Citations

Dr. Ju

37 Citations

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Anand, Preet, and Baldev Singh. “A Review on Cholinesterase Inhibitors for Alzheimer’s Disease.” Archives of Pharmacal Research, vol. 36, no. 4, Apr. 2013, pp. 375–99. Springer Link, doi:10.1007/s12272-013-0036-3.

Anggono, Victor, and Richard L. Huganir. “Regulation of AMPA Receptor Trafficking and Synaptic Plasticity.” Current Opinion in Neurobiology, vol. 22, no. 3, June 2012, pp. 461–69. PubMed Central, doi:10.1016/j.conb.2011.12.006.

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Bondi, Mark W., et al. “Alzheimer’s Disease: Past, Present, and Future.” Journal of the International Neuropsychological Society, vol. 23, no. 9–10, 2017, pp. 818–31. Scholars Portal Journals, doi:10.1017/S135561771700100X.

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Brothers, Holly M., et al. “The Physiological Roles of Amyloid-β Peptide Hint at New Ways to Treat Alzheimer’s Disease.” Frontiers in Aging Neuroscience, vol. 10, 2018. Frontiers, doi:10.3389/fnagi.2018.00118.

Chen, Ming. “The Maze of APP Processing in Alzheimer’s Disease: Where Did We Go Wrong in Reasoning?” Frontiers in Cellular Neuroscience, vol. 9, 2015. Frontiers, doi:10.3389/fncel.2015.00186.

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Cobar, Luis Fernando, Li Yuan, and Ayumu Tashiro. “Place Cells and Long-Term Potentiation in the Hippocampus.” Neurobiology of Learning and Memory, MCCS 2017, 138 (February 1, 2017): 206–14. https://doi.org/10.1016/j.nlm.2016.10.010.

Counts, Scott E., et al. “Biomarkers for the Early Detection and Progression of Alzheimer’s Disease.” Neurotherapeutics, vol. 14, no. 1, Jan. 2017, pp. 35–53. Springer Link, doi:10.1007/s13311-016-0481-z.

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Doherty, Gayle H., et al. “Leptin Prevents Hippocampal Synaptic Disruption and Neuronal Cell Death Induced by Amyloid β.” Neurobiology of Aging, vol. 34, no. 1, Jan. 2013, pp. 226–37. ScienceDirect, doi:10.1016/j.neurobiolaging.2012.08.003.

Fjell, Anders M., et al. “What Is Normal in Normal Aging? Effects of Aging, Amyloid and Alzheimer’s Disease on the Cerebral Cortex and the Hippocampus.” Progress in Neurobiology, vol. 117, June 2014, pp. 20–40. ScienceDirect, doi:10.1016/j.pneurobio.2014.02.004.

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Gad, Helge, et al. “Fission and Uncoating of Synaptic Clathrin-Coated Vesicles Are Perturbed by Disruption of Interactions with the SH3 Domain of Endophilin.” Neuron, vol. 27, no. 2, Aug. 2000, pp. 301–12. www.cell.com, doi:10.1016/S0896-6273(00)00038-6.

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Hess, Lisa M., et al. “Cognitive Function during and Six Months Following Chemotherapy for Front-Line Treatment of Ovarian, Primary Peritoneal or Fallopian Tube Cancer: An NRG Oncology/Gynecologic Oncology Group Study.” Gynecologic Oncology, vol. 139, no. 3, Dec. 2015, pp. 541–45. PubMed Central, doi:10.1016/j.ygyno.2015.10.003.

Holtzman, David M., et al. “Alzheimer’s Disease: The Challenge of the Second Century.” Science Translational Medicine, vol. 3, no. 77, Apr. 2011, p. 77sr1. PubMed Central, doi:10.1126/scitranslmed.3002369.

Hsieh, Helen, et al. “AMPAR Removal Underlies Aβ-Induced Synaptic Depression and Dendritic Spine Loss.” Neuron, vol. 52, no. 5, Dec. 2006, pp. 831–43. www.cell.com, doi:10.1016/j.neuron.2006.10.035.

