Serum levels and mutual correlations of amyloid β in patients with depression

Abstract

Aim: Epidemiological studies have shown that depression is a risk factor for Alzheimer's disease (AD). Although the biological mechanism underlying the link between depression and AD is unclear, altered amyloid β (Aβ) metabolism in patients with depression has been suggested as a potential mechanism. Results from previous studies of Aβ metabolism in patients with depression have been inconsistent, and Aβ polymerization, which is a crucial process in AD pathology, has not previously been assessed.Methods: Serum levels of Aβ40, Aβ42 and Aβ oligomers were evaluated in 104 inpatients with major depressive disorder (MDD) and 132 healthy control individuals.Results: Lower serum Aβ42 levels were observed in patients with MDD, but there was no difference in serum Aβ oligomer levels between the MDD group and the healthy control group, even in older adults. Interestingly, serum Aβ oligomer levels in patients with MDD were dependent on serum Aβ42 levels, regardless of age, and this relationship was not observed in the control group.Conclusions: These results suggest that Aβ42 is more prone to aggregation and polymerization in patients with depression than in healthy individuals, suggesting a possible mechanism underlying the transition from depression to AD. Geriatr Gerontol Int 2020; 20: 125-129.

Synergistic Effect of Depression and Cerebrovascular Disease in Mid- to Late-life on the Risk for Dementia: A Nationwide Population-based Cohort Study

“…Researchers suggest that chronic stress and hypercortisolemia can induce beta-amyloid accumulation, hyperphosphorylation of Tau proteins, and neurotoxicity [37]. A prior study reported that depressed patients have more beta-amyloid aggregation than healthy individuals [38]. Our ndings are also in line with an animal study, which reported chronic stress resulting in increased amyloid plaques in the hippocampus of female mice only, without changes in the cerebral cortices of both male and female mice [39].…”

Additive interaction of mid- to late-life depression and cerebrovascular disease on the risk of dementia: A nationwide population-based cohort study

“…Chronic stress and hypercortisolemia can induce beta-amyloid accumulation, hyperphosphorylation of Tau proteins, and neurotoxicity [45]. A prior study reported that depressed patients have higher beta-amyloid aggregation levels than healthy individuals [46]. The additive interaction of depression and CVD on the dementia risk in our study was more remarkable in women, who are known to be at risk of AD [1].…”

Additive interaction of mid- to late-life depression and cerebrovascular disease on the risk of dementia: A nationwide population-based cohort study

“…Chronic stress and hypercortisolemia can induce beta-amyloid accumulation, hyperphosphorylation of Tau proteins, and neurotoxicity [57]. A prior study reported that depressed patients have higher beta-amyloid aggregation levels than healthy individuals [58]. The additive interaction of depression and CVD on the dementia risk in our study was more remarkable in women, who are known to be at risk of AD [1].…”