Showing papers in "Journal of Neuroimmunology in 2009"

TL;DR: ASD patients displayed an increased innate and adaptive immune response through the Th1 pathway, suggesting that localized brain inflammation and autoimmune disorder may be involved in the pathogenesis of ASD.

TL;DR: In order to study the polarization induced by Abeta, microglia was stimulated with different forms of the peptide and found that the oligomeric Abeta is a stronger M1-inductor than the fibrillar form.

TL;DR: Elevated levels of endotoxin/lipopolysaccharide concentrations in plasma from patients with sporadic amyotrophic lateral sclerosis (sALS) and Alzheimer's (AD) as compared to healthy controls suggest that systemic LPS levels and activated monocyte/macrophages may play significant roles in the pathogenesis of sALS.

TL;DR: This study shows that TNF-alpha and elevated numbers of antibodies against periodontal bacteria associate with AD and contribute to the AD diagnosis.

TL;DR: G-1 is able to reduce the severity of disease in both active and passive EAE models of multiple sclerosis in SJL mice and that this effect is concomitant with a G-1-mediated decrease in proinflammatory cytokines, including IFN-gamma and IL-17, in immune cells harvested from these mice.

TL;DR: The hypothesis of an involvement of the adaptive immune system associated with a neuroinflammatory process in the pathobiology of ALS is strengthened.

TL;DR: It is demonstrated that the transplacental passage of IgG from MCAD is capable of inducing long-term behavioral consequences and pilot studies of immune markers in MCAD IgG-exposed embryonic brains suggest evidence of cytokine and glial activation.

TL;DR: The inhibition of microglial activation by ginseng saponins may be a good potential therapeutic modality for neurodegenerative diseases.

TL;DR: The emerging role of this neurotransmitter as a regulator of DC and T-cell physiology and, in turn, immune response is reviewed and how alterations in the dopamine-mediated immune regulatory mechanisms could contribute to the onset of immune-related disorders is discussed.

TL;DR: The importance of the Fok-I VDRG polymorphism for vitamin D metabolism should be taken into account in association and ultimately intervention studies on vitamin D and MS.

TL;DR: Intravenous transplantation of MSCs which protect dopaminergic neurons from MPTP toxicity may be engaged in anyone or a combination of these mechanisms: repair of the BBB, reduction of MBL in the brain, inhibition of microglial cytotoxicity, and direct protection of dopamine neurons.

TL;DR: The results corroborate the role of inflammatory events in the process of neurodegeneration in PD which can be of special relevance in the sporadic form of PD with later onset.

TL;DR: Results support the use of BMSCs as vehicles to deliver BDNF into the CNS of EAE animals and suggest a potentially novel therapeutic approach that might be used to deliverBDNF gene or genes for other therapeutic proteins into the central nervous system in MS or in other diseases of the CNS in which accessibility of therapeutic proteins is limited due to the blood-brain barrier.

TL;DR: This work prospectively assessed suppressive activities and frequencies of Treg and Treg subsets in 15 patients with RRMS undergoing long-term therapy with GA and concluded that the immunomodulatory action of glatiramer acetate includes effects on Treg function and frequencies.

TL;DR: Luteolin and diosmin inhibited neuronal JAK2/STAT3 phosphorylation both in vitro and in vivo following IL-6 challenge as well as significantly diminishing behavioral deficits in social interaction.

TL;DR: It is found that IFN-beta-1a(IM) treatment of relapsing-remitting MS subjects over 12 months significantly increased both percentage of CD56(bright) NK cells and Foxp3 mRNA expression compared to baseline values, untreated RRMS subjects and healthy controls (HC).

TL;DR: A considerable number of patients with Bickerstaff brainstem encephalitis have associated Guillain-Barré syndrome, indicative that these two disorders are closely related on a continuous spectrum.

TL;DR: A role for this epitope in the autoimmune pathogenesis of MS is suggested because antibodies against EBNA-1 in HLA DRB1*1501 positive individuals were associated with a 24-fold risk increase for MS.

TL;DR: There is evidence of immune activation and Treg cells in acute ischaemic stroke in patients with ischemic stroke compared to healthy subjects and patients with OND.

TL;DR: Intravenous administration of syngenic BMSCs to EAMG-model rats effectively ameliorated the disease, partially through a TGF-beta-dependent mechanism, and support a potential role for B MSCs in their treatment.

TL;DR: The data show that NMO-IgG induces a complement-dependent cytotoxicity of astrocytes in vitro, and suggest that a mechanism of cellular death by necrosis might be implicated in the pathophysiology of NMO.

TL;DR: Vascular alterations in MOG peptide-induced EAE in the mouse are accompanied by increased lesion-specific levels of VEGF, extensive laminin deposits in the tissue and altered transcription of numerous angiogenic factors.

TL;DR: It is shown that neurodegenerative lesions caused by human truncated tau promote inflammatory response manifested by upregulation of immune-molecules and morphological activation of microglial cells in a rat model of tauopathy.

TL;DR: It is suggested that MWCNTs could potentially be used as a novel and non-toxic vehicle for targeting MP in brain tumors.

TL;DR: The findings suggest that the mechanism of microglial activation during stress may differ from those of infection or inflammation and indicates that the neuronal cells expressing c-Fos protein may play some roles to trigger microglia activation.

TL;DR: A significant association was noted between the severity of neurological deficit at admission, the diagnostic subtype and some inflammatory variables.

TL;DR: MSC-CNTF may improve functional recovery in EAE mice, possibly by exerting their immunoregulatory activity, inhibiting inflammation, homing MSC- CNTF cells to the lesions, elevating CNTF expression, reducing demyelination, and stimulating oligodendrogenesis.

TL;DR: IL-1Ra and/or IL-1 RII increased in sera of all 10 investigated patients after the steroid treatment for relapse, suggesting the important beneficial role of the induction of IL- 1 RII and IL-2Ra in MS.

TL;DR: The results indicate that lupus mice develop depression and CNS dysfunction very early in the course of disease, in the absence of substantial pathology involving other target organs.

TL;DR: A role for CCR6-expressing PDL1(+) mDC in regulating EAE progression is suggested, and add back of mDC with increased PD-L1 expression to C CR6(-/-) mice reduced the severe chronic EAE disease phase to that of wild type controls.