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PubMed1995

Qualitative comparison of carbon dioxide-induced change in cerebral near-infrared spectroscopy versus jugular venous oxygen saturation in adults with acute brain disease.

OBJECTIVE: To compare carbon dioxide-induced changes in cerebral oxy- and deoxyhemoglobin, measured by near-infrared spectroscopy, with those changes in jugular venous oxygen saturation in adult patients with acute brain disease. DESIGN: A prospective study. SETTING: The medical and surgical intensive care unit of a university hospital. PATIENTS: Nine patients with head trauma (n = 4), cerebrovascular disease (n = 3), and meningitis (n = 2). A total of ten measurements were done, while PaCO2 was increased from hypocapnia toward normocapnia in the nine patients. INTERVENTIONS: Arterial and jugular bulb catheterization, and intracranial pressure monitoring were performed as a part of the clinical intervention. An increase in PaCO2 was obtained by inhalation of CO2 and, if necessary, by reducing the ventilator rate. MEASUREMENTS AND MAIN RESULTS: In each patient, the position of the jugular bulb catheter was ascertained by skull roentgenography. Near-infrared spectroscopic values for oxy- and deoxyhemoglobin were set at zero at the beginning of the study. An increase in PaCO2 from 29 +/- 1 (SEM) torr (3.9 +/- 0.2 kPa) to 39 +/- 2 torr (5.2 +/- 0.3 kPa) was accompanied by a significant increase in jugular venous oxygen saturation from 63 +/- 3% to 76 +/- 3%; a significant increase in oxyhemoglobin of 3.5 +/- 0.9 mumol/L (of the brain tissue); and a significant decrease in deoxyhemoglobin of 1.5 +/- 0.4 mumol/L. In nine of ten measurements, the slopes of changes in oxyhemoglobin against the slopes of change in jugular venous oxygen saturation were very similar. In one patient, oxyhemoglobin changed negligibly while jugular venous oxygen saturation increased by 20%. CONCLUSIONS: Jugular venous oxygen saturation consistently demonstrates cerebrovascular responsiveness to CO2. The direction and magnitude of changes in cerebral oxyhemoglobin, measured by near-infrared spectroscopy, were similar to those changes in jugular venous oxygen saturation in most of our cases. Interpretation of a negligible change in oxyhemoglobin in one patient, despite an obvious increase in jugular venous oxygen saturation, requires further study comparing near-infrared spectroscopy with standard techniques.

Acute Disease↗
PubMed1998

Cholinergic structures and neuropathologic alterations in the olfactory bulb of Alzheimer's disease brain samples.

This report describes the laminar distribution of acetylcholinesterase-positive structures and the neuropathologic alterations in the human olfactory bulb of control and Alzheimer's disease brain samples. The results suggests that no correlation exists between the distribution of cholinergic axons and the neuropathological alterations in the different layers in Alzheimer's disease.

Acetylcholinesterase↗
PubMed1993

Alterations of selected enzymes of phospholipid metabolism in Alzheimer's disease brain tissue as compared to non-Alzheimer's demented controls.

Previous studies have demonstrated elevated brain levels of phosphomonoesters in early stages of Alzheimer's disease and elevations of phosphodiesters later in the disease. In addition, preliminary quantitative analyses of the phospholipids of Alzheimer's brain reveals either decreases in some phospholipids or elevations followed by decreases in others. This study quantitated the activities of selected enzymes involved in phospholipid and choline metabolism and demonstrated elevated glycerol-3-phosphorylcholine phosphodiesterase and decreased choline kinase activities in Alzheimer's disease brain. The former could provide an enzymatic mechanism for the increased phosphorylcholine found in Alzheimer's disease brain.

Aged↗
PubMed1992

Heterogeneity of NMDA receptors labelled with [3H]3-((+-)-2-carboxypiperazin-4-yl) propyl-1-phosphonic acid ([3H]CPP): receptor status in Alzheimer's disease brains.

The binding of [3H]3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid ([3H]CPP) was studied in rat and human brain synaptic membranes. Specific binding was saturable, reversible and inhibited by a range of compounds active at N-methyl-D-aspartate (NMDA) receptors such as 2-amino-5-phosphonopentanoate (AP5), 2-amino-7-phosphonoheptanoate (AP7), NMDA and cis-2,4-methanoglutamate. Binding was heterogeneous as evidenced by non-linear Scatchard plots and Hill coefficients for binding inhibitors significantly different from unity. LIGAND analysis of the binding data indicated the likely presence of two distinct binding components for CPP, one of high (Kd values approx. = 70 nM) and the other of low (Kd values approx. 5 microM) affinity. Possible alterations in the binding of [3H]CPP to either site were investigated in medial frontal and medial temporal cortex from Alzheimer's disease brains and compared with control tissues, carefully matched for age and postmortem delay. While there were considerable inter-individual variations in binding, no significant differences were detected either between brain regions in either Alzheimer or control subjects, or between Alzheimer's disease and control brains. These data suggest the presence of at least two components of [3H]CPP binding in both rat and human brain tissue. The integrity of neither of these components is altered in Alzheimer's disease, consistent with a lack of gross alterations of NMDA receptors in this disorder.

2-Amino-5-phosphonovalerate↗
PubMed2004

Reorganisation of cerebral circuits in human ischemic brain disease.

