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Is Tourette's syndrome an autoimmune disease?
Tourette's syndrome is a childhood-onset neuropsychiatric disorder characterized by the presence of both multiple motor and vocal tics. While its pathogenesis at a molecular and cellular level remains unknown, recent research findings point to the possible involvement of autoimmunity in at least a subgroup of patients. These include the presence of antineuronal autoantibodies, findings of D8/17 B lymphocyte overexpression (a marker of chorea associated with streptococcal infection), reported associations of symptom severity fluctuations over time with preceding infections, and possible beneficial effects of immuno-modulatory intervention. We will critically review these findings, leading us to conclude that Tourette's syndrome is a heterogeneous disorder, and that immune factors may be involved in some patients
Ruolo della tomografia ad emissione di singoli fotoni nella diagnosi della demenza tipo Alzheimer
Apraxia of eyelid closure in autopsy-confirmed vascular progressive supranuclear palsy.
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Cerebral amino acid levels and uptake in rats after portocaval anastomosis: II. Regional studies in vivo.
Accumulo dell'acido glutammico e della glicina in tumori cerebrali umani in vitro. [Accumulation of glutamic acid and glycine in human cerebral tumors in vitro]
Preliminary results are given on transport of glycine and L-glutamate into human cerebral tissue, normal and tumoral. In comparison with normal tissue, glycine transport is diminished in meningioma and oligodendroblastoma, unaffected in neurinoma, sharply increased in medulloblastoma. Glutamic acid transport is lowered in neurinoma and oligodendroblastoma; increased in medulloblastoma. Such preliminary observations are briefly discussed
The tricyclic antidepressant clomipramine dose-dependently reduces regional cerebral metabolic rates for glucose in awake rats
The time course and the relation to dose of regional cerebral metabolic rates for glucose (rCMRglc) were measured in awake male Fischer-344 rats after administration of clomipramine (CMI), a serotonin (5-HT) uptake inhibitor and clinical antidepressant. rCMRglc was determined, using the quantitative autoradiographic [14C]2-deoxyglucose technique, in 64 brain regions at 20, 40, 60, 120, and 180 min after administration of CMI 50 mg/kg IP and 120 min after CMI 2 and 10 mg/kg IP. The peak metabolic effect was observed at 120 min after CMI. At that time, CMI 2 and 10 mg/kg IP significantly reduced rCMRglc from control values in 12 (19%) and 14 (22%) brain regions, which correspond to areas with high densities of 5-HT reuptake sites (e.g. visual and limbic areas and raphe nuclei). CMI 50 mg/kg produced widespread rCMRglc reductions in 34 (53%) brain regions, including cortical, hippocampal, raphe and cerebellar areas. The topographic distribution and the relation to time and dose of CMI effects on rCMRglc are different from those of 5-HT1A [8-hydroxy-2(di-N-propylamino) tetralin], 5-HT1B-C (m-chlorophenylpiperazine) and 5-HT3 (quipazine) agonists and resemble those produced by 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), an agonist of 5-HT2 receptors, suggesting that CMI may prefentially stimulate this 5-HT receptor subtype
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