Zobrazeno 1 - 10
of 40
pro vyhledávání: '"Maria I Fonseca"'
Autor:
Maria I Fonseca, Shuhui Chu, Aimee L Pierce, William D Brubaker, Richard E Hauhart, Diego Mastroeni, Elizabeth V Clarke, Joseph Rogers, John P Atkinson, Andrea J Tenner
Publikováno v:
PLoS ONE, Vol 11, Iss 2, p e0149792 (2016)
Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the C3b
Externí odkaz:
https://doaj.org/article/e80b68870340438f96ecae3c7cc77d03
Publikováno v:
Neurobiology of Disease, Vol 15, Iss 1, Pp 40-46 (2004)
Complement has been postulated to contribute to inflammatory reactions associated with the neuropathology of Alzheimer's disease (AD). C1q, an initial component of the complement cascade, is associated with neuritic plaques and with neurons in the hi
Externí odkaz:
https://doaj.org/article/c74d7e7f23cc488aba43663903ea8220
Autor:
Klebea Carvalho, Nicole D. Schartz, Gabriela Balderrama-Gutierrez, Heidi Y. Liang, Shu-Hui Chu, Purnika Selvan, Angela Gomez-Arboledas, Tiffany J. Petrisko, Maria I. Fonseca, Ali Mortazavi, Andrea J. Tenner
Publikováno v:
Journal of Neuroinflammation, Vol 19, Iss 1, Pp 1-21 (2022)
Abstract Background The complement system is part of the innate immune system that clears pathogens and cellular debris. In the healthy brain, complement influences neurodevelopment and neurogenesis, synaptic pruning, clearance of neuronal blebs, rec
Externí odkaz:
https://doaj.org/article/d254ddd8a4eb41ccbf2722299212173b
Autor:
Melisa A. Molina, Amanda Cazzaniga, Laura B. Milde, Sonia C. Sgroppo, Pedro D. Zapata, Maria I. Fonseca
Publikováno v:
Journal of Food Science. 88:1365-1377
Autor:
Lindsay A. Hohsfield, Michael X. Hernandez, Maria D. Torres, Melody J. Fang, Shan Jiang, Maria I. Fonseca, Shu Hui Chu, Kim N. Green, Ali Mortazavi, Rick A. Wetsel, Tracy A. Cole, Andrea J. Tenner
Publikováno v:
Molecular Neurodegeneration, Vol 12, Iss 1, Pp 1-19 (2017)
Hernandez, MX; Jiang, S; Cole, TA; Chu, S-H; Fonseca, MI; Fang, MJ; et al.(2017). Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss. MOLECULAR NEURODEGENERATION, 12. doi: 10.1186/s13024-017-0210-z. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/72n4f4fj
Molecular Neurodegeneration
Hernandez, MX; Jiang, S; Cole, TA; Chu, S-H; Fonseca, MI; Fang, MJ; et al.(2017). Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss. MOLECULAR NEURODEGENERATION, 12. doi: 10.1186/s13024-017-0210-z. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/72n4f4fj
Molecular Neurodegeneration
Background Pharmacologic inhibition of C5aR1, a receptor for the complement activation proinflammatory fragment, C5a, suppressed pathology and cognitive deficits in Alzheimer's disease (AD) mouse models. To validate that the effect of the antagonist
Autor:
Melody J. Fang, Grant R. MacGregor, Michael X. Hernandez, Andrea J. Tenner, Maria I. Fonseca, Shu-Hui Chu, Pooja Selvan, Lila Modarresi
Publikováno v:
Journal of Neuroinflammation
Fonseca, MI; Chu, S-H; Hernandez, MX; Fang, MJ; Modarresi, L; Selvan, P; et al.(2017). Cell-specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain. JOURNAL OF NEUROINFLAMMATION, 14. doi: 10.1186/s12974-017-0814-9. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/1ps011p3
Fonseca, MI; Chu, S-H; Hernandez, MX; Fang, MJ; Modarresi, L; Selvan, P; et al.(2017). Cell-specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain. JOURNAL OF NEUROINFLAMMATION, 14. doi: 10.1186/s12974-017-0814-9. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/1ps011p3
The complement cascade not only provides protection from infection but can also mediate destructive inflammation. Complement is also involved in elimination of neuronal synapses which is essential for proper development, but can be detrimental during
Publikováno v:
ASN Neuro, Vol 9 (2017)
Hernandez, MX; Namiranian, P; Nguyen, E; Fonseca, MI; & Tenner, AJ. (2017). C5a Increases the Injury to Primary Neurons Elicited by Fibrillar Amyloid Beta. ASN NEURO, 9(1). doi: 10.1177/1759091416687871. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/98f9g8zw
ASN NEURO
Hernandez, MX; Namiranian, P; Nguyen, E; Fonseca, MI; & Tenner, AJ. (2017). C5a Increases the Injury to Primary Neurons Elicited by Fibrillar Amyloid Beta. ASN NEURO, 9(1). doi: 10.1177/1759091416687871. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/98f9g8zw
ASN NEURO
C5aR1, the proinflammatory receptor for C5a, is expressed in the central nervous system on microglia, endothelial cells, and neurons. Previous work demonstrated that the C5aR1 antagonist, PMX205, decreased amyloid pathology and suppressed cognitive d
Autor:
John P. Atkinson, Diego Mastroeni, Andrea J. Tenner, Maria I. Fonseca, Joseph Rogers, Richard E. Hauhart, Aimee Pierce, Shu-Hui Chu, William D. Brubaker, Elizabeth V. Clarke
Publikováno v:
Fonseca, MI; Chu, S; Pierce, AL; Brubaker, WD; Hauhart, RE; Mastroeni, D; et al.(2016). Analysis of the Putative Role of CR1 in Alzheimer's Disease: Genetic Association, Expression and Function. PLOS ONE, 11(2). doi: 10.1371/journal.pone.0149792. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/532355p9
PloS one, vol 11, iss 2
PLoS ONE
PLoS ONE, Vol 11, Iss 2, p e0149792 (2016)
PloS one, vol 11, iss 2
PLoS ONE
PLoS ONE, Vol 11, Iss 2, p e0149792 (2016)
Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the C3b
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::225649cd6dbeac70bc9fe61cb1f3aedf
http://www.escholarship.org/uc/item/532355p9
http://www.escholarship.org/uc/item/532355p9
Publikováno v:
Molecular Immunology. 102:219
Autor:
Shu-Hui Chu, Enrico Gratton, Rachel Cinco, Rick A. Wetsel, Maria I. Fonseca, Andrea J. Tenner
Publikováno v:
Molecular Immunology. 102:218