ReviewCell communication and signaling : CCS2025
Bridging the gap in Parkinson's disease research: from general pathophysiology to advanced 3d cell culture models.
Review in Cell communication and signaling : CCS, 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.
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson’s disease (PD) is the second most common neurodegenerative disorder, having a substantial negative impact on the quality of life of patients with its wide range of motor and non-motor symptoms. PD has a complex etiology involving aging, genetic, and environmental factors. The hallmark of the pathology in PD is the accumulation of misfolded α-synuclein, a presynaptic vesicle-associated protein, in dopaminergic neurons, causing neuronal death in the substantia nigra pars compacta (SNpc) and other brain regions. This review focuses on the main pathophysiological mechanisms of PD and in vitro cell culture models. Conventional 2-dimensional (2D) systems can not properly mimic living tissue and reflect disease pathology. On the other hand, 3-dimensional (3D) cell culture models bring an innovative perspective to PD research because they offer tissue-like 3D environments that support the functioning and viability of cells. The potential use of spheroids and organoid systems, 3D bio-printing, microfluidic systems, and organ-on-chip models is discussed in comparison with traditional approaches using 2D. These methods have great potential for more realistic simulation of the dynamics of the disease, allowing the investigation of therapeutic molecules and targets. This review synthesizes current knowledge on PD mechanisms and 3D in vitro models, and explains why 3D offers advantages over 2D for studying disease and testing therapies.
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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.