Min Xu1, Xiao-Ying He2, Pan Huang3. 1. Department of Neurology, The Second People's Hospital of Deyang City, No. 340 Minjiang West Road, Deyang, Sichuan 618000, China. 2. Department of Neurology, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Street, Luzhou, Sichuan 646000, China. 3. Department of Neurology, People's Hospital of Deyang City, No. 173 TaiShan North Road, Deyang, Sichuan 618000, China.
Abstract
OBJECTIVE: This study was aimed at investigating the relationship between serum amyloid A (SAA) levels and cognitive dysfunction in patients with vascular dementia (VAD). METHODS: Using cross-sectional research methods, 146 patients with VAD were selected as the VAD group and 70 normal people were selected as the NC group. Upon admission, the clinical and biochemical characteristics of the two groups of study subjects were collected, and the MMSE scale was used to assess cognitive function. A sandwich enzyme-linked immunosorbent assay was used to detect SAA levels. RESULTS: There was no significant difference in clinical data and biochemical characteristics in the VAD group (p > 0.05). Compared with the VAD group, the NC group has a higher level of education (p < 0.05). The SAA level of the VAD group was higher than that of the NC group, and there was a significant difference (p < 0.05). Spearman correlation analysis showed that SAA and MMSE in the VAD group were negatively correlated. Further multiple regression analysis showed that the serum amyloid A level is an independent risk factor for cognitive dysfunction in VAD patients. CONCLUSION: The level of SAA in VAD patients is significantly increased, which can be used as a potential peripheral blood marker to predict cognitive impairment in VAD patients.
OBJECTIVE: This study was aimed at investigating the relationship between serum amyloid A (SAA) levels and cognitive dysfunction in patients with vascular dementia (VAD). METHODS: Using cross-sectional research methods, 146 patients with VAD were selected as the VAD group and 70 normal people were selected as the NC group. Upon admission, the clinical and biochemical characteristics of the two groups of study subjects were collected, and the MMSE scale was used to assess cognitive function. A sandwich enzyme-linked immunosorbent assay was used to detect SAA levels. RESULTS: There was no significant difference in clinical data and biochemical characteristics in the VAD group (p > 0.05). Compared with the VAD group, the NC group has a higher level of education (p < 0.05). The SAA level of the VAD group was higher than that of the NC group, and there was a significant difference (p < 0.05). Spearman correlation analysis showed that SAA and MMSE in the VAD group were negatively correlated. Further multiple regression analysis showed that the serum amyloid A level is an independent risk factor for cognitive dysfunction in VAD patients. CONCLUSION: The level of SAA in VAD patients is significantly increased, which can be used as a potential peripheral blood marker to predict cognitive impairment in VAD patients.
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