Animal experiments suggest that reorganisation of cerebral representations is the neurobiological basis of post-lesional recovery. In human ischemic brain disease recovery is a dynamic and sustained process beginning after stroke manifestation. The mechanisms underlying recovery can be investigated non-invasively in the human brain using functional neuroimaging and transcranial magnetic stimulation (TMS). In the acute stage, the mismatch area of the perfusion deficit and the impaired water diffusion as assessed by magnetic resonance imaging (MRI) shows the brain tissue that potentially can be rescued by thrombolysis or emergency carotid endarterectomy. Since spontaneous motor recovery is a function of the corticospinal tract integrity, early reperfusion of ischemic tissue is critical. In the subacute and chronic stage after stroke, recovery of motor function was shown to take place irrespective of a concomitant affection of the somatosensory system. Functional MRI with simultaneous recordings of the electromyogram provides evidence that the abnormal activation of motor and premotor cortical areas in both hemispheres related to finger movements has a large interindividual variability. As evident from TMS, recovery results from regression of perilesional inhibition and from remote intracortical disinhibition. Repetitive training, constraint induced training and motor imagery can augment recovery promoting a re-emerging activation in the affected hemisphere. Evolution of altered local perilesional and large-scale bihemispheric circuits appears to allow for post-lesional deficit compensation.

Brain Ischemia↗
PubMedDate not supplied

Elevated adenosine monophosphate deaminase activity in Alzheimer's disease brain.

Abnormal elevations in ammonia have been implicated in the pathogenesis of Alzheimer's disease. However, the biochemical mechanism(s) leading to increased ammonia in Alzheimer's disease have not yet been identified. A potential source of increased ammonia production is adenosine monophosphate (AMP) deaminase, an important enzyme in the regulation of the purine nucleotide cycle and adenylate energy charge. AMP deaminase activity is expressed in human brain and converts AMP to inosine monophosphate with the release of ammonia. We have investigated AMP deaminase activity in postmortem brain tissue from Alzheimer's disease subjects and age-matched controls. Compared to control brain, Alzheimer's disease brain AMP deaminase activity is 1.6- to 2.4-fold greater in the regions examined--the cerebellum, occipital cortex, and temporal cortex. Similar increases in AMP deaminase protein and mRNA levels are observed in Alzheimer's disease brain. These results suggest that increased AMP deaminase activity may augment ammonia levels in the brain in Alzheimer's disease.

AMP Deaminase↗
PubMed1995

Anion exchange proteins are a component of corpora amylacea in Alzheimer disease brain.

Corpora amylacea (CAm) are amorphous structures that increase in number in the brains of patients with neurodegenerative diseases. We found abundant CAm in the brains of Alzheimer disease (AD) patients. We show here that proteins of the anion exchanger (AE) gene family, related to erythrocyte band 3, are present in CAm. The presence of AE epitopes in CAm may be related to the presence of AE proteins in membranes of neurones, and their altered expression level in degenerating neurones in AD brains. Whereas the distribution of immunoreactivity was uniform over the CAm in control brains, there was much more variation in staining of CAm core and peripheral structures in AD brains. Our data support the suggestion that accumulation of altered neuronal membrane proteins may be involved in the pathogenesis of CAm in AD.

Aged↗
PubMed1998

Histochemical localization of glycoconjugates on microglial cells in Alzheimer's disease brain samples by using Abrus precatorius, Maackia amurensis, Momordica charantia, and Sambucus nigra lectins.

Four lectins (Abrus precatorius (APA), Maackia amurensis (MAA), Momordica charantia (MCA) and Sambucus nigra (SNA)) have been used to identify glycohistochemically the microglial cells (MGC) activation in autoptic brain samples from Alzheimer's disease (AD) subjects. Three of these lectins (APA, MAA and MCA) have utilized as microglial cell markers for the first time. The identification of new markers for the study of MGC is very important to better understand the role of these type of cells in the metabolic/dismetabolic control of betaA4 in AD which still represents a vexata questio.

Alzheimer Disease↗
PubMed2006

Choroid plexus transplants in the treatment of brain diseases.

The choroid plexus (CP) produces and secretes numerous biologically active neurotrophic factors into the cerebrospinal fluid (CSF). These circulate throughout the brain and spinal cord, maintaining neuronal networks and associated cells. In neurodegenerative disease and in acute brain injury there is local up-regulation of neurotrophin production close to the site of the lesion. Treatment by direct injection of neurotrophins and growth factors close to these lesion sites has repeatedly been demonstrated to improve recovery. It has therefore been proposed that transplanting viable choroid plexus cells close to the lesion might provide a novel means for continuous delivery of these molecules directly to the site of injury. Recent publications describe how transplanted CP, either free or in an immunoprotected encapsulated form, deliver therapeutic molecules to the desired site. This review briefly describes the accumulated evidence that CP cells support neuronal cells in vitro and have therapeutic properties when transplanted to treat acute and chronic brain disease and injury in animal models.

Animals↗
PubMed1994

Synaptophysin and chromogranin A immunoreactivities of Lewy bodies in Parkinson's disease brains.

Lewy bodies commonly observed in brains with Parkinson's disease (PD) histochemically contain both protein and lipid as chemical components. Ultrastructurally, they are composed of filamentous, vesicular and granular structures. We investigated PD brains with light and electron microscopic immunohistochemistry using antibodies against two marker proteins for neuronal secretory vesicles, synaptophysin and chromogranin A. Both antibodies immunolabeled the peripheral zones and occasionally central cores of Lewy bodies of the classical and intraneuritic types. In addition, the diffuse immunolabeling was observed in Lewy bodies of the cortical type. Furthermore, the ultrastructural immuno-decoration was found mainly in the vesicular structures, and also in the filamentous and granular structures of Lewy bodies. Immuno-blot analysis of each antibody showed no difference between PD and normal control brains. The present observations suggest that vesicular profiles of Lewy bodies represent presynaptic and dense core secretory vesicles, and therefore that the lipid elements of Lewy bodies are derived from membrane lipids of these vesicles.

Aged↗