Lashley, Tammaryn, et al. “Molecular Biomarkers of Alzheimer’s Disease: Progress and Prospects.” Disease Models & Mechanisms, vol. 11, no. 5, May 2018. PubMed Central, doi:10.1242/dmm.031781.

Lee, Sang Hyoung, et al. “Clathrin Adaptor AP2 and NSF Interact with Overlapping Sites of GluR2 and Play Distinct Roles in AMPA Receptor Trafficking and Hippocampal LTD.” Neuron, vol. 36, no. 4, Nov. 2002, pp. 661–74. DOI.org (Crossref), doi:10.1016/S0896-6273(02)01024-3.

Liu, Jinping, et al. “The Role of NMDA Receptors in Alzheimer’s Disease.” Frontiers in Neuroscience, vol. 13, 2019. Frontiers, doi:10.3389/fnins.2019.00043.

Marsh, Jade, and Pavlos Alifragis. “Synaptic Dysfunction in Alzheimer’s Disease: The Effects of Amyloid Beta on Synaptic Vesicle Dynamics as a Novel Target for Therapeutic Intervention.” Neural Regeneration Research 13, no. 4 (April 2018): 616–23. https://doi.org/10.4103/1673-5374.230276.

Milosevic, Ira, et al. “Recruitment of Endophilin to Clathrin-Coated Pit Necks Is Required for Efficient Vesicle Uncoating after Fission.” Neuron, vol. 72, no. 4, Nov. 2011, pp. 587–601. PubMed, doi:10.1016/j.neuron.2011.08.029.

Mu, Yangling, and Fred H. Gage. “Adult Hippocampal Neurogenesis and Its Role in Alzheimer’s Disease.” Molecular Neurodegeneration, vol. 6, no. 1, Dec. 2011, pp. 1–9. molecularneurodegeneration-biomedcentral-com.myaccess.library.utoronto.ca, doi:10.1186/1750-1326-6-85.

Murphy, M. Paul, and Harry LeVine. “Alzheimer’s Disease and the β-Amyloid Peptide.” Journal of Alzheimer’s Disease : JAD, vol. 19, no. 1, Jan. 2010, p. 311. PubMed Central, doi:10.3233/JAD-2010-1221.

Ossola, Dario, et al. “Force-Controlled Patch Clamp of Beating Cardiac Cells.” Nano Letters, vol. 15, no. 3, Mar. 2015, pp. 1743–50. ACS Publications, doi:10.1021/nl504438z.

Penn, A. C., et al. “Hippocampal LTP and Contextual Learning Require Surface Diffusion of AMPA Receptors.” Nature, vol. 549, no. 7672, Sept. 2017, pp. 384–88. www.nature.com, doi:10.1038/nature23658.

Rajasekhar, K., et al. “Function and Toxicity of Amyloid Beta and Recent Therapeutic Interventions Targeting Amyloid Beta in Alzheimer’s Disease.” Chemical Communications, vol. 51, no. 70, 2015, pp. 13434–50. Scholars Portal Journals, doi:10.1039/c5cc05264e.

Recent Developments in Alzheimer’s Disease Therapeutics | BMC Medicine | Full Text. https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-7-7. Accessed 21 Nov. 2019.

Ren, Yimin, et al. “Endophilin I Expression Is Increased in the Brains of Alzheimer Disease Patients.” Journal of Biological Chemistry, vol. 283, no. 9, Feb. 2008, pp. 5685–91. www.jbc.org, doi:10.1074/jbc.M707932200.

Reutens, Anne T., and C. Glenn Begley. “Endophilin-1: A Multifunctional Protein.” The International Journal of Biochemistry & Cell Biology, vol. 34, no. 10, Oct. 2002, pp. 1173–77. ScienceDirect, doi:10.1016/S1357-2725(02)00063-8.

Ringstad, Niels, et al. “Differential Expression of Endophilin 1 and 2 Dimers at Central Nervous System Synapses.” Journal of Biological Chemistry, vol. 276, no. 44, Nov. 2001, pp. 40424–30. www.jbc.org, doi:10.1074/jbc.M106338200.

