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PubMed2006

Mouse Models of Human Cancers Consortium Workshop on Nervous System Tumors.

Nervous system tumors are clinically challenging neoplasms that form within the central and peripheral nervous system. Although there have been many clinical trials using novel agents for the treatment of primary brain tumors, there have been few advances that positively affect overall patient survival. Over the past several years, there has been significant progress in the development of accurate small-animal spontaneous brain tumor models, small-animal neuroimaging, and tools for the bioinformatic analysis of complex molecular data sets, all of which have contributed to an improved understanding of the pathogenesis of human brain tumors. Whereas these models will continue to be of great value in basic science investigations, they can also be used to identify and validate potential therapies for brain tumors and to evaluate these drugs in preclinical trials. The National Cancer Institute recently convened a workshop to review the current state of small-animal brain tumor modeling and to make recommendations about the use of these models to improve the clinical outcome for patients with brain tumors. In this meeting report, we outline the current state of small-animal models for brain tumors, the potential applications of these models, and the recommendations made by the workshop participants for the use of mouse models in the preclinical evaluation of potential brain tumor therapies.

Animals↗
PubMed2000

Systemic and Central Nervous System Vasculitides.

The vasculitides are a collection of diseases sharing the central feature of tissue injury due to inflammation of blood vessels. Although some occur frequently, many are encountered uncommonly or rarely. Nonetheless, because peripheral or central nervous system abnormalities may be a prominent part of these disorders, neurologists should know or be able to refer to studies on the classification, pathophysiology, treatments, and long-term complications of vasculitis. Two central issues that confront us now are 1) improving the accuracy of diagnosis, including identifying any underlying infectious causes, and 2) limiting the long-term damage from both the disease and its therapies.

Journal Article↗
PubMed1999

[Aging in parts? Systemic aging of the nervous system].

Neurons of the central nervous system in general do not multiply after birth. Therefore, no replacement or biological renewal of individual cells affected by aging or death is possible. Morphological changes occurring in the aging brain are found substantially more pronounced in neurodegenerative diseases. Systemic degenerations of selective brain areas in these disorders, e.g. in Alzheimer's, Parkinson's, Huntington's disease or in amyotrophic lateral sclerosis, may be considered as models of accelerated aging and may allow to study the genetic and environmental influences of selective aging and cell death in modules of the central nervous system. Although neurodegenerative diseases are disparate disorders on the basis of their symptomatology and the anatomic distribution of pathologic lesions, they actually share key attributes with respect to biochemical and cellular determinants of selective vulnerability. Most strikingly, many show a conversion of disease specific and only recently identified proteins into unsoluble aggregates which form intra- or extracellular deposits. These protein aggregates may, over time, affect neuronal function, eventually leading to neurodegeneration and neurodegenerative pathology. The pathological process is counterbalanced by protective mechanisms that may loose their efficacy during normal aging. This could explain the late onset of even the inherited neurodegenerative disorders. Since the expression of disease-specific proteins is often not restricted to the affected brain areas (as exemplified by the expression of polyglutamine containing proteins in trinucleotide repeat disorders in non-affected brain areas and even outside the brain), the anatomical specificity of the degenerative process may be determined by associated binding proteins. Therapeutic strategies include the reinforcement of physiological defense mechanisms and intervention at early phases of the pathological biochemistry of disease specific proteins.

Animals↗
PubMed2000

Modulation of the immune system by the autonomic nervous system and its implication in immunological changes after training.

This review examines the role of the autonomic nervous system in the regulation of the immune system to understand the alteration of immunological parameters under the influence of stressors and exercise. Sympathetic innervation in secondary lymphoid organs plays a major role in immune regulation. Catecholamine released from the nerve terminal serves as the major mediator when bound to adrenergic receptors present on immunocompetent cells. Experiments using chemical and surgical denervation, catecholamine knock-out mice, and receptor antagonist and agonists revealed several important points. Sympathetic nerve activity is generally suppressive for the immunocompetent cells in the blood stream except neutrophils. Sympathetic activity facilitates detachment of T cells and NK cells from blood vessels without affecting functional adhesion molecule expression. Th1 cells express more beta 2 adrenergic receptors than Th2 cells, indicating a greater influence of sympathetic activity on Th1 response. Sympathetic action was also shown to regulate the production of chemokines. Taken together, the sympathetic nervous system does not simply suppress the immune system but might help organize the immune response sequentially and spatially by modulating the distribution of immunocompetent cells.

