Imperial College London
Alternate

Professor Richard Reynolds, BSc AKC PhD

Faculty of Medicine, Department of Brain Sciences

Professor of Cellular Neurobiology
 
 
 
//

Contact

 

+44 (0)20 7594 6668r.reynolds

 
 
//

Location

 

E414Burlington DanesHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Tu:2022:10.1186/s12868-021-00687-4,
author = {Tu, H and Zhang, ZW and Qiu, L and Lin, Y and Jiang, M and Chia, S-Y and Wei, Y and Ng, ASL and Reynolds, R and Tan, E-K and Zeng, L},
doi = {10.1186/s12868-021-00687-4},
journal = {BMC Neurosci},
pages = {3--3},
title = {Increased expression of pathological markers in Parkinson's disease dementia post-mortem brains compared to dementia with Lewy bodies.},
url = {http://dx.doi.org/10.1186/s12868-021-00687-4},
volume = {23},
year = {2022}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 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 hydroxylase (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.
AU  - Tu,H
AU  - Zhang,ZW
AU  - Qiu,L
AU  - Lin,Y
AU  - Jiang,M
AU  - Chia,S-Y
AU  - Wei,Y
AU  - Ng,ASL
AU  - Reynolds,R
AU  - Tan,E-K
AU  - Zeng,L
DO  - 10.1186/s12868-021-00687-4
EP  - 3
PY  - 2022///
SP  - 3
TI  - Increased expression of pathological markers in Parkinson's disease dementia post-mortem brains compared to dementia with Lewy bodies.
T2  - BMC Neurosci
UR  - http://dx.doi.org/10.1186/s12868-021-00687-4
UR  - https://www.ncbi.nlm.nih.gov/pubmed/34983390
UR  - https://bmcneurosci.biomedcentral.com/articles/10.1186/s12868-021-00687-4
UR  - http://hdl.handle.net/10044/1/93740
VL  - 23
ER  -
Download