The Down Syndrome-Associated Protein, Regulator of Calcineurin-1, is Altered in Alzheimer’s Disease and Dementia with Lewy Bodies
Received Date: Jan 21, 2019 / Accepted Date: Feb 27, 2019 / Published Date: Mar 06, 2019
Abstract
There is a known relationship between Alzheimer’s disease (AD) and Down syndrome (DS), with the latter typically developing AD-like neuropathology in mid-life. In order to further understand this relationship we examined intersectin-1 (ITSN1) and the regulator of calcineurin-1 (RCAN1), proteins involved in endosomal and lysosomal trafficking that are over-expressed in DS. We examined RCAN1 and ITSN1 levels (both long (-L) and short (-S) isoforms) and the level of endogenous metals in White Blood Cells (WBCs) collected from AD patients who were enrolled in the Australian Imaging, Biomarker and Lifestyle Study on Ageing (AIBL). We also examined RCAN1 and ITSN1-S and -L in post-mortem brain tissue in a separate cohort of patients with AD or other types of dementia including Dementia with Lewy Bodies (DLB) and non-Alzheimer’s disease dementia. We found that RCAN1 was significantly elevated in AD and DLB brain compared with controls, but there was no difference in the level of RCAN1 in WBCs of AD patients. There were no differences in the levels of ITSN1-L and –S between AD and the control, nor between other types of dementia and the control. We found that there were no differences in the levels of metals between AD and the control WBCs. In conclusion, our data demonstrate that RCAN1 is differentially regulated between the peripheral and central compartments in AD and should be further investigated to understand its potential role in dementia of AD and DLB.
Keywords: Alzheimer’s disease; Down syndrome; Dementia
Citation: Malakooti N, AIBL Research Group, Fowler C, Volitakis I, McLean CA, et al. (2019) The Down Syndrome-Associated Protein, Regulator of Calcineurin-1, is Altered in Alzheimer’s Disease and Dementia with Lewy Bodies. J Alzheimers Dis Parkinsonism 9: 462. Doi: 10.4172/2161-0460.1000462
Copyright: © 2019 Malakooti N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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