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Title: Increased expression of pathological markers in Parkinson's disease dementia post-mortem brains compared to dementia with Lewy bodies
Authors: Tu, Haitao
Zhang, Zhi Wei
Qiu, Lifeng
Lin, Yuning
Jiang, Mei
Chia, Sook-Yoong
Wei, Yanfei
Ng, Adeline S. L.
Reynolds, Richard
Tan, Eng-King
Zeng, Li
Keywords: Science::Medicine
Issue Date: 2022
Source: Tu, H., Zhang, Z. W., Qiu, L., Lin, Y., Jiang, M., Chia, S., Wei, Y., Ng, A. S. L., Reynolds, R., Tan, E. & Zeng, L. (2022). Increased expression of pathological markers in Parkinson's disease dementia post-mortem brains compared to dementia with Lewy bodies. BMC Neuroscience, 23(1), 3-.
Project: LCG002–SPARK II 
NMRC/ OFIRG/0074/2018 
Journal: BMC Neuroscience 
Abstract: Background: Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) are common age-related neurodegenerative diseases comprising Lewy body spectrum disorders associated with cortical and subcortical Lewy body pathology. Over 30% of PD patients develop PD dementia (PDD), which describes dementia arising in the context of established idiopathic PD. Furthermore, Lewy bodies frequently accompany the amyloid plaque and neurofibrillary tangle pathology of Alzheimer’s disease (AD), where they are observed in the amygdala of approximately 60% of sporadic and familial AD. While PDD and DLB share similar pathological substrates, they differ in the temporal onset of motor and cognitive symptoms; however, protein markers to distinguish them are still lacking. Methods: Here, we systematically studied a series of AD and PD pathogenesis markers, as well as mitochondria, mitophagy, and neuroinflammation-related indicators, in the substantia nigra (SN), temporal cortex (TC), and caudate and putamen (CP) regions of human post-mortem brain samples from individuals with PDD and DLB and condition-matched controls. Results: We found that p-APPT668 (TC), α-synuclein (CP), and LC3II (CP) are all increased while the tyrosine hydroxy lase (TH) (CP) is decreased in both PDD and DLB compared to control. Also, the levels of Aβ42 and DD2R, IBA1, and p-LRRK2S935 are all elevated in PDD compared to control. Interestingly, protein levels of p-TauS199/202 in CP and DD2R, DRP1, and VPS35 in TC are all increased in PDD compared to DLB. Conclusions: Together, our comprehensive and systematic study identified a set of signature proteins that will help to understand the pathology and etiology of PDD and DLB at the molecular level.
ISSN: 1471-2202
DOI: 10.1186/s12868-021-00687-4
Schools: Lee Kong Chian School of Medicine (LKCMedicine) 
Organisations: National Neuroscience Institute, Singapore
DUKE‑NUS Graduate Medical School
Research Centres: Centre for Molecular Neuropathology
Rights: © The Author(s) 2021. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver (http://creativeco applies to the data made available in this article, unless otherwise stated in a credit line to the data.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:LKCMedicine Journal Articles

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