Feng G, Pang J, Yi X, Song Q, Zhang J, Li C, He G, Ping Y. Down-Regulation of K(V)4 Channel in Drosophila Mushroom Body Neurons Contributes to Aβ42-Induced Courtship Memory Deficits. Neuroscience. 2018 Feb 1;370:236-245. doi: 10.1016/j.neuroscience.2017.06.008. Epub 2017 Jun 13. PubMed PMID: 28627422.
From the abstract: "Accumulation of amyloid-β (Aβ) is widely believed to be an early event in the pathogenesis of Alzheimer's disease (AD). Kv4 is an A-type K+ channel, and our previous report shows the degradation of Kv4, induced by the Aβ42 accumulation, may be a critical contributor to the hyperexcitability of neurons in a Drosophila AD model. Here, we used well-established courtship memory assay to investigate the contribution of the Kv4 channel to short-term memory (STM) deficits in the Aβ42-expressing AD model. ... These data highlight causal relationship between region-specific Kv4 degradation and age-dependent learning decline in the AD model, and provide a mechanism for the disturbed cognitive function in AD."
Lee BI, Suh YS, Chung YJ, Yu K, Park CB. Shedding Light on Alzheimer's β-Amyloidosis: Photosensitized Methylene Blue Inhibits Self-Assembly of β-Amyloid Peptides and Disintegrates Their Aggregates. Sci Rep. 2017 Aug 8;7(1):7523. doi: 10.1038/s41598-017-07581-2. PubMed PMID: 28790398; PubMed Central PMCID: PMC5548810.
From the abstract: "Abnormal aggregation of β-amyloid (Aβ) peptides is a major hallmark of Alzheimer's disease (AD). ... Among many candidate chemicals, methylene blue (MB) has proved its therapeutic potential for AD in a number of in vitro and in vivo studies; but the result of recent clinical trials performed with MB and its derivative was negative. Here ... we first report that photoexcited MB molecules can block Aβ42 aggregation in vitro. Furthermore, our in vivo study using Drosophila AD model demonstrates that photoexcited MB is highly effective in suppressing synaptic toxicity ... Our work suggests that light illumination can provide an opportunity to boost the efficacies of MB toward photodynamic therapy of AD in future."
Papanikolopoulou K, Grammenoudi S, Samiotaki M, Skoulakis EMC. Differential effects of 14-3-3 dimers on Tau phosphorylation, stability and toxicity in vivo. Hum Mol Genet. 2018 Jul 1;27(13):2244-2261. doi: 10.1093/hmg/ddy129. PubMed PMID: 29659825.
From the abstract: "Neurodegenerative dementias collectively known as Tauopathies involve aberrant phosphorylation and aggregation of the neuronal protein Tau. ... We use .. the Drosophila system to investigate in vivo whether 14-3-3s are causal or synergistic with Tau accumulation in precipitating pathogenesis. ... Our collective data demonstrate the complexity of 14-3-3/Tau interactions in vivo and suggest that 14-3-3 attenuation is not appropriate ameliorative treatment of Tauopathies. ..."
No comments:
Post a Comment