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Updated: Jun 15, 2025
Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
Published on: April 23, 2021
Correlation between Non-HDL-C/HDL-C and Aβ1-42 levels in cerebral infarction-related cognitive dysfunction
Xiufang Shi1, Xiaoqing Zhang1, Jia-Fu Ao1
1The Clinical Laboratory of Bozhou People's Hospital, BoZhou 236800, China.
Insights
Elevated non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (Non-HDL-C/HDL-C) and beta-amyloid 1-42 (Aβ-1-42) levels in peripheral blood are risk factors for cognitive dysfunction after cerebral infarction. Early detection of these markers may aid in managing cognitive impairment.
Area of Science:
- Neuroscience
- Cardiovascular Medicine
- Biochemistry
Background:
- Early detection of cognitive impairment post-cerebral infarction is crucial for effective treatment and delaying cognitive decline.
- Non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (Non-HDL-C/HDL-C) reflects the burden of atherogenic lipoproteins.
- Beta-amyloid 1-42 (Aβ-1-42) is a key component of cerebrovascular amyloid deposits.
Purpose of the Study:
- To investigate the association between Non-HDL-C/HDL-C ratio and Aβ-1-42 levels in peripheral blood.
- To determine the relationship between these biomarkers and cognitive dysfunction secondary to cerebral infarction.
Main Methods:
- 83 cerebral infarction patients were assessed and divided into cognitive dysfunction (n=30) and non-cognitive dysfunction (n=53) groups based on MMSE scores.
- A control group (n=34) with transient cerebral insufficiency or stenosis was included.
- Logistic regression analysis identified risk factors for cognitive dysfunction, including lipid indexes, Non-HDL-C/HDL-C, and Aβ1-42 levels.
Main Results:
- Hypertensive patients with cognitive dysfunction showed greater brain region involvement and lower MMSE scores.
- Significantly higher levels of homocysteine (HCY), Non-HDL-C/HDL-C, and Aβ1-42 were found in the cognitive dysfunction group.
- Peripheral blood Non-HDL-C/HDL-C and Aβ1-42 levels were identified as significant risk factors for secondary cognitive dysfunction.
Conclusions:
- Peripheral blood Non-HDL-C/HDL-C and Aβ1-42 levels are risk factors for cognitive dysfunction following cerebral infarction.
- These findings offer insights into the mechanisms of cognitive dysfunction in cerebrovascular disorders.
- Potential for developing novel early interventions for preventing or treating cognitive impairment in these patients.
Objective:
Cerebral infarction treatments are most effective if used early after stroke symptoms occur. Also, early detection is crucial for delaying and improving cognitive impairment. This study investigated the relationship between the ratio of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol (Non-HDL-C/HDL-C), which reflects the entire burden of the cholesterol transported in atherogenic lipoproteins, and the level of β-amyloid 1-42 (Aβ-1-42), a major component of cerebrovascular amyloid deposits, in peripheral blood and cognitive dysfunction secondary to cerebral infarction.
Methods:
A total of 83 patients with cerebral infarction admitted to Bozhou People's Hospital between June 2019 and June 2022 were assessed. The patients were divided into two groups based on their Mini-Mental State Scale (MMSE) scores: cognitive dysfunction group (n = 30) and non-cognitive dysfunction group (n = 53). In addition, a control group comprising 34 patients with transient cerebral insufficiency or cerebrovascular stenosis was selected. The groups were compared in terms of various clinical factors, including gender, age, hypertension, hyperlipidemia, lipid indexes, Non-HDL-C/HDL-C, and Aβ1-42 levels. Logistic regression analysis was used to identify the risk factors associated with cognitive dysfunction.
Results:
The results showed that hypertensive patients with cognitive dysfunction secondary to cerebral infarction had a higher proportion of frontal lobe, temporal lobe, and thalamus involvement and lower scores on the MMSE compared to the non-cognitive impairment group and control group (p < 0.05). Additionally, the levels of homocysteine (HCY), Non-HDL-C/HDL-C, and Aβ1-42 in peripheral blood were significantly higher in hypertensive patients with cognitive dysfunction compared to the other two groups (all p < 0.05) and were identified as risk factors for cognitive dysfunction secondary to cerebral infarction. Peripheral blood levels of Non-HDL-C/HDL-C and Aβ1-42 are risk factors for secondary cognitive dysfunction following a cerebral infarction.
Conclusion:
These data have important clinical implications for understanding the mechanisms underlying cognitive dysfunction in individuals with cerebrovascular disorders, potentially leading to new early interventions for preventing or treating such diseases.
