Abstract:
:Amyloid beta (A beta) immunization of amyloid precursor protein (APP)-transgenic (tg) mice with human A beta induces humoral immunity, however, the immune response to endogenous rodent A beta is unknown. Fourteen-month J20 APP-tg mice and non-tg littermates were immunized subcutaneously followed by chronic intranasal boosting with human or rodent A beta peptide and adjuvant LT(R192G). Rodent A beta-immunized APP-tg mice had anti-rodent A beta antibody levels of 257.8 micrograms/ml and those immunized with human A beta had anti-human A beta antibodies of 120.8 micrograms/ml. Non-tg littermates had anti-rodent and anti-human A beta antibody concentrations of 98.8 and 231.1 microgram/ml, respectively. Inter-species cross-reactivity was minimal. Anti-human A beta antibodies were predominately IgG1 and IgG2b, while anti-rodent A beta antibodies were equally IgG1, IgG2a, and IgG2b. Anti-human A beta antibodies recognized an epitope within human A beta1-9. Anti-rodent A beta antibodies did not stain Alzheimer's disease (AD) plaques but bound some plaques in APP-tg mice. Splenocytes proliferated modestly to their respective antigen and secreted low levels of IL-2 and IFN-gamma. Therefore, immunizing APP-tg and non-tg mice with rodent A beta resulted in a species-specific humoral response with modest T cell reactivity.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Seabrook TJ,Bloom JK,Iglesias M,Spooner ET,Walsh DM,Lemere CAdoi
10.1016/j.neurobiolaging.2003.12.008subject
Has Abstractpub_date
2004-10-01 00:00:00pages
1141-51issue
9eissn
0197-4580issn
1558-1497pii
S0197458004000284journal_volume
25pub_type
杂志文章abstract::We investigated the effect of apolipoprotein E (apoE) genotype on amyloid load in the frontal and cerebellar cortices of 24 patients with definite Alzheimer disease (AD) and 19 controls. Amyloid load was examined by using two methods: 1) acid-extractable amyloid beta-protein (A beta) and insoluble A beta levels of fro...
journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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更新日期:1997-07-01 00:00:00
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2013.12.009
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2013.01.009
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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abstract::The apolipoprotein E (ApoE) ε4 allele has consistently been established as an Alzheimer's disease (AD) risk factor, but its pathological contribution to AD is obscure. Certain butyrylcholinesterase (BuChE) polymorphisms together with the ApoE ε4 allele synergistically increase the risk of AD. In addition, AD risk fact...
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