Disease relevance of Central Nervous System Diseases

• Vasopressin (ADH) was measured in CSF and plasma in 75 evaluable patients with known or suspected CNS metastases from small-cell bronchogenic carcinoma (SCBC), and in 66 control patients having neither malignant disease nor organic CNS disease [1].
• Cryostat sections of central nervous system (CNS) tissues of patients with multiple sclerosis (MS) and other CNS diseases were stained with antibodies to fibronectin, a macrophage fibronectin receptor component, fibrin/fibrinogen, and albumin using immunoperoxidase [2].
• RESULTS: In the group of lupus patients with CNS involvement, intrathecal levels of NFL and GFAP were increased an average of 7-fold (P </= 0.0001) and 3-fold (P </= 0.05), respectively, compared with the levels in SLE patients without overt CNS disease [3].
• These results demonstrate that the severity of CNS disease can be reduced through the use of a neutralizing mAb directed against CCL5 in a viral model of demyelination [4].
• The lack of neuronal HSP72 expression in this model suggests that at least some of the events leading to neuronal injury in meningitis are unique, when compared with CNS diseases associated with HSP72 induction [5].

Psychiatry related information on Central Nervous System Diseases

• OBJECTIVE: Elevated plasma homocysteine has been found to be a risk factor for Alzheimer's disease as well as cerebral vascular disease, suggesting that some risk factors can accelerate or increase the severity of several CNS disease processes [6].
• Raised CSF concentrations of TNF-alpha (greater than 40 ng/l) were detected both in patients with AIDS dementia complex (ADC) (6/9) and with CNS opportunistic infections (10/19) and, less commonly, in HIV infected subjects without CNS diseases (2/14) and in anti-HIV negative controls (1/14) [7].
• Present or past alcohol abuse and respiratory, liver, cardiac or CNS diseases of different degrees seemed to be features in common for the patients possibly rendering them susceptible to the suggested detrimental effect of chlormethiazole therapy [8].

High impact information on Central Nervous System Diseases

• CNTF is a major protective factor in demyelinating CNS disease: a neurotrophic cytokine as modulator in neuroinflammation [9].
• These data suggest that oligodendrocytes share with neurons a high vulnerability to AMPA/kainate receptor-mediated death, a mechanism that may contribute to white matter injury in CNS disease [10].
• In contrast, LCMV-infected, nontransgenic littermates and mice expressing other gene products from the NSE promoter showed no CNS disease, no increased intraparenchymal CTL, and no blood-brain barrier damage after the adoptive transfer of antiviral CTL [11].
• This observation suggests a possible role for brain-reactive lymphocytotoxic antibodies in the development of CNS disease in SLE [12].
• Hyponatraemia and hypoosmolality in patients with central nervous system (CNS) disease or trauma are often ascribed to inappropriate secretion of antidiuretic hormone [13].

Chemical compound and disease context of Central Nervous System Diseases

• In patients with CNS disease or injured brains intravenous fluid intake should be limited to about 1 litre (of 2.5% glucose in 0.45% saline for a 70 kg adult) per day during the acute stress [13].
• Tumor necrosis factor (TNF) is up-regulated in a variety of central nervous system (CNS) diseases with diverse etiology and pathologic manifestation [14].
• Treatment consisted essentially of a 4-drug combination (cytoxan, adriamycin, vincristine, and prednisone) alternating with a 42-hr methotrexate infusion, followed by leukovorin rescue, and included intrathecal prophylactic therapy against central nervous system (CNS) disease [15].
• Generalized CNS disease and massive GM1-ganglioside accumulation in mice defective in lysosomal acid beta-galactosidase [16].
• Untreated the disease is invariably fatal, and melarsoprol, the only available and effective treatment for CNS disease, is associated in up to 10% of cases with a severe post-treatment reactive encephalopathy (PTRE), which can itself cause death [17].

