Facial reconstruction

Search LJMU Research Online

Browse Repository | Browse E-Theses

Plasma Amyloid-β Dynamics in late-life major depression: A longitudinal study

Pomara, N, Bruno, D, Reichert Plaska, C, Ramos Cejudo, J, Osorio, R, Pillai, A, Imbimbo, B, Zetterberg, H and Blennow, K (2022) Plasma Amyloid-β Dynamics in late-life major depression: A longitudinal study. Translational Psychiatry, 12 (301).

Plasma Amyloid dynamics in latelife major depression a longitudinal study.pdf - Published Version
Available under License Creative Commons Attribution.

Download (978kB) | Preview


Depressed individuals are twice as likely to develop Alzheimer’s disease (AD) as compared to controls. Brain amyloid-β (Aβ) deposition is believed to have a major role in AD pathogenesis but studies also suggest associations of Aβ dynamics and depression. The aim of this study was to test if plasma Aβ levels are longitudinally associated to late-life depression. We measured plasma levels of amyloid-β1-40 (Aβ40) and amyloid-β1-42 (Aβ42) peptides longitudinally for three consecutive years in 48 cognitively intact elderly subjects with late-life major depressive disorder (LLMD) and 45 age-matched cognitively healthy controls. We found that the Aβ42/Aβ40 plasma ratio was significantly and steadily lower in depressed subjects compared to controls (p < 0.001). At screening, Aβ42/Aβ40 plasma did not correlate with depression severity (as measured with Hamilton Depression Scale) or cognitive performance (as measured with Mini-Mental State Examination) but was associated to depression severity at 3 years after adjustment for age, education, cognitive performance, and antidepressants use. This study showed that reduced plasma Aβ42/ Aβ40 ratio is consistently associated with LLMD diagnosis and that increased severity of depression at baseline predicted low Aβ42/Aβ40 ratio at 3 years. Future studies are needed to confirm these findings and examine if the consistently lower plasma Aβ42/Aβ40 ratio in LLMD reflects increased brain amyloid deposition, as observed in AD subjects, and an increased risk for progressive cognitive decline and AD.

Item Type: Article
Uncontrolled Keywords: 1103 Clinical Sciences; 1117 Public Health and Health Services; 1701 Psychology
Subjects: B Philosophy. Psychology. Religion > BF Psychology
R Medicine > RA Public aspects of medicine > RA0421 Public health. Hygiene. Preventive Medicine
R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Divisions: Psychology (from Sep 2019)
Publisher: Nature Publishing Group
SWORD Depositor: A Symplectic
Date Deposited: 02 Aug 2022 09:19
Last Modified: 02 Aug 2022 09:30
DOI or ID number: 10.1038/s41398-022-02077-8
URI: https://researchonline.ljmu.ac.uk/id/eprint/17254
View Item View Item