ArticlePloS one2013
Cyclophilin D deficiency rescues axonal mitochondrial transport in Alzheimer's neurons.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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.
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Who cites it
68 citing papers in PubMed, 118 citations in OpenAlex.
- Sex differences in brain glucose metabolism and Alzheimer's disease risk and progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- A Proteomics Profiling Reveals the Neuroprotective Effects of Melatonin on Exogenous β-amyloid-42 Induced Mitochondrial Impairment, Intracellular β-amyloid Accumulation and Tau Hyperphosphorylation in Human SH-SY5Y Cells.Cell biology international · 2025Article
- New cyclophilin D inhibitor rescues mitochondrial and cognitive function in Alzheimer's disease.Brain : a journal of neurology · 2024Article
- Review
- Caspase-3 cleaved tau impairs mitochondrial function through the opening of the mitochondrial permeability transition pore.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Mitochondrial dysfunction and Alzheimer's disease: pathogenesis of mitochondrial transfer.Frontiers in aging neuroscience · 2024Review
- Potential Retinal Biomarkers in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Disruption of axonal transport in neurodegeneration.The Journal of clinical investigation · 2023Review
- Common mechanisms underlying axonal transport deficits in neurodegenerative diseases: a mini review.Frontiers in molecular neuroscience · 2023Review
- Mitochondrial Dysfunction Links to Impaired Hippocampal Serotonin Release in a Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- Mitochondrial behavior when things go wrong in the axon.Frontiers in cellular neuroscience · 2022Review
- Redox signaling and metabolism in Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Disentangling Mitochondria in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Mitochondrial Permeability Transition: A Pore Intertwines Brain Aging and Alzheimer's Disease.Cells · 2021Review
- Electrophysiological properties of the mitochondrial permeability transition pores: Channel diversity and disease implication.Biochimica et biophysica acta. Bioenergetics · 2021Review
- Modulation of OSCP mitigates mitochondrial and synaptic deficits in a mouse model of Alzheimer's pathology.Neurobiology of aging · 2021Article
- Mitochondrial Quality Control Strategies: Potential Therapeutic Targets for Neurodegenerative Diseases?Frontiers in neuroscience · 2021Review
- Recent progress in the use of mitochondrial membrane permeability transition pore in mitochondrial dysfunction-related disease therapies.Molecular and cellular biochemistry · 2021Review
- Mitochondrial Behavior in Axon Degeneration and Regeneration.Frontiers in aging neuroscience · 2021Review
- Relationships between Mitochondrial Dysfunction and Neurotransmission Failure in Alzheimer's Disease.Aging and disease · 2020Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Normal axonal mitochondrial transport and function is essential for the maintenance of synaptic function. Abnormal mitochondrial motility and mitochondrial dysfunction within axons are critical for amyloid β (Aβ)-induced synaptic stress and the loss of synapses relevant to the pathogenesis of Alzheimer's disease (AD). However, the mechanisms controlling axonal mitochondrial function and transport alterations in AD remain elusive. Here, we report an unexplored role of cyclophilin D (CypD)-dependent mitochondrial permeability transition pore (mPTP) in Aβ-impaired axonal mitochondrial trafficking. Depletion of CypD significantly protects axonal mitochondrial motility and dynamics from Aβ toxicity as shown by increased axonal mitochondrial density and distribution and improved bidirectional transport of axonal mitochondria. Notably, blockade of mPTP by genetic deletion of CypD suppresses Aβ-mediated activation of the p38 mitogen-activated protein kinase signaling pathway, reverses axonal mitochondrial abnormalities, improves synaptic function, and attenuates loss of synapse, suggesting a role of CypD-dependent signaling in Aβ-induced alterations in axonal mitochondrial trafficking. The potential mechanisms of the protective effects of lacking CypD on Aβ-induced abnormal mitochondrial transport in axon are increased axonal calcium buffer capability, diminished reactive oxygen species (ROS), and suppressing downstream signal transduction P38 activation. These findings provide new insights into CypD-dependent mitochondrial mPTP and signaling on mitochondrial trafficking in axons and synaptic degeneration in an environment enriched for Aβ.
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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.