Nathanael J Lee

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UNLABELLED Much of the molecular understanding of synaptic pathology in Alzheimer's disease (AD) comes from studies of various mouse models that express familial AD (FAD)-linked mutations, often in combinations. Most studies compare the absolute magnitudes of long-term potentiation (LTP) and long-term depression (LTD) to assess deficits in bidirectional(More)
Our recent study demonstrated that an amyloid-β binding molecule, BTA-EG4, increases dendritic spine number via Ras-mediated signaling. To potentially optimize the potency of the BTA compounds, we synthesized and evaluated an amyloid-β binding analog of BTA-EG4 with increased solubility in aqueous solution, BTA-EG6. We initially examined the effects of(More)
Recent studies demonstrated that the antihypertensive drug Valsartan improved spatial and episodic memory in mouse models of Alzheimer's Disease (AD) and human subjects with hypertension. However, the molecular mechanism by which Valsartan can regulate cognitive function is still unknown. Here, we investigated the effect of Valsartan on dendritic spine(More)
Andrea Megill,1 Trinh Tran,1 X Kiara Eldred,2 X Nathanael J. Lee,3 Philip C. Wong,1,4 Hyang-Sook Hoe,3 Alfredo Kirkwood,1 and X Hey-Kyoung Lee1,2 1Solomon H. Snyder Department of Neuroscience, Zanvyl-Krieger Mind/Brain Institute, and 2Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, 3Department of Neuroscience, Georgetown(More)
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