Inherited Indicators: Plasma Biomarkers in Adult Children of Parents with Alzheimer’s

Published on August 30, 2022

Think of it like inheriting your parents’ eye color or musical talent. Just as genetics can shape physical characteristics, they may also influence our health. In the case of late-onset Alzheimer’s disease (AD), a family history (FH) can play a role in certain changes found in the cerebrospinal fluid (CSF) biomarkers of cognitively normal individuals. But what about plasma biomarkers? This study sheds light on this lesser-known area by investigating potential plasma biomarkers and their correlation in cognitively normal adult children (AC) whose parents have AD. The researchers compared the plasma samples of AC to those of their AD parents and unrelated non-demented controls (NC). The results revealed that the AC group showed some significant similarities to their AD parents in terms of elevated levels of Aβ1–40, phosphorylated tau (P-tau), and P-tau/T-tau ratio, along with reduced levels of Aβ1–42 and Aβ1–42/Aβ1–40 ratio. Importantly, a correlation between Aβ1–42 and Aβ1–40, as well as T-tau and P-tau, was observed only in the AC group. This suggests that disrupted correlation patterns between Aβ and tau could potentially serve as a biomarker for the development of AD in AC. The findings underscore the complex interplay between genetic factors and disease outcomes, emphasizing the need for further longitudinal studies to deepen our understanding of this inherited link to AD.

Family history (FH) of late-onset Alzheimer’s disease (AD) is associated with changes in several cerebrospinal fluid (CSF) biomarkers in cognitively normal individuals. However, potential changes in plasma biomarkers remain unknown. This study aimed to evaluate potential plasma biomarkers and their correlation in cognitively normal adult children (AC) and to compare this data with their AD parents and unrelated non-demented controls (NC). Participants with dementia due to AD, their AC and NC were recruited. Plasma samples were assessed for amyloid beta (Aβ)1–42, Aβ1–40, total tau (T-tau) and phosphorylated tau (P-tau). Kruskal–Wallis test was used for the comparison of this data between the three groups. Spearman rank correlation was used for evaluation of the correlations between Aβ1–40 and Aβ1–42, and T-tau and P-tau in the AD and AC groups. A total of 99 subjects completed the assessment (30 had AD; 38 were AC group; and 31 were NC). Compared with the NC group, there were significantly higher levels of Aβ1–40, P-tau, and P-tau/T-tau ratio, and lower levels of Aβ1–42 and Aβ1–42/Aβ1–40 ratio in the AD and AC groups. The correlation between the level of Aβ1–42 and Aβ1–40 and level of T-tau and P-tau was only observed in the AC but not in the AD group. AC of AD parents demonstrate some indicators of AD like their parents. Disruption to the correlation between Aβ and tau in AD may be a biomarker for the development of AD in AC, which should be examined in a longitudinal cohort.

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