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Introduction: Patients with Alzheimer disease (AD) suffer from psychotic symptoms including pain. The current antipsychotic drugs confer limited effectiveness, and hence new strategies are being designed to decrease pain in order to increase antipsychological effectiveness. Vitamin B12 is a safe supplementary drug to decrease pain. Additionally, cytokines participate in the pathogenesis of immune-related diseases such as AD. Thus, the main aim of this clinical trial study was to determine the effects of treatment with risperidone and quetiapine, as antipsychotic drugs, with and without vitamin B12 on the psychotic symptoms of AD patients and the expression of IL-6, IL-8, tumor growth factor (TGF)-β, tumor necrosis factor (TNF)-α, and endothelin (ET)-1). Material and Methods: Serum levels of IL-6, IL-8, TGF-β, TNF-α, and ET-1 were evaluated in the following groups: healthy controls, nonpsychotic AD patients, psychotic AD patients, psychotic AD patients under treatment with risperidone, psychotic AD patients under treatment with risperidone plus vitamin B12, psychotic AD patients under treatment with quetiapine, and psychotic AD patients under treatment with quetiapine plus vitamin B12. Results: Treatment with antipsychotic drugs plus vitamin B12 led to a decreased expression of IL-8 and TNF-α and an increased expression of TGF-β. Vitamin B12 in association with quetiapine reduced the pain in psychotic AD patients. Discussion: Proinflammatory cytokines play important roles in the pathogenesis of psychosis in AD patients. Antipsychotic drugs plus vitamin B12 can reduce and induce the expression of proinflammatory and anti-inflammatory cytokines to improve psychotic symptoms in AD patients.

Objectives: Interferon-β 1a (IFN-β 1a) is a common strategy therapy for multiple sclerosis (MS) with unknown mechanisms. S100A12 (S100 calcium-binding protein A12) is a damage-associated molecular pattern molecule which binds to its receptor, RAGE (receptor for advanced glycation end products), and activates nuclear factor-κB (NF-κB). NF-κB is transcribed from proinflammatory molecules, which may participate in the pathogenesis of MS. Therefore, the aims of this study were to compare mRNA levels of S100A12, RAGE, and NF-κB in newly diagnosed MS patients with healthy controls and determine whether IFN-β 1a therapy affects the expression of the molecules. Methods: S100A12, RAGE, and NF-κB mRNA levels in 30 new cases of untreated MS patients and 35 healthy controls were evaluated using the real-time PCR technique. The mRNA levels were also evaluated in the MS patients after 6 months of IFN-β 1a therapy. Results: S100A12, RAGE, and NF-κB mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. IFN-β 1a therapy results in upregulation of RAGE in MS patients, but not S100A12 and NF-κB. Conclusions: It appears that S100A12 participates in the pathogenesis of MS, and it seems that IFN-β 1a modulates immune responses in an S100A12-independent manner. Based on the reported anti-inflammatory effects of RAGE, it seems that RAGE may be considered as a mechanism by IFN-β 1a to modulate immune responses. NF-κB is produced permanently in the human cells and is inactive in the cytoplasm; therefore, the effects of IFN-β 1a may be related to its functions rather than expressions.

Patients with Alzheimer disease (AD) suffer from psychotic symptoms including pain. The current antipsychotic drugs confer limited effectiveness, and hence new strategies are being designed to decrease pain in order to increase antipsychological effectiveness. Vitamin B12 is a safe supplementary drug to decrease pain. Additionally, cytokines participate in the pathogenesis of immune-related diseases such as AD. Thus, the main aim of this clinical trial study was to determine the effects of treatment with risperidone and quetiapine, as antipsychotic drugs, with and without vitamin B12 on the psychotic symptoms of AD patients and the expression of IL-6, IL-8, tumor growth factor (TGF)-β, tumor necrosis factor (TNF)-α, and endothelin (ET)-1).Serum levels of IL-6, IL-8, TGF-β, TNF-α, and ET-1 were evaluated in the following groups: healthy controls, nonpsychotic AD patients, psychotic AD patients, psychotic AD patients under treatment with risperidone, psychotic AD patients under treatment with risperidone plus vitamin B12, psychotic AD patients under treatment with quetiapine, and psychotic AD patients under treatment with quetiapine plus vitamin B12.Treatment with antipsychotic drugs plus vitamin B12 led to a decreased expression of IL-8 and TNF-α and an increased expression of TGF-β. Vitamin B12 in association with quetiapine reduced the pain in psychotic AD patients.Proinflammatory cytokines play important roles in the pathogenesis of psychosis in AD patients. Antipsychotic drugs plus vitamin B12 can reduce and induce the expression of proinflammatory and anti-inflammatory cytokines to improve psychotic symptoms in AD patients.

Interferon-β 1a (IFN-β 1a) is a common strategy therapy for multiple sclerosis (MS) with unknown mechanisms. S100A12 (S100 calcium-binding protein A12) is a damage-associated molecular pattern molecule which binds to its receptor, RAGE (receptor for advanced glycation end products), and activates nuclear factor-κB (NF-κB). NF-κB is transcribed from proinflammatory molecules, which may participate in the pathogenesis of MS. Therefore, the aims of this study were to compare mRNA levels of S100A12, RAGE, and NF-κB in newly diagnosed MS patients with healthy controls and determine whether IFN-β 1a therapy affects the expression of the molecules.S100A12, RAGE, and NF-κB mRNA levels in 30 new cases of untreated MS patients and 35 healthy controls were evaluated using the real-time PCR technique. The mRNA levels were also evaluated in the MS patients after 6 months of IFN-β 1a therapy.S100A12, RAGE, and NF-κB mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. IFN-β 1a therapy results in upregulation of RAGE in MS patients, but not S100A12 and NF-κB.It appears that S100A12 participates in the pathogenesis of MS, and it seems that IFN-β 1a modulates immune responses in an S100A12-independent manner. Based on the reported anti-inflammatory effects of RAGE, it seems that RAGE may be considered as a mechanism by IFN-β 1a to modulate immune responses. NF-κB is produced permanently in the human cells and is inactive in the cytoplasm; therefore, the effects of IFN-β 1a may be related to its functions rather than expressions.