The association between mean arterial pressure and memory decline in preeclampsia patients: a mediation analysis of serum amyloid-β 1-42 and phosphorylated tau 181
摘要
Preeclampsia (PE) can damage the central nervous system of pregnant women, leading to a decline in cognitive function, and this effect can persist for several decades after childbirth. Amyloid-β 1-42 (Aβ1-42) had neurotoxicity and excessive deposition can damage neural synapses. Excessive production of phosphorylated tau 181 (P-tau181) can reduce the transport efficiency of axons in nerve cells, leading to degeneration of nerve cell protrusions and cell death. The aim of our study was to compare memory function status and serum Aβ1-42 and P-tau181 levels in PE patients and healthy controls to explore the related factors affecting memory function in PE patients and the possible pathogenic mechanism leading to the decline in memory function.
MethodsOne hundred and fifteen PE patients, forty-eight nonpregnant healthy controls (NPHCs) and forty-seven pregnant healthy controls (PHCs) were included. The clinical data of each participants, included blood pressure, were collected. Neurological examinations and neuropsychological tests effectively evaluate all participants’ memory status. Among these, the Auditory Verbal Learning Test–Huashan Version (AVLT-H) is particularly useful. The levels of serum Aβ1-42 and P-tau181 were detected by enzyme linked immunosorbent assay. The associations between the mean arterial pressure (MAP), total AVLT-H score and serum Aβ1-42 and P-tau181 levels were investigated by mediation analysis. The contribution ratio of each factor affecting the total AVLT-H score was obtained by principal component analysis.
ResultsThere were obvious differences in the total AVLT-H score and the levels of serum Aβ1-42 and P-tau181 among the PE patients and healthy controls (p < 0.05). Mediation analysis revealed that the MAP affected the total AVLT-H score in three ways. The principal component analysis showed that the main factors affecting memory function were the serum Aβ1-42 and P-tau181 levels and the MAP, in that order of contribution.
ConclusionsThese findings highlight that the elevated blood pressure can lead to decreased memory function in PE patients through the mediating effect of serum Aβ1-42 and P-tau181 levels. Blood pressure monitoring and early detection of memory decline should be strictly and regularly carried out in PE patients.