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Goll_2014_Neurodegener.Dis_13_58

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Title : Sustained Alzheimer's amyloid pathology in myeloid differentiation protein-88-deficient APPswe\/PS1 mice - Goll_2014_Neurodegener.Dis_13_58
Author(s) : Goll Y , Bekenstein U , Barbash S , Greenberg DS , Zangen R , Shoham S , Soreq H
Ref : Neurodegener Dis , 13 :58 , 2014
Abstract :

BACKGROUND: Most Alzheimer's disease (AD) cases arise sporadically and may involve innate immune activation of microglial expressed Toll-like receptors regulated through the myeloid differentiation protein 88 (MyD88) pathway. OBJECTIVE: It was the aim of this study to test the innate immune involvement in AD pathology.
METHODS: We mated APPsw/PS1DeltaE9 mice with MyD88-deficient mice.
RESULTS: Progeny mice had similar levels of soluble amyloid-beta peptides, amyloid plaque density and neuroimmune staining patterns. However, double-transgenic mice did show a significantly reduced life expectancy. CONCLUSION: Our findings indicate that impaired innate immune responses may play a role in AD pathology.
PubMedSearch : Goll_2014_Neurodegener.Dis_13_58
PubMedID: 24192711

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Citations formats

Goll Y, Bekenstein U, Barbash S, Greenberg DS, Zangen R, Shoham S, Soreq H (2014)
Sustained Alzheimer's amyloid pathology in myeloid differentiation protein-88-deficient APPswe\/PS1 mice
Neurodegener Dis 13 :58

Goll Y, Bekenstein U, Barbash S, Greenberg DS, Zangen R, Shoham S, Soreq H (2014)
Neurodegener Dis 13 :58