Animals↗
PubMed1986

Zuelzer-Wilson's syndrome and absence of the enteric nervous system. Two rare forms of anomalies of the enteric nervous system with identical clinical symptoms.

47 children have been treated in Basel for aganglionosis (Hirschsprung's disease) during the last 25 years. Six children presented severe vomiting and an ileus as leading symptoms instead of chronic constipation, the classical leading symptom of Hirschsprung's disease. Clinical, radiological and intraoperative findings were virtually identical in these 6 patients. However, enzyme histochemical and immunocytochemical investigations disclosed an aganglionosis of the entire colon (Zuelzer-Wilson's disease) in 3 patients, absence of the enteric nervous system in the small and large intestine in 2 patients, and a combination of both in 1 patient. In contrast to children suffering from aganglionosis of the entire colon, the chance of survival for patients with an absence of the enteric nervous system is extremely small. It is therefore necessary in presence of severe vomiting and an ileus to take intraoperative biopsies from the large and the small intestine. The precise diagnosis can be made only by using enzyme histochemical and immunocytochemical techniques.

Cholinergic Fibers↗
PubMed1996

[Free radicals in the central nervous system].

Central nervous system has a low antioxidative capacity, which is formed mainly by ascorbic acid. Therefore the cerebral tissue is threatened by the increased formation of free radicals and their metabolites (ROS--reactive oxygen species). ROS are formed such as in reperfusion phase after ischemia and in catecholamine metabolism, in oxidative stress due to hyperglycaemia. Polyunsaturated fatty acids (PUFA) are peroxidased by ROS; proteins and DNK are damaged as well. Free radicals are involved in etiology and pathogenesis of many CNS diseases, such as neuritis, Alzheimer disease, Parkinson disease, Huntington disease, aging and atherosclerosis of the brain, epilepsy, etc. During the antioxidant therapy it is necessary to consider the types of ROS, their origin and their mode of action, whether to administer hydrophilic or lipophilic antioxidants, eventually chelate agents, etc. Hydrophylic antioxidants are acting very soon after the administration, whereas the lipophilic ones reach their target tissues with a great delay. Therefore it is better to apply them preferentially like a prevention, if possible. Enzymatic antioxidants (SOD, GSPHx and catalase and others) are usually acting only for a short time. The methods of estimation of free radicals attacks are discussed as well their possible pathophysiological effects.

Animals↗
PubMed1985

Central nervous system morbidity following an initial isolated central nervous system relapse and its subsequent therapy in childhood acute lymphoblastic leukemia.

The frequency and types of major CNS toxicity and morbidity were analyzed in 107 children with acute lymphoblastic leukemia (ALL) following an isolated primary CNS relapse. Seventy-nine (73%) have had multiple subsequent marrow or CNS relapses requiring intensive and prolonged therapy to the CNS. Median survival time is two years. Of these 79 patients, two thirds have had one or more types of major CNS toxicity, including epileptiform seizures (35), moderate to severe structural abnormalities (24 of 27 evaluated), major motor disabilities (9), blindness (2), CNS infection (6), cranial nerve palsies (2), and intracranial lymphoma (2). The remaining 28 patients (26%) have had no or one additional CNS relapse and have received therapy for a median of eight years. One half of this surviving group of patients have had major CNS toxicity, including seizures (9), major motor disability (2), and intracranial calcifications (12/19). When neuropsychologic evaluations were compared between the 28 survivors and 50 of their contemporaries who had been in initial continuous complete remission, the CNS survivors had significantly lower Full Scale IQ scores (83 +/- 16 v 99 +/- 14, P = less than .001) with similarly lower measures of academic performance. The relative contributions of meningeal leukemia itself and intrathecal or radiation therapy to these effects cannot be determined. Since major CNS sequelae occurred in the majority of patients who had a primary isolated CNS relapse, and the frequency of CNS relapse is dependent on the efficacy of the method of CNS prophylaxis, the best method of avoiding major CNS sequelae is the most effective form of CNS prophylaxis.

Acute Disease↗
PubMed1994

Biology of the mononuclear phagocyte system of the central nervous system and HIV infection.

