Abstract

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. Serum levels of Aβ40, Aβ42 and Aβ oligomers were evaluated in 104 inpatients with major depressive disorder (MDD) and 132 healthy control individuals. 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. 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.

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