ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Pan-neuronal expression of APL-1, an APP-related protein, disrupts olfactory, gustatory, and touch plasticity in Caenorhabditis elegans.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 26 citations in OpenAlex.
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- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Modeling neurodegeneration inDisease models & mechanisms · 2020Review
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- Caenorhabditis elegans hub genes that respond to amyloid beta are homologs of genes involved in human Alzheimer's disease.PloS one · 2019Article
- Small molecule modulator of sigma 2 receptor is neuroprotective and reduces cognitive deficits and neuroinflammation in experimental models of Alzheimer's disease.Journal of neurochemistry · 2017Article
- Alzheimer-related protein APL-1 modulates lifespan through heterochronic gene regulation in Caenorhabditis elegans.Aging cell · 2016Article
- The C. elegans adult neuronal IIS/FOXO transcriptome reveals adult phenotype regulators.Nature · 2016Article
- Using C. elegans to discover therapeutic compounds for ageing-associated neurodegenerative diseases.Chemistry Central journal · 2015Review
- Longevity pathways and memory aging.Frontiers in genetics · 2014Review
- Epigenetic effect of testosterone in the behavior of C. elegans. A clue to explain androgen-dependent autistic traits?Frontiers in cellular neuroscience · 2014Article
- Use of Caenorhabditis elegans as a model to study Alzheimer's disease and other neurodegenerative diseases.Frontiers in genetics · 2014Review
- Neuronal aging: learning from C. elegans.Journal of molecular signaling · 2013Article
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7 authors at 3 institutions in 1 country.
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Abstract
Patients with Alzheimer's disease show age-related cognitive decline. Postmortem autopsy of their brains shows the presence of large numbers of senile plaques, whose major component is the β-amyloid peptide. The β-amyloid peptide is a cleavage product of the amyloid precursor protein (APP). In addition to the neurodegeneration associated with β-amyloid aggregation in Alzheimer's disease patients, mutations in APP in mammalian model organisms have also been shown to disrupt several behaviors independent of visible amyloid plaque formation. However, the pathways in which APP function are unknown and difficult to unravel in mammals. Here we show that pan-neuronal expression of APL-1, the Caenorhabditis elegans ortholog of APP, disrupts several behaviors, such as olfactory and gustatory learning behavior and touch habituation. These behaviors are mediated by distinct neural circuits, suggesting a broad impact of APL-1 on sensory plasticity in C. elegans. Furthermore, we found that disruption of these three behaviors requires activity of the TGFβ pathway and reduced activity of the insulin pathway. These results suggest pathways and molecular components that may underlie behavioral plasticity in mammals and in patients with Alzheimer's disease.
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