Infection of the central nervous system by HIV-1 results in widespread neuropathology and neurological symptoms. The cells infected in the brain belong to the mononuclear phagocyte lineage. We review aspects of the biology of the macrophage populations associated with the central nervous system and consider their distribution, phenotype, and kinetics in relation to HIV pathology.

Central Nervous System↗
PubMed2005

Progressive central nervous system metastases in responder patients for outside central nervous system metastases on trastuzumab-based therapy--report of two cases of refractory breast cancer.

We report two cases of central nervous system (CNS) metastases during systemic response to trastuzumab in combination with chemotherapy for refractory breast cancer. The patients responded to trastuzumab in combination with chemotherapy. During combination treatment, the patients developed cerebellar metastases. A follow-up computed tomography scan revealed that their diseases continued to respond outside the CNS. These cases suggest that the failure of trastuzumab to cross the blood-brain barrier may compromise its overall effectiveness and raises the possibility that CNS metastasis may become clinically more significant in patients receiving antibody-based therapies, including patients responding to therapy outside the CNS. Additionally, repeated stereotactic radiosurgery as gammaknife combination therapy synchronously with systematic trastuzumab-based therapy was useful for the treatment of metastatic breast carcinoma.

Adult↗
PubMedDate not supplied

[Neuroimmunomodulation. The bi- and unilateral correlations between the nervous system and the immune system].

The nervous system-immune system relationships, namely the modulatory effects of the former upon the latter and vice versa, have been considered both in physiological and pathological conditions. The nervous system communicates with the immune system in two biochemical ways, by means of neurohormones and neurotransmitters, using anatomical and functional pathways related to the pituitary system (the manifold endocrine axes between hypophysis and peripheral endocrine glands) and autonomic system (especially the orthosympathetic one, and to much lesser extent the parasympathetic system). The immune system is able to modulate some nervous functions via cytokines, peptidic molecules produced by immunocytes, that can also be secreted in certain conditions by neural cells, such as astrocytes, microgliocytes and even neurons. The knowledge of physiology of the neuroimmunomodulation and related pathological changes may be very useful for understanding the pathogenesis and the pathophysiology of neuroimmunological diseases, and for their diagnosis and treatment.

Animals↗
PubMed1989

[Immunology of tumors of the central nervous system].

Central nervous system (CNS) tumours possess special immunological features resulting from their development in an organ having a privileged immunological status. The following review gives a summary of actual data concerning their tumour-associated antigens, the immunological responses of their hosts and the mechanisms permitting them to escape from these responses. There is presently no proof of the existence of tumour-specific antigens on spontaneous glial tumours. Much progress has been made in this area with the development of monoclonal antibodies technology which mainly disclosed the profound antigenic heterogeneity of brain tumours. This heterogeneity could favour the escape of brain tumours from immunosurveillance; furthermore, it represents a major limitation to the use of monoclonal antibodies for diagnosis or therapy. Regarding the immunological responses of brain tumour patients, the main feature is a profound depression of cellular immunity creating an anergic state toward a large number of antigens. In vitro, it concerns specifically T4 helper lymphocytes: their mitogenic responses and secretion of interleukin-2 after antigenic stimuli are drastically reduced. Three phenomena have also been incriminated to explain the defect of immunosurveillance in brain tumour patients: 1) the synthesis by tumour cells of a protective mucopolysaccharidic coat, 2) the secretion by these cells of specific immunosuppressive factors related to cytokines, 3) the isolation of CNS maintained by the blood-brain barrier which regulates the circulation of immunocompetent cells between the intra- and extracerebral compartments. Currents efforts are focused on the individualization of therapy based on these biologic principles.

Antibodies, Monoclonal↗
PubMed1985

Developmental expression of the myelin-associated glycoprotein in the peripheral nervous system is different from that in the central nervous system.

We recently characterized two developmentally regulated myelin-associated glycoprotein (MAG) polypeptides synthesized by mouse brain mRNA in vitro. We now extended these studies to include the peripheral nervous system (PNS). Total cytoplasmic RNA was isolated from the sciatic nerves of 7-, 12-, and 17-day-old and adult rats and translated in vitro in a rabbit reticulocyte lysate system. In contrast to results in the CNS, it appears that only one MAG polypeptide, p67MAG, is synthesized by PNS mRNA at all ages. The implications of these findings are discussed with respect to recent observations concerning both the localization of MAG and the synthesis of MAG in the PNS of dysmyelinating mutant mice.

Animals↗