%0 Journal Article
%T Immunolocalization of Kisspeptin Associated with Amyloid-¦Â Deposits in the Pons of an Alzheimer¡¯s Disease Patient
%A Amrutha Chilumuri
%A Maria Ashioti
%A Amanda N. Nercessian
%A Nathaniel G. N. Milton
%J Journal of Neurodegenerative Diseases
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/879710
%X The pons region of the Alzheimer¡¯s disease (AD) brain is one of the last to show amyloid-¦Â (A¦Â) deposits and has been suggested to contain neuroprotective compounds. Kisspeptin (KP) is a hormone that activates the hypothalamic-pituitary-gonadal axis and has been suggested to be neuroprotective against A¦Â toxicity. The localization of KP, plus the established endogenous neuroprotective compounds corticotropin releasing hormone (CRH) and catalase, in tissue sections from the pons region of a male AD subject has been determined in relation to A¦Â deposits. Results showed A¦Â deposits also stained with KP, CRH, and catalase antibodies. At high magnification the staining of deposits was either KP or catalase positive, and there was only a limited area of the deposits with KP-catalase colocalization. The CRH does not bind A¦Â, whilst both KP and catalase can bind A¦Â, suggesting that colocalization in A¦Â deposits is not restricted to compounds that directly bind A¦Â. The neuroprotective actions of KP, CRH, and catalase were confirmed in vitro, and fibrillar A¦Â preparations were shown to stimulate the release of KP in vitro. In conclusion, neuroprotective KP, CRH, and catalase all colocalize with A¦Â plaque-like deposits in the pons region from a male AD subject. 1. Introduction The deposition of the amyloid-¦Â (A¦Â) peptide within plaques in the Alzheimer¡¯s disease (AD) brain is a central feature of the disease pathology [1, 2]. A sequential pattern of A¦Â deposition within different regions of the brain has been suggested as AD progresses [3¨C6]. The staging of A¦Â deposition by Thal et al. (2002) [3] identified the cerebellum plus brainstem nuclei including the pons as the last to show A¦Â deposits. In transgenic mice overexpressing the human amyloid precursor protein (APP) the A¦Â deposition showed a similar sequential pattern, with the cerebellum and pons again the last to show A¦Â deposits [7]. The apparent resistance of the cerebellum and pons to neurodegenerative changes suggests that endogenous neuroprotective processes may play a role in these tissues. A range of endogenous compounds have been suggested to have neuroprotective properties against A¦Â in AD models [8¨C16]. In a recent study kisspeptin (KP) peptides were suggested to have neuroprotective properties against A¦Â plus related amyloid proteins [17]. The KP peptide is a reproductive hormone [18], and the female hypothalamic levels of KP show elevations after menopause that are not seen in males [19]. Female AD onset is typically postmenopausal, and there is significantly less neurodegeneration in the
%U http://www.hindawi.com/journals/jnd/2013/879710/