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Prophylactic active immunization with a novel epitope vaccine improves cognitive ability by decreasing amyloid plaques and neuroinflammation in APP/PS1 transgenic mice.

Abstract：

:Both amyloid-β peptide (Aβ) deposition and neuroinflammation are considered to be early events that play pivotal roles in Alzheimer's disease (AD) pathogenesis and its associated cognitive impairment. Prophylactic anti-Aβ active immunotherapy is a promising therapeutic strategy for AD, if the Aβ-specific autoimmune responses to self T cell epitopes of Aβ can be avoided. This can be achieved by the use of antigen, which contains the B cell epitope of Aβ and excludes the Aβ-specific T cell epitope. In this study, we developed a novel peptide epitope vaccine, Aβ3-10-KLH, by coupling the B cell epitope Aβ3-10 to keyhole limpet hemocyanin (KLH) as the carrier protein, and subcutaneously injected it into 2.5-month-old APP/PS1 transgenic mice. Aβ3-10-KLH immunization induced high levels of anti-Aβ antibodies and significantly improved cognitive ability in APP/PS1 transgenic mice. Immunohistochemistry and immunofluorescence revealed that Aβ3-10-KLH immunization significantly reduced cerebral amyloid plaque formation and alleviated gliosis. The results indicate that Aβ3-10-KLH immunization successfully rescued cognitive impairment in APP/PS1 transgenic mice via decreasing cerebral Aβ deposition and neuroinflammation. Aβ3-10-KLH may potentially be safe and effective for prevention and treatment of AD.

journal_name

Neurosci Res

journal_title

Neuroscience research

authors

Ding L,Meng Y,Zhang HY,Yin WC,Yan Y,Cao YP

doi

10.1016/j.neures.2017.01.003

subject

Has Abstract

pub_date

2017-06-01 00:00:00

pages

7-14

eissn

0168-0102

issn

1872-8111

pii

S0168-0102(17)30035-4

journal_volume

119

pub_type

杂志文章

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