ReviewNeurobiology of disease2022
The roles of connectivity and neuronal phenotype in determining the pattern of α-synuclein pathology in Parkinson's disease.
Review in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 36 citations in OpenAlex.
- Selective molecular and network architecture features underlie brain cortical atrophy in dementia with Lewy bodies.Journal of biomedical science · 2026Article
- Mapping cellular vulnerability in Parkinson's disease using retro-AAVs and preformed α-synuclein fibrils.Translational neurodegeneration · 2026Article
- Emodin, a Potent Anthraquinone Mitigates MPTP-Induced Parkinsons' Disease Pathology by Regulating Nrf2 and Its Downstream Targets: In Silico and In Vivo Approach.Molecular neurobiology · 2025Article
- Pathological α-synuclein elicits granulovacuolar degeneration independent of tau.Translational neurodegeneration · 2025Article
- Choroid plexus enlargement contributes to motor severity via regional glymphatic dysfunction in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Research Priorities on the Role of α-Synuclein in Parkinson's Disease Pathogenesis.Movement disorders : official journal of the Movement Disorder Society · 2024Review
- A topographical atlas of α-synuclein dosage and cell type-specific expression in adult mouse brain and peripheral organs.NPJ Parkinson's disease · 2024Article
- Dopaminergic neuron loss in mice due to increased levels of wild-type human α-Synuclein only takes place under conditions of accelerated aging.Scientific reports · 2024Article
- Intercellular transmission of alpha-synuclein.Frontiers in molecular neuroscience · 2024Review
- Mitochondrial dysfunction in Parkinson's disease - a key disease hallmark with therapeutic potential.Molecular neurodegeneration · 2023Review
- Advances in understanding the function of alpha-synuclein: implications for Parkinson's disease.Brain : a journal of neurology · 2023Review
- Hippocampal subfield vulnerability to α-synuclein pathology precedes neurodegeneration and cognitive dysfunction.NPJ Parkinson's disease · 2023Article
- Article
- Hippocampal subfield vulnerability to α-synuclein pathology precedes neurodegeneration and cognitive dysfunction.bioRxiv : the preprint server for biology · 2023Article
- Article
- Physiological and Pathological Functions of Neuronal Hemoglobin: A Key Underappreciated Protein in Parkinson's Disease.International journal of molecular sciences · 2022Review
- The Role of Rab Proteins in Parkinson's Disease Synaptopathy.Biomedicines · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is the most common neurodegenerative movement disorder, and motor dysfunction has been attributed to loss of dopaminergic neurons. However, motor dysfunction is only one of many symptoms experienced by patients. A neuropathological hallmark of PD is intraneuronal protein aggregates called Lewy pathology (LP). Neuropathological staging studies have shown that dopaminergic neurons are only one of the many cell types prone to manifest LP. Progressive appearance of LP in multiple brain regions, as well as peripheral nerves, has led to the popular hypothesis that LP and misfolded forms of one of its major components - α-synuclein (aSYN) - can spread through synaptically connected circuits. However, not all brain regions or neurons within connected circuits develop LP, suggesting that cell autonomous factors modulate the development of pathology. Here, we review studies about how LP develops and progressively engages additional brain regions. We focus on how connectivity constrains progression and discuss cell autonomous factors that drive pathology development. We propose a mixed model of cell autonomous factors and trans-synaptic spread as mediators of pathology progression and put forward this model as a framework for future experiments exploring PD pathophysiology.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.