ArticleNeurobiology of disease2015
Increased cortical synaptic activation of TrkB and downstream signaling markers in a mouse model of Down Syndrome.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Impaired BDNF-TrkB trafficking and signalling in Down syndrome basal forebrain neurons.Cell death & disease · 2026Article
- The role of Down syndrome cell adhesion molecule in Down syndrome.Medical review (2021) · 2024Review
- DSCAM gene triplication causes excessive GABAergic synapses in the neocortex in Down syndrome mouse models.PLoS biology · 2023Article
- Targeting increased levels of APP in Down syndrome: Posiphen-mediated reductions in APP and its products reverse endosomal phenotypes in the Ts65Dn mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Article
- Intellectual disability: dendritic anomalies and emerging genetic perspectives.Acta neuropathologica · 2021Review
- Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons: Converging Insights From Alternative Hypotheses.Frontiers in neuroscience · 2019Review
- Q&A: Array tomography.BMC biology · 2018Article
- Dysregulation of neurotrophin signaling in the pathogenesis of Alzheimer disease and of Alzheimer disease in Down syndrome.Free radical biology & medicine · 2018Review
- Aerobic exercise and a BDNF-mimetic therapy rescue learning and memory in a mouse model of Down syndrome.Scientific reports · 2017Article
- Amyloid precursor protein-mediated endocytic pathway disruption induces axonal dysfunction and neurodegeneration.The Journal of clinical investigation · 2016Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Down Syndrome (DS), trisomy 21, is characterized by synaptic abnormalities and cognitive deficits throughout the lifespan and with development of Alzheimer's disease (AD) neuropathology and progressive cognitive decline in adults. Synaptic abnormalities are also present in the Ts65Dn mouse model of DS, but which synapses are affected and the mechanisms underlying synaptic dysfunction are unknown. Here we show marked increases in the levels and activation status of TrkB and associated signaling proteins in cortical synapses in Ts65Dn mice. Proteomic analysis at the single synapse level of resolution using array tomography (AT) uncovered increased colocalization of activated TrkB with signaling endosome related proteins, and demonstrated increased TrkB signaling. The extent of increases in TrkB signaling differed in each of the cortical layers examined and with respect to the type of synapse, with the most marked increases seen in inhibitory synapses. These findings are evidence of markedly abnormal TrkB-mediated signaling in synapses. They raise the possibility that dysregulated TrkB signaling contributes to synaptic dysfunction and cognitive deficits in DS.
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Registered trials
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