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Serum Leptin is not Altered nor Related to Cognitive Decline in Alzheimer's Disease

Article type: Research Article

Authors: Teunissen, Charlotte E.a; * | van der Flier, Wiesje M.b; c | Scheltens, Philipb | Duits, Annelia | Wijnstok, Nienked; e | Nijpels, Giele; f | Dekker, Jacqueline M.c; e | Blankenstein, M.A.a | Heijboer, Annemieke C.a

Affiliations: [a] Department of Clinical Chemistry, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, the Netherlands | [b] Alzheimer center & Department of Neurology, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, the Netherlands | [c] Department of Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, the Netherlands | [d] Department of Health Sciences, Faculty of Earth and Life Sciences, VU University, Amsterdam, the Netherlands | [e] EMGO + Institute for Health and Care Research, VU University Medical Center, Amsterdam, the Netherlands | [f] Department of General Practice, VU University Medical Center, Amsterdam, the Netherlands

Correspondence: [*] Correspondence to: Charlotte Teunissen, Neurochemistry Laboratory and Biobank, Department of Clinical Chemistry, VU University Medical Center, Amsterdam, PO Box 7057, 1007 MB Amsterdam, the Netherlands. Tel.: +31 20 4443680; Fax: +31 20 4443895; E-mail: c.teunissen@vumc.nl.

Keywords: Alzheimer's disease, atrophy, blood-based biomarker, cognition, leptin, vascular dementia

DOI: 10.3233/JAD-141503

Journal: Journal of Alzheimer's Disease, vol. 44, no. 3, pp. 809-813, 2015

Accepted 23 September 2014
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Published: 6 February 2015
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Abstract

Background:

Low plasma leptin levels can be a risk factor for Alzheimer's disease (AD) but the relation of leptin with disease progression in clinical AD is unknown.

Objective:

The aim of this study was to investigate the relation between serum leptin concentrations and cognitive decline in clinical AD.

Methods:

Serum leptin levels were analyzed in 295 non-obese subjects including healthy controls (n = 65), patients with subjective memory complaints (n = 99), patients with AD (n = 100), and patients with vascular dementia (n = 31). Leptin levels were related to hippocampal atrophy, baseline Mini-Mental State Examination (MMSE) scores and annual decline in MMSE measured over 2 years (range 0.4–4.5 years).

Results:

Serum leptin levels were similar in AD patients compared to healthy controls and patients with subjective memory complaints. No correlation was observed between leptin concentrations and MMSE, annual change in MMSE during follow-up or atrophy.

Conclusion:

Serum leptin levels are not altered in this population of relatively young AD or vascular dementia patients (mean 60) compared to healthy and clinical control groups and were not related to cognitive decline. These results suggest that peripheral leptin levels do not play a role in evolution of AD pathology.

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