ArticleBMC neuroscience2022
Increased expression of pathological markers in Parkinson's disease dementia post-mortem brains compared to dementia with Lewy bodies.
Article in BMC neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Systematic review of differentially abundant proteins in people with Lewy body dementia.Acta neuropsychiatrica · 2025Pooled it
- CSF1R T567M mutation induces microglial dysfunction and synaptic impairment in patient iPSC-derived cerebral organoids of CSF1R-related disorder.Cell death discovery · 2026Article
- Pharmacological inhibition of O-GlcNAcase reduces pS129-α-synuclein positive aggregates in the substantia nigra of mThy1-hSNCA mice.Journal of Parkinson's disease · 2026Article
- Early α-Synuclein Pathology Induces Neuroinflammation and Decreases Topoisomerase IIβ Expression in A53T Mice.Inflammation · 2025Article
- LRRK2 kinase-mediated accumulation of lysosome-associated phospho-Rabs in tauopathies and synucleinopathies.Acta neuropathologica · 2025Article
- Single-nucleus transcriptomics reveals a distinct microglial state and increased MSR1-mediated phagocytosis as common features across dementia subtypes.Genome medicine · 2025Article
- The Mitochondrial Foundations of Parkinson's Disease: Therapeutic Implications.Aging and disease · 2025Review
- α-synuclein and tau: interactions, cross-seeding, and the redefinition of synucleinopathies as complex proteinopathies.Frontiers in neuroscience · 2025Review
- Interplay of oxidative stress and Inflammasome activation and clinical indices in Parkinson's disease: insights from serum SIRT1, Nrf2, and NLRP3 levels and PDQ-39-a cross-sectional study.Frontiers in neuroscience · 2025Article
- NOTCH2NLC GGC intermediate repeat with serine induces hypermyelination and early Parkinson's disease-like phenotypes in mice.Molecular neurodegeneration · 2024Article
- Neuroinflammation is associated with Alzheimer's disease co-pathology in dementia with Lewy bodies.Acta neuropathologica communications · 2024Article
- Pathobiology of Cognitive Impairment in Parkinson Disease: Challenges and Outlooks.International journal of molecular sciences · 2023Review
- β-Glucan Regulates Lipopolysaccharide Induced Genotoxic Damage to The Liver through The Induction of BRCA1 Protein Expression.Cell journal · 2023Article
- Investigation of Inflammation in Lewy Body Dementia: A Systematic Scoping Review.International journal of molecular sciences · 2023Article
- Morphological characteristics differentiate dementia with Lewy bodies from Parkinson disease with and without dementia.Journal of neural transmission (Vienna, Austria : 1996) · 2023Article
- Morphological basis of Parkinson disease-associated cognitive impairment: an update.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Dynamic Interrogation of Stochastic Transcriptome Trajectories Using Disease Associated Genes Reveals Distinct Origins of Neurological and Psychiatric Disorders.Frontiers in neuroscience · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParkinson'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.
methodsHere, 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.
resultsWe found that p-APP
conclusionsTogether, 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.
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