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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-49561

Brunner, P; Sözer-Topcular, N; Jockers, R; Ravid, R; Angeloni, D; Fraschini, F; Eckert, A; Müller-Spahn, F; Savaskan, E (2006). Pineal and cortical melatonin receptors MT1 and MT2 are decreased in Alzheimer's disease. European Journal of Histochemistry, 50(4):311-316.

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Abstract

The pineal hormone melatonin is involved in physiological transduction of temporal information from the light dark cycle to circadian and seasonal behavioural rhythms, as well as possessing neuroprotective properties. Melatonin and its receptors MT1 and MT2, which belong to the family of G protein-coupled receptors, are impaired in Alzheimer's disease (AD) with severe consequences to neuropathology and clinical symptoms. The present data provides the first immunohistochemical evidence for the cellular localization of the both melatonin receptors in the human pineal gland and occipital cortex, and demonstrates their alterations in AD. We localized MT1 and MT2 in the pineal gland and occipital cortex of 7 elderly controls and 11 AD patients using immunohistochemistry with peroxidase-staining. In the pineal gland both MT1 and MT2 were localized to pinealocytes, whereas in the cortex both receptors were expressed in some pyramidal and non-pyramidal cells. In patients with AD, parallel to degenerative tissue changes, there was an overall decrease in the intensity of receptors in both brain regions. In line with our previous findings, melatonin receptor expression in AD is impaired in two additional brain areas, and may contribute to disease pathology.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Psychiatric University Hospital Zurich > Division of Psychiatric Research and Clinic for Psychogeriatric Medicine
DDC:610 Medicine & health
Language:English
Date:2006
Deposited On:13 Sep 2011 07:35
Last Modified:23 Nov 2012 12:41
Publisher:Pagepress
ISSN:1121-760X
Publisher DOI:10.4081/1002
PubMed ID:17213040

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