Abstract:
:The focus of this study is the expression of Toll-like receptor-3 (TLR-3), a receptor for double-stranded RNA, in human brains affected by Alzheimer's disease (AD) pathology. Toll-like receptors are a family of pattern recognition molecules primarily involved in host defenses to microbial pathogens, but roles in neurodegenerative disease have also been shown, as amyloid beta (Aβ) can be a ligand for TLR-2 and -4 and α-synuclein for TLR-1 and TLR-2, while TLR-9 activation promotes Aβ removal. However, involvement of TLR-3 in AD has not been rigorously studied. Immunohistochemical analyses in human temporal cortical sections with a validated antibody for TLR-3 predominantly identified microglia, particularly strongly in cells associated with amyloid plaques, also brain vascular endothelial cells and subsets of astrocytes, but not neurons or p62-immunoreactive structures. Microglial TLR-3 colocalized with the endosomal/lysosomal marker CD68, which identifies phagocytic cells. Quantitative analyses of neuropathologically-staged human brain middle temporal gyrus samples using immunohistochemistry and mRNA expression methods demonstrated increased TLR-3 immunoreactivity and increased TLR-3 mRNA in AD compared to non-demented cases. There were significant positive correlations between TLR-3 mRNA levels and plaque or tangle loads in both series of samples. Increased expression of interferon beta (IFN-β) and interferon regulatory factor (IRF)-3 mRNA, two factors induced by TLR-3 signaling, were detected in the AD cases. Increased expression of TLR-4 and TLR-9 mRNA was also observed in these same samples, but not TLR-2. In vitro cultured human brain microglia responses to Aβ inflammatory activation were not altered by TLR-3 activation with activator polyinosinic;polycytidylic acid (poly I:C), while human brain endothelial cells showed reduction in responses when stimulated with both agents. Treatment of microglia with poly I:C did not increase their uptake and breakdown of Aβ.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Walker DG,Tang TM,Lue LFdoi
10.1016/j.expneurol.2018.07.016subject
Has Abstractpub_date
2018-11-01 00:00:00pages
91-106eissn
0014-4886issn
1090-2430pii
S0014-4886(18)30279-6journal_volume
309pub_type
杂志文章abstract::Golgi and computer morphometric analysis of neuronal dendrites was done on four cases, one each of Tay-Sachs disease, infantile type 2 sialidosis, Hurler's syndrome, and Sanfilippo's syndrome. There were large meganeurites on pyramidal neurons in Tay-Sachs disease, and small ones in Hurler's and Sanfilippo's syndromes...
journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
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pub_type: 杂志文章,评审
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journal_title:Experimental neurology
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2003.10.002
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(87)90065-3
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1998.7005
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pub_type: 杂志文章
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journal_title:Experimental neurology
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pub_type: 杂志文章
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
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