ReviewF1000Research2016
Transporting mitochondria in neurons.
Review in F1000Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- Inhibition of mitochondrial dynamics inFrontiers in cell and developmental biology · 2026Article
- Alkaloids from Caliphruria subedentata (Amaryllidaceae) as Regulators of AChE, BuChE, NMDA and GSK3 Activity: An In Vitro and In Silico Approach for Mimicking Alzheimer´s Disease.Neurochemical research · 2025Article
- Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Novel Insights into Psychosis and Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes.International journal of molecular sciences · 2024Review
- Insomnia in Forensic Detainees: Is Salience Network the Common Pathway for Sleep, Neuropsychiatric, and Neurodegenerative Disorders?Journal of clinical medicine · 2024Review
- NR2F1 shapes mitochondria in the mouse brain, providing new insights into Bosch-Boonstra-Schaaf optic atrophy syndrome.Disease models & mechanisms · 2023Article
- Mitochondria on the move: Horizontal mitochondrial transfer in disease and health.The Journal of cell biology · 2023Article
- Mitochondrial transport in neurons and evidence for its involvement in acute neurological disorders.Frontiers in neuroscience · 2023Review
- Protein misfolding and clearance in the pathogenesis of a new infantile onset ataxia caused by mutations in PRDX3.Human molecular genetics · 2022Article
- Role of Impaired Mitochondrial Dynamics Processes in the Pathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Structural regulation and dynamic behaviour of organelles during plant meiosis.Frontiers in cell and developmental biology · 2022Review
- Human iPSC-Derived Neurons as A Platform for Deciphering the Mechanisms behind Brain Aging.Biomedicines · 2021Review
- Mitochondrial support and local translation of mitochondrial proteins in synaptic plasticity and function.Histology and histopathology · 2021Review
- Autophagic Pathways to Clear the Tau Aggregates in Alzheimer's Disease.Cellular and molecular neurobiology · 2021Review
- Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson's Disease.Frontiers in neuroscience · 2021Review
- The Emerging Role ofFrontiers in neurology · 2020Review
- Changes in PGC-1α/SIRT1 Signaling Impact on Mitochondrial Homeostasis in Amyloid-Beta Peptide Toxicity Model.Frontiers in pharmacology · 2020Article
- Article
- Strategies for the Treatment of Parkinson's Disease: Beyond Dopamine.Frontiers in aging neuroscience · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Neurons demand vast and vacillating supplies of energy. As the key contributors of this energy, as well as primary pools of calcium and signaling molecules, mitochondria must be where the neuron needs them, when the neuron needs them. The unique architecture and length of neurons, however, make them a complex system for mitochondria to navigate. To add to this difficulty, mitochondria are synthesized mainly in the soma, but must be transported as far as the distant terminals of the neuron. Similarly, damaged mitochondria-which can cause oxidative stress to the neuron-must fuse with healthy mitochondria to repair the damage, return all the way back to the soma for disposal, or be eliminated at the terminals. Increasing evidence suggests that the improper distribution of mitochondria in neurons can lead to neurodegenerative and neuropsychiatric disorders. Here, we will discuss the machinery and regulatory systems used to properly distribute mitochondria in neurons, and how this knowledge has been leveraged to better understand neurological dysfunction.
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.