Sadigh-Eteghad, Saeed, et al. “Amyloid-Beta: A Crucial Factor in Alzheimer’s Disease.” Medical Principles and Practice, vol. 24, no. 1, 2015, pp. 1–10. www.karger.com, doi:10.1159/000369101.

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Segev, Amir, et al. “Whole-Cell Patch-Clamp Recordings in Brain Slices.” Journal of Visualized Experiments : JoVE, no. 112, June 2016. PubMed Central, doi:10.3791/54024.

Shankar, Ganesh M., Brenda L. Bloodgood, Matthew Townsend, Dominic M. Walsh, Dennis J. Selkoe, and Bernardo L. Sabatini. “Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway.” The Journal of Neuroscience 27, no. 11 (March 14, 2007): 2866–75. https://doi.org/10.1523/JNEUROSCI.4970-06.2007.

Solinas, Sergio M. G., et al. “A Kinetic Model for Brain-Derived Neurotrophic Factor Mediated Spike Timing-Dependent LTP.” PLoS Computational Biology, vol. 15, no. 4, Apr. 2019, p. e1006975. doaj.org, doi:10.1371/journal.pcbi.1006975.

Steven A. Connor, Peter V. Nguyen. “Noradrenergic Regulation of Hippocampus-Dependent Memory.” Central Nervous System Agents in Medicinal Chemistry, November 30, 2019. http://www.eurekaselect.com/173665/article.

Suk, Ho-Jun, et al. “Advances in the Automation of Whole-Cell Patch Clamp Technology.” Journal of Neuroscience Methods, vol. 326, Oct. 2019, p. 108357. DOI.org (Crossref), doi:10.1016/j.jneumeth.2019.108357.

Tabatabaei‐Jafari, Hossein, et al. “The Cerebellum Shrinks Faster than Normal Ageing in Alzheimer’s Disease but Not in Mild Cognitive Impairment.” Human Brain Mapping, vol. 38, no. 6, 2017, pp. 3141–50. Scholars Portal Journals, doi:10.1002/hbm.23580.

“The Need for Early Detection and Treatment in Alzheimer’s Disease.” EBioMedicine, vol. 9, July 2016, pp. 1–2. PubMed Central, doi:10.1016/j.ebiom.2016.07.001.

Ting, Jonathan T., et al. “Amyloid Precursor Protein Overexpression Depresses Excitatory Transmission through Both Presynaptic and Postsynaptic Mechanisms.” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 1, 2007, pp. 353–58.

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Wang, Shaoxun, et al. “Is Beta-Amyloid Accumulation a Cause or Consequence of Alzheimer’s Disease?” Journal of Alzheimer’s Parkinsonism & Dementia, vol. 1, no. 2, 2016. PubMed Central, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5555607/.

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Wattmo, Carina, and Åsa K. Wallin. “Early- versus Late-Onset Alzheimer’s Disease in Clinical Practice: Cognitive and Global Outcomes over 3 Years.” Alzheimer’s Research & Therapy, vol. 9, no. 1, Dec. 2017, pp. 1–13. alzres-biomedcentral-com.myaccess.library.utoronto.ca, doi:10.1186/s13195-017-0294-2.

Yin, Yichen, et al. “Endophilin 1 Knockdown Prevents Synaptic Dysfunction Induced by Oligomeric Amyloid β.” Molecular Medicine Reports, vol. 19, no. 6, June 2019, pp. 4897–905. www.spandidos-publications.com, doi:10.3892/mmr.2019.10158.

Yu, Qing, et al. “Overexpression of Endophilin A1 Exacerbates Synaptic Alterations in a Mouse Model of Alzheimer’s Disease.” Nature Communications, vol. 9, no. 1, July 2018, pp. 1–14. www.nature.com, doi:10.1038/s41467-018-04389-0.

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Zhang, Jifeng, Minghui Tan, et al. “Distinct Functions of Endophilin Isoforms in Synaptic Vesicle Endocytosis.” Neural Plasticity, vol. 2015, Jan. 2015. doaj.org, doi:10.1155/2015/371496.

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