{"date_published":"2003-12-19T00:00:00Z","citation":{"mla":"Bell, Karen, et al. “Structural Involvement of the Glutamatergic Presynaptic Boutons in a Transgenic Mouse Model Expressing Early Onset Amyloid Pathology.” <i>Neuroscience Letters</i>, vol. 353, no. 2, Elsevier, 2003, pp. 143–47, doi:<a href=\"https://doi.org/10.1016/j.neulet.2003.09.027\">10.1016/j.neulet.2003.09.027</a>.","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,” <i>Neuroscience Letters</i>, vol. 353, no. 2. Elsevier, pp. 143–147, 2003.","apa":"Bell, K., De Kort, G. J., Steggerda, S., Shigemoto, R., Ribeiro Da Silva, A., &#38; Cuello, A. (2003). Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology. <i>Neuroscience Letters</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neulet.2003.09.027\">https://doi.org/10.1016/j.neulet.2003.09.027</a>","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. <i>Neuroscience Letters</i>. 2003;353(2):143-147. doi:<a href=\"https://doi.org/10.1016/j.neulet.2003.09.027\">10.1016/j.neulet.2003.09.027</a>","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.” <i>Neuroscience Letters</i>. Elsevier, 2003. <a href=\"https://doi.org/10.1016/j.neulet.2003.09.027\">https://doi.org/10.1016/j.neulet.2003.09.027</a>.","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.","short":"K. Bell, G.J. De Kort, S. Steggerda, R. Shigemoto, A. Ribeiro Da Silva, A. Cuello, Neuroscience Letters 353 (2003) 143–147."},"publist_id":"4262","issue":"2","day":"19","quality_controlled":0,"title":"Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology","author":[{"first_name":"Karen","full_name":"Bell, Karen F","last_name":"Bell"},{"full_name":"De Kort, G J","last_name":"De Kort","first_name":"G J"},{"first_name":"S","last_name":"Steggerda","full_name":"Steggerda, S"},{"first_name":"Ryuichi","full_name":"Ryuichi Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","last_name":"Shigemoto"},{"first_name":"Alfredo","last_name":"Ribeiro Da Silva","full_name":"Ribeiro-da-Silva, Alfredo"},{"first_name":"Augusto","last_name":"Cuello","full_name":"Cuello, Augusto C"}],"date_created":"2018-12-11T11:58:48Z","intvolume":"       353","page":"143 - 147","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"}],"type":"journal_article","doi":"10.1016/j.neulet.2003.09.027","month":"12","date_updated":"2021-01-12T06:58:44Z","extern":1,"publication_status":"published","publisher":"Elsevier","status":"public","_id":"2637","year":"2003","publication":"Neuroscience Letters","volume":353}