{"publisher":"Elsevier","year":"2003","publist_id":"4262","volume":353,"date_created":"2018-12-11T11:58:48Z","intvolume":" 353","status":"public","quality_controlled":0,"title":"Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology","date_updated":"2021-01-12T06:58:44Z","month":"12","doi":"10.1016/j.neulet.2003.09.027","page":"143 - 147","author":[{"full_name":"Bell, Karen F","first_name":"Karen","last_name":"Bell"},{"full_name":"De Kort, G J","first_name":"G J","last_name":"De Kort"},{"full_name":"Steggerda, S","last_name":"Steggerda","first_name":"S"},{"first_name":"Ryuichi","last_name":"Shigemoto","full_name":"Ryuichi Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444"},{"first_name":"Alfredo","last_name":"Ribeiro Da Silva","full_name":"Ribeiro-da-Silva, Alfredo"},{"full_name":"Cuello, Augusto C","last_name":"Cuello","first_name":"Augusto"}],"day":"19","publication":"Neuroscience Letters","type":"journal_article","abstract":[{"text":"While the cholinergic depletion in Alzheimer's disease (AD) has been known for some time, a definitive involvement of other neurotransmitter systems has been somewhat more elusive. Our study demonstrates a clear involvement of both glutamatergic and, to a lesser extent, GABAergic neurons in an early onset transgenic mouse model of AD-like amyloid pathology. Immunohistochemical staining and subsequent quantification has revealed a statistically significant increased density of glutamatergic and GABAergic presynaptic boutons in both the plaque free and plaque adjacent cortical neuropile areas of transgenic mice as compared to non-transgenic controls. Furthermore, amyloid plaque size was shown to have a statistically significant effect on the relative area occupied by dystrophic glutamatergic neurites in the peri-plaque neuropile. These findings support our hypothesis that the amyloid pathology progresses in a time and neurotransmitter specific manner, first in the cholinergic system which appears to be most vulnerable, followed by the glutamatergic presynaptic boutons and finally the somewhat more resilient GABAergic terminals.","lang":"eng"}],"_id":"2637","issue":"2","date_published":"2003-12-19T00:00:00Z","publication_status":"published","citation":{"short":"K. Bell, G.J. De Kort, S. Steggerda, R. Shigemoto, A. Ribeiro Da Silva, A. Cuello, Neuroscience Letters 353 (2003) 143–147.","ista":"Bell K, De Kort GJ, Steggerda S, Shigemoto R, Ribeiro Da Silva A, Cuello A. 2003. Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology. Neuroscience Letters. 353(2), 143–147.","chicago":"Bell, Karen, G J De Kort, S Steggerda, Ryuichi Shigemoto, Alfredo Ribeiro Da Silva, and Augusto Cuello. “Structural Involvement of the Glutamatergic Presynaptic Boutons in a Transgenic Mouse Model Expressing Early Onset Amyloid Pathology.” Neuroscience Letters. Elsevier, 2003. https://doi.org/10.1016/j.neulet.2003.09.027.","apa":"Bell, K., De Kort, G. J., Steggerda, S., Shigemoto, R., Ribeiro Da Silva, A., & Cuello, A. (2003). Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology. Neuroscience Letters. Elsevier. https://doi.org/10.1016/j.neulet.2003.09.027","ama":"Bell K, De Kort GJ, Steggerda S, Shigemoto R, Ribeiro Da Silva A, Cuello A. Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology. Neuroscience Letters. 2003;353(2):143-147. doi:10.1016/j.neulet.2003.09.027","ieee":"K. Bell, G. J. De Kort, S. Steggerda, R. Shigemoto, A. Ribeiro Da Silva, and A. Cuello, “Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology,” Neuroscience Letters, vol. 353, no. 2. Elsevier, pp. 143–147, 2003.","mla":"Bell, Karen, et al. “Structural Involvement of the Glutamatergic Presynaptic Boutons in a Transgenic Mouse Model Expressing Early Onset Amyloid Pathology.” Neuroscience Letters, vol. 353, no. 2, Elsevier, 2003, pp. 143–47, doi:10.1016/j.neulet.2003.09.027."},"extern":1}