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Aging, Metabolism, Synaptic Activity, and Aβ in Alzheimer's Disease.
Front Aging Neurosci. 2019 Jul 23;11:185. doi: 10.3389/fnagi.2019.00185. eCollection 2019.
2
Regulation of Synaptic Amyloid-β Generation through BACE1 Retrograde Transport in a Mouse Model of Alzheimer's Disease.
J Neurosci. 2017 Mar 8;37(10):2639-2655. doi: 10.1523/JNEUROSCI.2851-16.2017. Epub 2017 Feb 3.
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Reciprocal Predictive Relationships between Amyloid and Tau Biomarkers in Alzheimer's Disease Progression: An Empirical Model.
J Neurosci. 2019 Sep 11;39(37):7428-7437. doi: 10.1523/JNEUROSCI.1056-19.2019. Epub 2019 Jul 26.
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The inside-out amyloid hypothesis and synapse pathology in Alzheimer's disease.
Neurodegener Dis. 2014;13(2-3):142-6. doi: 10.1159/000354776. Epub 2013 Sep 24.
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Inhibition of Drp1 Ameliorates Synaptic Depression, Aβ Deposition, and Cognitive Impairment in an Alzheimer's Disease Model.
J Neurosci. 2017 May 17;37(20):5099-5110. doi: 10.1523/JNEUROSCI.2385-16.2017. Epub 2017 Apr 21.
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Concerted changes in transcripts in the prefrontal cortex precede neuropathology in Alzheimer's disease.
Brain. 2010 Dec;133(Pt 12):3699-723. doi: 10.1093/brain/awq258. Epub 2010 Oct 1.

本文引用的文献

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Therapeutic Potential of AMP-Activated Protein Kinase in Alzheimer's Disease.
J Alzheimers Dis. 2019;68(1):33-38. doi: 10.3233/JAD-181043.
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Tau impairs neural circuits, dominating amyloid-β effects, in Alzheimer models in vivo.
Nat Neurosci. 2019 Jan;22(1):57-64. doi: 10.1038/s41593-018-0289-8. Epub 2018 Dec 17.
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Evidence of intraneuronal Aβ accumulation preceding tau pathology in the entorhinal cortex.
Acta Neuropathol. 2018 Dec;136(6):901-917. doi: 10.1007/s00401-018-1922-z. Epub 2018 Oct 25.
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Impact of late-onset Alzheimer's genetic risk factors on beta-amyloid endocytic production.
Cell Mol Life Sci. 2018 Jul;75(14):2577-2589. doi: 10.1007/s00018-018-2825-9. Epub 2018 Apr 27.
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Endosomal Traffic Jams Represent a Pathogenic Hub and Therapeutic Target in Alzheimer's Disease.
Trends Neurosci. 2017 Oct;40(10):592-602. doi: 10.1016/j.tins.2017.08.003.
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Aβ accumulation causes MVB enlargement and is modelled by dominant negative VPS4A.
Mol Neurodegener. 2017 Aug 23;12(1):61. doi: 10.1186/s13024-017-0203-y.
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Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis.
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