ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Expression of beta-amyloid induced age-dependent presynaptic and axonal changes in Drosophila.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- Vitamin K2 Promotes Mitochondrial Structural and Functional Homeostasis to Ameliorate Alzheimer Pathology by Targeting the EGFR-Ras-ERK Signaling Axis.International journal of molecular sciences · 2026Article
- Genetic architecture of human aging and longevity: Insights from genome-wide association studies.BMB reports · 2026Review
- Deep learning analysis of urine-derived stem cell mitochondrial morphology as a non-invasive Alzheimer's disease biomarker.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Insights into the molecular mechanism of neurological diseases and their pathophysiological responses.Archives of toxicology · 2025Review
- Therapeutic potential of melatonin-induced mitophagy in the pathogenesis of Alzheimer's disease.Inflammopharmacology · 2025Review
- Single-cell type analysis of wing premotor circuits in the ventral nerve cord ofbioRxiv : the preprint server for biology · 2025Article
- Polarized localization of kinesin-1 and RIC-7 drives axonal mitochondria anterograde transport.The Journal of cell biology · 2024Article
- Icaritin greatly attenuates β-amyloid-induced toxicity in vivo.CNS neuroscience & therapeutics · 2024Article
- Trehalose improves the movement ability of AβTranslational neuroscience · 2024Article
- Mitophagy in Alzheimer's Disease: A Bibliometric Analysis from 2007 to 2022.Journal of Alzheimer's disease reports · 2024Article
- The effect of lipid metabolism on age-associated cognitive decline: Lessons learned from model organisms and human.IBRO neuroscience reports · 2023Article
- Discoveries and future significance of research into amyloid-beta/α7-containing nicotinic acetylcholine receptor (nAChR) interactions.Pharmacological research · 2023Review
- Policosanol protects against Alzheimer's disease-associated spatial cognitive decline in male rats: possible involved mechanisms.Psychopharmacology · 2023Article
- The Novel Role of Mitochondrial Citrate Synthase and Citrate in the Pathophysiology of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Insights fromFrontiers in neuroscience · 2023Review
- Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.Neuron · 2022Review
- Synapses: The Brain's Energy-Demanding Sites.International journal of molecular sciences · 2022Review
- Excitotoxicity, calcium and mitochondria: a triad in synaptic neurodegeneration.Translational neurodegeneration · 2022Review
- Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope.Oxidative medicine and cellular longevity · 2022Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is attributable to synapse dysfunction and loss, but the nature and progression of the presynaptic structural and functional changes in AD are essentially unknown. We expressed wild-type or arctic form of beta amyloid(1-42) (Abeta) in a small group of neurons in the adult fly and performed extensive time course analysis of the function and structure of both axon and presynaptic terminals at the identified single-neuron level. Abeta accumulated intracellularly and induced a range of age-dependent changes, including depletion of presynaptic mitochondria, slowdown of bi-directional transports of axonal mitochondria, decreased synaptic vesicles, increased large vacuoles, and elevated synaptic fatigue. These structural and functional synaptic changes correlated with age-dependent deficit in motor behavior. All these alterations were accelerated in flies expressing the arctic form of Abeta. The depletion of presynaptic mitochondria was the earliest detected phenotype and was not caused by the change in axonal transport of mitochondria. Moreover, axonal mitochondria exhibited a dramatic reduction in number but a significant increase in size in aged Abeta-expressing flies, indicating a global depletion of mitochondria in the neuron and an impairment of mitochondria fission. These results suggest that Abeta accumulation depletes presynaptic and axonal mitochondria, leading to other presynaptic deficits.
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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.