Correlation between serum S100β protein levels and cognitive dysfunction in patients with cerebral small vessel disease: a case-control study.

The present study was designed to explore the correlation between serum S100β levels and cognitive dysfunction in patients with cerebral small vessel disease (SVD). A total of 172 SVD patients participated in the study, and they were assigned to patients with no cognitive impairment (NCI group) and those with vascular cognitive impairment no dementia (VCIND group). In total, 105 people were recruited into the normal control group. Serum S100β protein level was detected by ELISA. A receiver operating characteristic (ROC) curve was employed for the predictive value of serum S100β in diagnosing SVD with cognitive dysfunction. Pearson correlation analysis was used to examine the association of S100β level with mini-mental state examination (MMSE) and Montreal cognitive assessment (MoCA) and the association of S100β levels with hypertension. Logistic regression analysis was used to analyze risk factors of SVD. The serum S100β levels in the VCIND group were higher than those in the NCI and normal control groups. Logistic regression analysis revealed that a high serum S100β protein level, hypertension, and high low density lipoprotein-cholesterol (LDL-C) level were the independent risk factors for SVD. In addition, hypertension patients showed higher S100β levels than those with normal blood pressure and the normal control group, and there was a positive correlation between S100β level and blood pressure. The concentration of serum S100β level was related to impairment of cognition function of VCIND patients, therefore, early detection of serum S100β was of great value for diagnosis of SVD.

Wang F ，Zou ZR ，Yuan D ，Gong Y ，Zhang L ，Chen X ，Sun T ，Yu HL ... -  《-》

Plasma S100β is a predictor for pathology and cognitive decline in Alzheimer's disease.

Blood-brain barrier dysfunction is one characteristic of Alzheimer's disease (AD) and is recognized as both a cause and consequence of the pathological cascade leading to cognitive decline. The goal of this study was to assess markers for barrier dysfunction in postmortem tissue samples from research participants who were either cognitively normal individuals (CNI) or diagnosed with AD at the time of autopsy and determine to what extent these markers are associated with AD neuropathologic changes (ADNC) and cognitive impairment. We used postmortem brain tissue and plasma samples from 19 participants: 9 CNI and 10 AD dementia patients who had come to autopsy from the University of Kentucky AD Research Center (UK-ADRC) community-based cohort; all cases with dementia had confirmed severe ADNC. Plasma samples were obtained within 2 years of autopsy. Aβ40, Aβ42, and tau levels in brain tissue samples were quantified by ELISA. Cortical brain sections were cleared using the X-CLARITY™ system and immunostained for neurovascular unit-related proteins. Brain slices were then imaged using confocal microscopy and analyzed for microvascular diameters and immunoreactivity coverage using Fiji/ImageJ. Isolated human brain microvessels were assayed for tight-junction protein expression using the JESS™ automated Western blot system. S100 calcium-binding protein B (S100β), matrix metalloproteinase (MMP)-2, MMP-9, and neuron-specific enolase (NSE) levels in plasma were quantified by ELISA. All outcomes were assessed for linear associations with global cognitive function (MMSE, CDR) and cerebral atrophy scores by Pearson, polyserial, or polychoric correlation, as appropriate, along with generalized linear modeling or generalized linear mixed-level modeling. As expected, we detected elevated Aβ and tau pathology in brain tissue sections from AD patients compared to CNI. However, we found no differences in microvascular diameters in cleared AD and CNI brain tissue sections. We also observed no differences in claudin-5 protein levels in capillaries isolated from AD and CNI tissue samples. Plasma biomarker analysis showed that AD patients had 12.4-fold higher S100β plasma levels, twofold lower NSE plasma levels, 2.4-fold higher MMP-9 plasma levels, and 1.2-fold lower MMP-2 plasma levels than CNI. Data analysis revealed that elevated S100β plasma levels were predictive of AD pathology and cognitive impairment. Our data suggest that among different markers relevant to barrier dysfunction, plasma S100β is the most promising diagnostic biomarker for ADNC. Further investigation is necessary to assess how plasma S100β levels relate to these changes and whether they may predict clinical outcomes, particularly in the prodromal and early stages of AD.

Nehra G ，Maloney BJ ，Smith RR ，Chumboatong W ，Abner EL ，Nelson PT ，Bauer B ，Hartz AMS ... -  《Fluids and Barriers of the CNS》

Brachial-Ankle Pulse Wave Velocity is Associated with Incident Dementia in Patients with Cerebral Small-Vessel Disease.

Yamagishi S ，Yoshizawa H ，Hosoya M ，Seki M ，Toi S ，Kitagawa K ... -  《-》

[Cognitive function status and its correlation with blood pressure control in patients with hypertension in China].

Li Y ，Su XM ，Ge JZ ，Li ST ，Li J ... -  《-》

[Changes and correlation between serum β-amyloid 1-42 and total bilirubin in patients with Alzheimer's disease].

Wang XY ，Deng H ，Li W ，Zhou YF ，Pan SJ ... -  《-》