Correlation between Non-HDL-C/HDL-C and Aβ1-42 levels in cerebral infarction-related cognitive dysfunction.

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.