RESUMO
Objective:To investigate the roles of S100B protein and anti-brain antibody (ABAb) in the pathophysiology of Alzheimer's disease (AD) by analyzing the changes of the serum levels of S100B and ABAb and the relationships of the measures with cognition deficits in patients with AD.Methods:In this study,32 patients with AD(AD group) and 40 age-matched volunteers without cognitive impairment(control group) were enrolled.The diagnosis was made according to the Diagnostic and Statistical Manual of Mental Disorders,Fourth Edition (DSM-Ⅳ).The mental and social functional conditions were assessed with the Mini-Mental State Examination (MMSE) and Activity of Daily Living Scale(ADL),the cognitive function of patients was evaluated with the Alzheimer's Disease Assessment Scale-cognitive subscale(ADAS-Cog).The serum S100B proteinand ABAb levels were examined by enzyme-linked immuno sorbent assay(ELISA).Results:The serum S100B protein[(0.66 ± 0.17) μg/L vs.(0.30 ± 0.04)μg/L] and ABAb [(1.93 ± 0.95) U/L vs.(1.31 ± 0.25) U/L] levels were higher in AD patients than in the controls (Ps ＜ 0.01).In AD patients,the serum S 100B protein markedly negatively correlated with the scores of the MMSE(r =-0.66),while positively correlated with ADL and ADAS-Cog(r =0.57,r =0.53)(Ps ＜ 0.005).ABAb levels negatively correlated with the scores of the MMSE(r =-0.57),while positively correlated with ADL and ADAS-Cog(r =0.52,r =0.34)(Ps ＜0.05).The serum S100B protein levels were positively related to ABAb levels in AD group(r =0.51.P ＜0.005),but not in control group(r =0.076,P =0.654).Conclusions:It suggests that the serum levels of S100B protein and ABAb are related with cognitive function in patients with Alzheimer's disease,and S100B protein and ABAb might play key roles in mechanism of Alzheimer's disease.
RESUMO
Objective To investigate the efficacy of treatment and prevention of VitE on vacuous chewing move-ments (VCMs) of haloperidol-induced tardive dyskinesia (TD) rats and serum levels of brain-derived neurotrophic fac-tor ( BDNF) and total antioxidant capacity ( TAC) , and to explore the possible mechanisms.Methods Thirty-two male Sprague-Dawley (SD) rats were randomly divided into TD, P-Vit E, T-Vit E and control group (n=8), receiving to-week treatment with Haloperidol (Hal)+NS, Hal+Vit E (medicated at the baseline), Hal+VitE (medicated at the fifth week) or normal saline (NS), respectively.VCM was evaluated at each week.ELISA and spectrophotometer were used to detect the serum levels of BDNF and TAC, respectively.Results The VCM score of both TD group and T-Vit E group increased at the 2nd weekend, reached the peak at the 5th weekend.VCM score of T-Vit E group declined gradually at the 6th weekend and was significantly lower than that in the TD group [(6.5 ±3.3) vs.(27.9 ±5.8), P0.05) at the 10th weekend.There was no significant difference in VCM score between P-Vit E group and control group for ten weeks(P>0.05).At the 10th weekend, serum BDNF [(6.9 ±1.0) pg/mL] and TAC [(11.9 ±3.2) U/mL] levels of TD group were significantly lower than those of the controls [BDNF (8.6 ±2.5) pg/mL, TAC (18.2 ±5.5) U/mL] and T-Vit E group [BDNF (8.7 ±2.0) pg/mL, (18.6 ±5.9) U/mL] (P0.05).Conclusions Vit E may relieve and prevent VCM in TD model rats though alleviation of free radical damage.