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Article type: Short Communication
Authors: Yamazaki, Chiemi | Tamaoki, Toshio | Nunomura, Akihiko* | Tamai, Kenichi | Yasuda, Kazuyuki | Motohashi, Nobutaka
Affiliations: Department of Neuropsychiatry, Graduate School of Medical Science, University of Yamanashi, Chuo, Yamanashi, Japan
Correspondence: [*] Correspondence to: Akihiko Nunomura, MD, PhD, Department of Neuropsychiatry, Graduate School of Medical Science, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi 409-3898, Japan. Tel.: +81 55 273 9847; Fax: +81 55 273 6765; E-mail: [email protected].
Abstract: To elucidate an involvement of amyloid dysmetabolism in the pathophysiology of depression, we investigated associations of plasma amyloid-β (Aβ) levels with Alzheimer’s disease-related changes in neuroimaging and cognitive dysfunction in patients with late-life depression. Higher plasma Aβ40, but not Aβ42 nor Aβ40/Aβ42 ratio, was associated with higher degree of parahippocampal atrophy and lower verbal fluency performance. Indeed, high plasma Aβ40 predicted poor cognitive prognosis of depressed patients with mild cognitive impairment. As an anti-depressive treatment, electroconvulsive therapy (ECT) resulted in a marginally significant reduction of plasma Aβ40 compared to pharmacotherapy alone, suggesting protective effects of ECT against amyloid dysmetabolism.
Keywords: Alzheimer’s disease, amyloid-β, electroconvulsive therapy, late-life depression, mild cognitive impairment, neuroimaging, parahippocampal atrophy, plasma biomarker
DOI: 10.3233/JAD-170111
Journal: Journal of Alzheimer's Disease, vol. 58, no. 2, pp. 349-354, 2017
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