ArticleMolecular neurobiology2025
Proteasome Dysregulation in Parkinson's Disease: Insights from Blood-Based Analyses.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Copper Dyshomeostasis Affects α-Synuclein Clearance Mechanisms in Parkinson's Disease: Insights from In Vitro Models and Translational Evidence.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder that is characterized by α-synuclein aggregation, mitochondrial dysfunction, and impaired proteostasis. The peripheral biomarkers that reflect these cellular perturbations remain incompletely defined. This study aimed to evaluate the enzymatic activity and gene expression of two key protein degradation enzymes, Acyl PEptide Hydrolase (APEH) and Proteasome Subunit Beta Type-5 (PSMB5), in the peripheral blood of PD patients and to relate these findings to the severity of the disease. Thirteen PD patients and 13 age-matched healthy controls (HLT) were recruited. APEH and PSMB5 chymotrypsin-like (CT-like) activity were measured in whole blood, erythrocytes and immune cell fractions. Gene expression analysis was performed for APEH and PSMB5 and their related genes, plus other genes typical of parkinsonism or indicative of metabolic alterations: N(alpha)-acetyltransferase (NAA10) Aminoacylase 1 (ACY1), Ubiquitin-activating enzyme 1 (UBA1), Ubiquitin conjugating enzyme E2 I (UBE2I), Parkin RBR E3 ubiquitin protein ligase (PRKN), Alpha-synuclein (SNCA), Parkinsonism associated deglycase DJ-1 (PARK7), and mitochondrial Mn-SOD (SOD2). APEH activity did not differ significantly between PD and HLT in whole blood cells or cellular fractions. Conversely, PSMB5 CT-like activity was reduced in lymphocytes from PD patients, whereas erythrocytes and whole blood exhibited elevated activity. No changes in APEH and PSMB5 expression were observed, while PARK7 significantly decreased in patients with PD. Correlation analysis showed that proteasomal changes correlated with disease severity, and cognitive impairment. Our findings revealed compartment-specific proteasomal dysregulation in the peripheral blood of PD patients, suggesting systemic proteostasis imbalance. These alterations appeared more pronounced in patients with more severe clinical progression. This study supports the potential of peripheral proteasomal activity profiles as biomarkers linked to PD progression, warranting further investigation in larger cohorts.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.