ArticleMolecular brain2017
An iTRAQ-based proteomic analysis reveals dysregulation of neocortical synaptopodin in Lewy body dementias.
Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- VGF Peptides in Cerebrospinal Fluid of Patients with Dementia with Lewy Bodies.International journal of molecular sciences · 2019Trial
- Phosphoproteomic profiling reveals post-translational dysregulation in Huntington's disease patient-derived neurons.Cellular & molecular biology letters · 2026Article
- Neuronal Calcium Signaling and Cytoskeletal Dynamics in Neurodegeneration.International journal of molecular sciences · 2026Review
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- Genome-wide association neural networks identify genes linked to family history of Alzheimer's disease.Briefings in bioinformatics · 2024Article
- Article
- A NAC domain mutation (E83Q) unlocks the pathogenicity of human alpha-synuclein and recapitulates its pathological diversity.Science advances · 2022Article
- Piperine promotes autophagy flux by P2RX4 activation inAutophagy · 2022Article
- Proteomic Characterization of the Olfactory Molecular Imbalance in Dementia with Lewy Bodies.International journal of molecular sciences · 2020Article
- Comparative proteomics combined with analyses of transgenic plants reveal ZmREM1.3 mediates maize resistance to southern corn rust.Plant biotechnology journal · 2019Article
- Proteomics of neurodegenerative diseases: analysis of human post-mortem brain.Journal of neurochemistry · 2019Review
- Quantitative iTRAQ-based proteomic analysis of differentially expressed proteins in aging in human and monkey.BMC genomics · 2019Article
- The Effects of Maternal Obesity on Porcine Placental Efficiency and Proteome.Animals : an open access journal from MDPI · 2019Article
- BAG3 and SYNPO (synaptopodin) facilitate phospho-MAPT/Tau degradation via autophagy in neuronal processes.Autophagy · 2019Article
- Synaptopodin Deficiency Ameliorates Symptoms in the 3xTg Mouse Model of Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Brains for Dementia Research: The Importance of Cohorts in Brain Banking.Neuroscience bulletin · 2019Article
- Gut Mucosal Proteins and Bacteriome Are Shaped by the Saturation Index of Dietary Lipids.Nutrients · 2019Article
- Mass synaptometry: High-dimensional multi parametric assay for single synapses.Journal of neuroscience methods · 2019Article
- Dementia with Lewy bodies and Parkinson's disease-dementia: current concepts and controversies.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Kinome and phosphoproteome of high-grade meningiomas reveal AKAP12 as a central regulator of aggressiveness and its possible role in progression.Scientific reports · 2018Article
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8 authors at 3 institutions in 3 countries.
Funding
Abstract
Lewy body dementias are the second most common cause of neurodegenerative dementia in the elderly after Alzheimer's disease (AD). The two clinical subgroups of Lewy body dementias, namely, dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), are differentiated by the chronology of cognitive symptoms relative to parkinsonism. At present, there remains a debate on whether DLB and PDD are separate disease entities, or fall within the same spectrum of Lewy body dementias. In this study, we compared the detergent-soluble proteome via an 8-plex isobaric tag for relative and absolute quantitation (iTRAQ) analysis of pooled lysates from the prefrontal cortex (BA9) of DLB (n = 19) and PDD (n = 21) patients matched a priori for amyloid (total Aβ42) burden, semi-quantitative scores for Lewy bodies and neurofibrillary tangles together with age-matched control (n = 21) subjects. A total of 1914 proteins were confidently identified by iTRAQ (false discovery rate = 0%). None of the proteins showed a significant yet opposite regulation in between DLB and PDD when compared to aged controls in the proteomic data set as well as following immunoblot analysis of the pooled and individual lysates involving all 61 subjects. The postsynaptic protein, synaptopodin (SYNPO) was significantly down-regulated in both DLB and PDD subgroups, suggesting a defective synaptic transmission in the demented patients. In conclusion, the largely similar proteome of DLB and PDD matched for amyloid burden suggests that variations in concomitant AD-related pathology, abnormal post-translational modifications or protein-protein interactions, defective intracellular trafficking or misfolding of proteins could play a part in driving the clinically observed differences between these two subgroups of Lewy body dementias. This further indicates that amyloid-targeting therapeutic strategies may show different efficacies in DLB versus PDD.
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