ArticleTranslational neurodegeneration2013
Insights on altered mitochondrial function and dynamics in the pathogenesis of neurodegeneration.
Article in Translational neurodegeneration, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
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- Positron Emission Computed Tomography Imaging of Synaptic Vesicle Glycoprotein 2A in Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Effects of air pollution on mitochondrial function, mitochondrial DNA methylation, and mitochondrial peptide expression.Mitochondrion · 2019Article
- Understanding Miro GTPases: Implications in the Treatment of Neurodegenerative Disorders.Molecular neurobiology · 2018Review
- Clinical, pathological and functional characterization of riboflavin-responsive neuropathy.Brain : a journal of neurology · 2017Article
- Relationship Between β-Amyloid and Mitochondrial Dynamics.Cellular and molecular neurobiology · 2017Review
- Water-Soluble Coenzyme Q10 Reduces Rotenone-Induced Mitochondrial Fission.Neurochemical research · 2017Article
- The Endoplasmic Reticulum Unfolded Protein Response in Neurodegenerative Disorders and Its Potential Therapeutic Significance.Frontiers in molecular neuroscience · 2017Review
- Mitochondrial Effects of PGC-1alpha Silencing in MPPFrontiers in molecular neuroscience · 2017Article
- Intracellular Calcium Dysregulation: Implications for Alzheimer's Disease.BioMed research international · 2016Review
- Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds.Frontiers in neuroscience · 2016Review
- Low Cerebral Glucose Metabolism: A Potential Predictor for the Severity of Vascular Parkinsonism and Parkinson's Disease.Aging and disease · 2015Article
- Non-signalling energy use in the brain.The Journal of physiology · 2015Review
- Chaperone-mediated autophagy and neurodegeneration: connections, mechanisms, and therapeutic implications.Neuroscience bulletin · 2015Review
- OUTER RETINAL TUBULATION IN ADVANCED AGE-RELATED MACULAR DEGENERATION: Optical Coherence Tomographic Findings Correspond to Histology.Retina (Philadelphia, Pa.) · 2015Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In neurons, mitochondria are enriched to provide energy and calcium buffering required for synaptic transmission. Additionally, mitochondria localize to the synapse, where they are critical for the mobilization of reserve pool vesicles and for neurotransmitter release. Previously, functional defects in mitochondria were considered to be downstream effects of neurodegenerative diseases. However, more recent findings suggest mitochondria may serve as key mediators in the onset and progression of some types of neurodegeneration. In this review, we explore the possible roles of altered mitochondrial function and dynamics in the pathogenesis of neurodegenerative disorders, with a particular focus on Alzheimer's disease (AD) and Parkinson's disease (PD), which have highlighted the important role of mitochondria in neurodegeneration. While inheritable diseases like Charcot-Marie-Tooth disease type 2A are concretely linked to gene mutations affecting mitochondrial function, the cause of mitochondrial dysfunction in primarily sporadic diseases such as AD and PD is less clear. Neuronal death in PD is associated with defects in mitochondrial function and dynamics arising from mutations in proteins affecting these processes, including α-synuclein, DJ-1, LRRK2, Parkin and Pink1. In the case of AD, however, the connection between mitochondria and the onset of neurodegeneration has been less clear. Recent findings, however, have implicated altered function of ER-mitochondria contact sites and amyloid beta- and/or tau-induced defects in mitochondrial function and dynamics in the pathogenesis of AD, suggesting that mitochondrial defects may act as key mediators in the pathogenesis of AD as well. With recent findings at hand, it may be postulated that defects in mitochondrial processes comprise key events in the onset of neurodegeneration.
Identifiers
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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.