Biological context of Central Nervous System Diseases

• CNS disease associated with the N-terminal portion of the Fr98 env gene was preceded by upregulation of cytokines and chemokines [18].
• Except for the previously reported pathogenicity of beta-synuclein, none of the 68 peptides from 39 proteins was found to induce CNS disease in recipient rats [19].
• Here we show that transgenic (tg) mice that overexpress bioactive (TGF-beta 1 in the central nervous system (CNS) and show no overt phenotype in the unmanipulated state, are more susceptible to the immune-mediated CNS disease experimental autoimmune encephalomyelitis (EAE) [20].
• The association of viral infections with autoimmune central nervous system (CNS) diseases such as post-infectious encephalomyelitis and possibly multiple sclerosis (MS) prompted the investigation to understand how virus infection could modulate autoimmune responses [21].

Anatomical context of Central Nervous System Diseases

• Major illnesses presenting with psychiatric symptoms in order of frequency were infectious, pulmonary, thyroid, diabetic, hematopoietic, hepatic and CNS diseases [22].
• In order to determine whether patients with active CNS-SS have cerebrospinal fluid (CSF) abnormalities indicative of CNS inflammation, CSF analyses from 30 patients with active CNS-SS (SSA) were contrasted with those from 20 SS patients without CNS involvement (SSI) and 20 patients with systemic lupus erythematosus and active CNS disease (SLEA) [23].
• TNFR1 signalling is critical for the development of demyelination and the limitation of T-cell responses during immune-mediated CNS disease [24].
• It is known that there is restricted clonality of the B-cell immunoglobulin response in the CSF compartment with inflammatory CNS diseases, and with infections the majority of these so-called oligoclonal antibodies are directed against the exciting antigen and are synthesized in the CNS [25].
• These results suggest that the envelope protein of CasBrE is not itself neurotoxic but that virus infectious events beyond binding and fusion in microglia are necessary for the induction of CNS disease [26].

Gene context of Central Nervous System Diseases

• Thus, TGF-beta1 may exert a protective role in CNS diseases characterized by microglial cell activation by proinflammatory stimulants [27].
• In this review, we focus on the biological functions of OSM, the signaling pathways of OSM in the CNS, and OSM involvement in CNS diseases [28].
• This shift from classically neuroprotective to neurodegenerative MAPK pathways suggests that agents that inhibit activation of JNK/p38 may be protective against HIV-associated CNS disease [29].
• First, we note that purified recombinant MOBP inoculated into SJL/J mice produces CNS disease [30].
• Further, it is possible that an as yet unidentified cell found more abundantly in LT-alpha -/- than in LT-beta -/- mice may assist in the amplification of scrapie infection in the periphery and favor susceptibility to CNS disease following peripheral routes of infection [31].

Analytical, diagnostic and therapeutic context of Central Nervous System Diseases

• In three separate experiments, no mouse sensitized for EAE and then treated with anti-TNF by intraperitoneal injection developed signs of central nervous system (CNS) disease [32].
• PCR detected B burgdorferi OspA DNA in CSF of (1) 10 of 11 patients with Lyme encephalopathy, (2) 28 of 37 patients with inflammatory CNS disease, (3) seven of seven seronegative patients with Lyme-compatible disorders, and (4) zero of 23 patient controls [33].
• We used a newly developed enzyme immunoassay and the polymerase chain reaction to investigate the association of R henselae infection with HIV-related CNS disease and found that whereas seroprevalence rates in HIV-positive patients unselected for neurologic disease were 4% to 5.5%, those with neurologic disease had seroprevalence rates of 32% [34].
• Intrathecal chemotherapy (methotrexate, hydrocortisone and cytarabine) was given to prevent CNS disease, and CNS irradiation was used only for patients with leukemia and an initial WBC of >50,000/microl or patients with active CNS disease at diagnosis [35].
• Rhesus monkeys infected with simian immunodeficiency virus (SIV) manifest immunosuppression and CNS disease that is pathologically [L. R. Sharer et al. (1991) J. Med. Primatol. 20, 211-217] and behaviorally [E. A. Murray et al. (1992) Science 255, 1246-1249] similar to humans [36].

References