ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
Distinctive roles of different beta-amyloid 42 aggregates in modulation of synaptic functions.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Exploring the versatility ofFly · 2025Review
- Key questions for the future of amyloid research in dementia: a framework for integrating complex datasets.Molecular psychiatry · 2025Review
- Amyloid in the ageing brain: New frameworks and perspectives.Aging brain · 2021Article
- Modeling Neurodegenerative Disorders inInternational journal of molecular sciences · 2020Review
- Phenotypic differences betweenAnimal cells and systems · 2017Article
- Uncoupling neuronal death and dysfunction in Drosophila models of neurodegenerative disease.Acta neuropathologica communications · 2016Article
- Modeling the complex pathology of Alzheimer's disease in Drosophila.Experimental neurology · 2015Review
- Lack of evidence of the interaction of the Aβ peptide with the Wnt signaling cascade in Drosophila models of Alzheimer's disease.Molecular brain · 2014Article
- Intraneuronal accumulation of Aβ42 induces age-dependent slowing of neuronal transmission in Drosophila.Neuroscience bulletin · 2014Article
- Synaptic abnormalities in a Drosophila model of Alzheimer's disease.Disease models & mechanisms · 2014Article
- Cholesterol increases ventricular volume in a rabbit model of Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2012Article
- Inhibitory Effects of Quercetin on Muscle-type of Nicotinic Acetylcholine Receptor-Mediated Ion Currents Expressed in Xenopus Oocytes.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Characterization of a Drosophila Alzheimer's disease model: pharmacological rescue of cognitive defects.PloS one · 2011Article
- PI3 kinase signaling is involved in Abeta-induced memory loss in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Transgenic Drosophila models of Alzheimer's disease and tauopathies.Brain structure & function · 2010Review
- Mitochondrial mislocalization underlies Abeta42-induced neuronal dysfunction in a Drosophila model of Alzheimer's disease.PloS one · 2009Article
- Article
- Ascidians: an invertebrate chordate model to study Alzheimer's disease pathogenesis.Disease models & mechanismsArticle
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Abstract
To determine how endogenously secreted beta-amyloid 42 (Abeta42) aggregates regulate synaptic functions, we examined effects of Abeta42 at the neuromuscular junction of Drosophila larvae. Voltage-clamp recordings of synaptic transmission and optical analysis of vesicle recycling at presynaptic terminals show that expression of Abeta42 in neurons leads to a reduction of neurotransmitter release. However, expression of Abeta42 in postsynaptic muscle cells enhanced neurotransmitter release. Both effects are neutralized by Abeta antibody, suggesting a role for secreted Abeta42 peptides. Application of exogenously prepared Abeta42 oligomers leads to a reduction in synaptic responses, whereas mixed Abeta42 aggregates with mainly fibrils elicit an opposite effect by increasing synaptic transmission. Further analysis of long-term depression (LTD) confirms differential effects of different Abeta42 aggregates. Taken together, our data suggest that Abeta42 is secreted from neurons primarily as oligomers that inhibit neurotransmitter release and exert no effect on LTD. Whereas larger-sized aggregates, possibly fibrils, are major components secreted from muscle cells, which enhance synaptic transmission and LTD. Thus, different types of cells may secrete distinct forms of Abeta42 aggregates, leading to different modulation of synaptic functions.
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