repulsive guidance molecule of the semaphorin/collapsin family, may help to explain deranged migration and histogenesis of DS brain and wiring of AD brain.

Aged↗
PubMed2005

Truncation and activation of calcineurin A by calpain I in Alzheimer disease brain.

A disturbance of calcium homeostasis is believed to play an important role in the neurodegeneration of the brains of Alzheimer disease (AD) patients, but the molecular pathways by which it contributes to the disease are not well understood. Here we studied the activation of two major Ca(2+)-regulated brain proteins, calpain and calcineurin, in AD brain. We found that calpain I is activated, which in turn cleaves and activates calcineurin in AD brain. Mass spectrometric analysis indicated that the cleavage of calcineurin by calpain I is at lysine 501, a position C-terminal to the autoinhibitory domain, which produces a 57-kDa truncated form. The 57-kDa calcineurin maintains its Ca(2+)/calmodulin dependence of the phosphatase activity, but the phosphatase activity is remarkably activated upon truncation. The cleavage and activation of calcineurin correlate to the number of neurofibrillary tangles in human brains. These findings suggest that the overactivation of calpain I and calcineurin may mediate the role of calcium homeostatic disturbance in the neurodegeneration of AD.

Aged↗
PubMed1999

Assignment of the muscle-eye-brain disease gene to 1p32-p34 by linkage analysis and homozygosity mapping.

Muscle-eye-brain disease (MEB) is an autosomal recessive disease of unknown etiology characterized by severe mental retardation, ocular abnormalities, congenital muscular dystrophy, and a polymicrogyria-pachygyria-type neuronal migration disorder of the brain. A similar combination of muscle and brain involvement is also seen in Walker-Warburg syndrome (WWS) and Fukuyama congenital muscular dystrophy (FCMD). Whereas the gene underlying FCMD has been mapped and cloned, the genetic location of the WWS gene is still unknown. Here we report the assignment of the MEB gene to chromosome 1p32-p34 by linkage analysis and homozygosity mapping in eight families with 12 affected individuals. After a genomewide search for linkage in four affected sib pairs had pinpointed the assignment to 1p, the MEB locus was more precisely assigned to a 9-cM interval flanked by markers D1S200 proximally and D1S211 distally. Multipoint linkage analysis gave a maximum LOD score of 6.17 at locus D1S2677. These findings provide a starting point for the positional cloning of the disease gene, which may play an important role in muscle function and brain development. It also provides an opportunity to test other congenital muscular dystrophy phenotypes, in particular WWS, for linkage to the same locus.

Blindness↗
PubMed1990

The need for specialists in biologically-based brain diseases.

Because neuroscience research has documented that mental illnesses are biologically-based brain diseases, our country should start training programs to create BBBD specialists. The National Alliance for the Mentally Ill has proposed a 2-track training system for psychiatric professionals--(1) A BBBD track and (2) a "mental health" track.

Biological Psychiatry↗
PubMed1976

GM2 ganglioside in fetal Tay-Sachs disease brain cultures: a model system for the disease.

Cultured cells derived from Tay-Sachs disease (TSD) fetal cerebellum were shown to accumulate GM2 ganglioside when compared with control cultures. In contrast, fibroblasts derived from TSD fetal lung do not contain GM2. GM2 was identified by thin-layer chromatography (TLC) and confirmed by gas-liquid chromatography (GLC). Unlike fetal TSD brain, the cell cultures established from fetal TSD brain have high concentrations of globoside and GD3 and little or no asialo GM2(GA2). The GM2 and related glycosphingolipids in these cultured cells contain a high percentage of C24:0 and C24:1 fatty acids. In spite of these differences, this TSD cell strain is unique in that it accumulates GM2, and can therefore serve as a useful in vitro model for the study of TSD.

Cells, Cultured↗
PubMed1995

Muscle-eye-brain disease and Fukuyama type congenital muscular dystrophy are not allelic.

Muscle-Eye-Brain disease (MEB) and Fukuyama type congenital muscular dystrophy (FCMD) are clinically similar autosomal recessive diseases, characterized by congenital muscular dystrophy and severe mental retardation, raising the possibility that they might be caused by mutations of the same gene. Recently FCMD was localized to chromosome 9q31-33 by linkage. We performed a linkage study in seven Finnish MEB families with 12 affected patients using markers D9S53, D9S58, D9S59 and HXB. The MEB phenotype was not linked to any of the markers. A multipoint linkage analysis excluded the entire region harboring FCMD. We thus conclude that MEB and FCMD are not allelic.

Adolescent↗
PubMedDate not supplied

[Congenital muscular dystrophies: muscle-eye-brain disease].

Three rare autosomal recessive disorders share the combination of congenital muscular dystrophy and brain malformations including a neuronal migration defect: muscle-eye-brain disease (MEB), Walker-Warburg syndrome (WWS), and Fukuyama congenital muscular dystrophy (FCMD). In addition, ocular abnormalities are a constant feature in MEB and WWS. We report on two brothers with MEB. The clinical and radiological characteristics are demonstrated.

Brain↗