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The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|November 1, 1995
Regulated secretion of beta-amyloid precursor protein in rat brainS A Farber, R M Nitsch, J G Schulz, et al.Neuro-Degenerative Diseases|May 16, 2012
Inhibition of microglial activation protects hippocampal neurogenesis and improves cognitive deficits in a transgenic mouse model for Alzheimer's diseaseBarbara Biscaro, Olle Lindvall, Giuseppina Tesco, et al.Annals of Neurology|December 16, 2000
The selective muscarinic M1 agonist AF102B decreases levels of total Abeta in cerebrospinal fluid of patients with Alzheimer's diseaseR M Nitsch, M Deng, M Tennis, et al.Proceedings of the National Academy of Sciences of the United States of America|August 15, 1995
Amyloid precursor protein processing is stimulated by metabotropic glutamate receptorsR K Lee, R J Wurtman, A J Cox, et al.Proceedings of the National Academy of Sciences of the United States of America|June 1, 1993
Release of amyloid beta-protein precursor derivatives by electrical depolarization of rat hippocampal slicesR M Nitsch, S A Farber, J H Growdon, et al.The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|July 20, 2007
Abeta oligomer-mediated long-term potentiation impairment involves protein phosphatase 1-dependent mechanismsMarlen Knobloch, Mélissa Farinelli, Uwe Konietzko, et al.Frontiers in Immunology|June 26, 2020
Oligomeric Forms of Human Amyloid-Beta(1-42) Inhibit Antigen PresentationChristoph Gericke, Anna Mallone, Britta Engelhardt, et al.Journal of Neural Transmission (Vienna, Austria : 1996)|December 30, 1998
Lu 25-109, a combined m1 agonist and m2 antagonist, modulates regulated processing of the amyloid precursor protein of Alzheimer's diseaseD Müller, H Wiegmann, U Langer, et al.Science (New York, N.Y.)|October 9, 1992
Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptorsR M Nitsch, B E Slack, R J Wurtman, et al.Cell Death & Disease|June 19, 2015
Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic lossJ H Birnbaum, J Bali, L Rajendran, et al.Pageof 28