ArticleLife science alliance2022
Decreasing pdzd8-mediated mito-ER contacts improves organismal fitness and mitigates Aβ
Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 40 citations in OpenAlex.
- PDZD8 overexpression alleviates early brain injury via regulating MERCs integrity after experimental subarachnoid hemorrhage.Journal of neuroinflammation · 2026Article
- Mitochondrial interplay with membrane organelles in health and disease.Cell communication and signaling : CCS · 2026Review
- Mitochondria-ER contact sites in neurological disorders.Animal cells and systems · 2026Review
- Mitochondrial origins of the pressure to sleep.Nature · 2025Article
- PDZD8 promotes autophagy at ER-lysosome membrane contact sites to regulate activity-dependent synaptic growth.Cell reports · 2025Article
- Mitochondrial complexity is regulated at ER-mitochondria contact sites via PDZD8-FKBP8 tethering.Nature communications · 2025Article
- Tracking spatiotemporal distribution of organelle contacts in vivo with SPLICS reporters.Cell death & disease · 2025Article
- Quercetin preserves mitochondria-endoplasmic reticulum contact sites improving mitochondrial dynamics in aged myocardial cells.Biogerontology · 2024Article
- ER-mitochondria association negatively affects wound healing by regulating NLRP3 activation.Cell death & disease · 2024Article
- Genome-wide CRISPR/Cas9 screen shows that loss of GET4 increases mitochondria-endoplasmic reticulum contact sites and is neuroprotective.Cell death & disease · 2024Article
- COPI-regulated mitochondria-ER contact site formation maintains axonal integrity.Cell reports · 2023Article
- Optogenetic cleavage of the Miro GTPase reveals the direct consequences of real-time loss of function in Drosophila.PLoS biology · 2023Article
- Role of Mitochondria-ER Contact Sites in Mitophagy.Biomolecules · 2023Review
- Insights fromFrontiers in neuroscience · 2023Review
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Transcriptome Profile in the Mouse Brain of Hepatic Encephalopathy and Alzheimer's Disease.International journal of molecular sciences · 2022Article
- 1-L Transcription in Alzheimer's Disease.Current issues in molecular biology · 2022Article
- The Potential of Small Molecules to Modulate the Mitochondria-Endoplasmic Reticulum Interplay in Alzheimer's Disease.Frontiers in cell and developmental biology · 2022Review
- Endoplasmic reticulum-Mitochondria Coupling in Alzheimer's Disease.Contact (Thousand Oaks (Ventura County, Calif.))Review
- Recent Advances on Synaptotagmin-Like Mitochondrial-Lipid Binding Protein Domain Containing Lipid Transfer Proteins.Contact (Thousand Oaks (Ventura County, Calif.))Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitochondria-ER contact sites (MERCs) orchestrate many important cellular functions including regulating mitochondrial quality control through mitophagy and mediating mitochondrial calcium uptake. Here, we identify and functionally characterize the Drosophila ortholog of the recently identified mammalian MERC protein, Pdzd8. We find that reducing pdzd8-mediated MERCs in neurons slows age-associated decline in locomotor activity and increases lifespan in Drosophila. The protective effects of pdzd8 knockdown in neurons correlate with an increase in mitophagy, suggesting that increased mitochondrial turnover may support healthy aging of neurons. In contrast, increasing MERCs by expressing a constitutive, synthetic ER-mitochondria tether disrupts mitochondrial transport and synapse formation, accelerates age-related decline in locomotion, and reduces lifespan. Although depletion of pdzd8 prolongs the survival of flies fed with mitochondrial toxins, it is also sufficient to rescue locomotor defects of a fly model of Alzheimer's disease expressing Amyloid β
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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.