Trial reportThe American journal of pathology2013
Mitochondrial abnormality associates with type-specific neuronal loss and cell morphology changes in the pedunculopontine nucleus in Parkinson disease.
Trial report in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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
32 citing papers in PubMed, 66 citations in OpenAlex.
- Exercise Intervention for REM Sleep Behavior Disorder in Parkinson's Disease: Mechanisms and Implications for Neurorehabilitation.CNS neuroscience & therapeutics · 2026Review
- Stereological analysis of cholinergic neurons within bilateral pedunculopontine nuclei in health and when affected by Parkinson's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- Article
- α-Synuclein pathology disrupts mitochondrial function in dopaminergic and cholinergic neurons at-risk in Parkinson's disease.Molecular neurodegeneration · 2024Article
- Advances in the study of cholinergic circuits in the central nervous system.Annals of clinical and translational neurology · 2023Review
- Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson's Disease Model by Alleviating Mitochondrial Dysfunction.International journal of molecular sciences · 2023Article
- The Therapeutic Potential of Mitochondria Transplantation Therapy in Neurodegenerative and Neurovascular Disorders.Current neuropharmacology · 2023Review
- The PPN and motor control: Preclinical studies to deep brain stimulation for Parkinson's disease.Frontiers in neural circuits · 2023Review
- Exploring the Role of Lipid-Binding Proteins and Oxidative Stress in Neurodegenerative Disorders: A Focus on the Neuroprotective Effects of Nutraceutical Supplementation and Physical Exercise.Antioxidants (Basel, Switzerland) · 2022Review
- The roles of connectivity and neuronal phenotype in determining the pattern of α-synuclein pathology in Parkinson's disease.Neurobiology of disease · 2022Review
- Protective effect of curcumin against rotenone-induced substantia nigra pars compacta neuronal dysfunction.Metabolic brain disease · 2022Article
- Cholinergic systems, attentional-motor integration, and cognitive control in Parkinson's disease.Progress in brain research · 2022Review
- Single-Cell Approaches for Studying the Role of Mitochondrial DNA in Neurodegenerative Disease.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Progressive Pontine-Medullary Dysfunction Leads to REM Sleep Behavior Disorder Symptoms in a Chronic Model of Parkinson's Disease.Nature and science of sleep · 2021Article
- Determinants of seeding and spreading of α-synuclein pathology in the brain.Science advances · 2020Article
- Calcium, Bioenergetics, and Parkinson's Disease.Cells · 2020Review
- Dissecting Brainstem Locomotor Circuits: Converging Evidence for Cuneiform Nucleus Stimulation.Frontiers in systems neuroscience · 2020Article
- Nurr1, Pitx3, and α7 nAChRs mRNA Expression in Nigral Tissue of Rats with Pedunculopontine Neurotoxic Lesion.Medicina (Kaunas, Lithuania) · 2019Article
- Regional mitochondrial DNA and cell-type changes in post-mortem brains of non-diabetic Alzheimer's disease are not present in diabetic Alzheimer's disease.Scientific reports · 2019Observational
- The pedunclopontine nucleus and Parkinson's disease.Neurobiology of disease · 2019Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Cholinergic neuronal loss in the pedunculopontine nucleus (PPN) associates with abnormal functions, including certain motor and nonmotor symptoms. This realization has led to low-frequency stimulation of the PPN for treating patients with Parkinson disease (PD) who are refractory to other treatment modalities. However, the molecular mechanisms underlying PPN neuronal loss and the therapeutic substrate for the clinical benefits following PPN stimulation remain poorly characterized, hampering progress toward designing more efficient therapies aimed at restoring the PPN's normal functions during progressive parkinsonism. Here, we investigated postmortem pathological changes in the PPN of PD cases. Our study detected a loss of neurons producing gamma-aminobutyric acid (GABA) as their output and glycinergic neurons, along with the pronounced loss of cholinergic neurons. These losses were accompanied by altered somatic cell size that affected the remaining neurons of all neuronal subtypes studied here. Because studies showed that mitochondrial dysfunction exists in sporadic PD and in PD animal models, we investigated whether altered mitochondrial composition exists in the PPN. A significant up-regulation of several mitochondrial proteins was seen in GABAergic and glycinergic neurons; however, cholinergic neurons indicated down-regulation of the same proteins. Our findings suggest an imbalance in the activity of key neuronal subgroups of the PPN in PD, potentially because of abnormal inhibitory activity and altered cholinergic outflow.
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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.