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Retracted: Mechanisms and effects of curcumin on spatial learning and memory improvement in APPswe/PS1dE9 mice
Author(s) -
Wang Pengwen,
Su Caixin,
Li Ruisheng,
Wang Hong,
Ren Ying,
Sun Haiyun,
Yang Jinduo,
Sun Jianning,
Shi Jing,
Tian Jinzhou,
Jiang Shucui
Publication year - 2014
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23322
Subject(s) - curcumin , insulin degrading enzyme , neprilysin , genetically modified mouse , pharmacology , amyloid (mycology) , presenilin , hippocampal formation , morris water navigation task , amyloid precursor protein , chemistry , transgene , alzheimer's disease , medicine , biochemistry , enzyme , disease , inorganic chemistry , gene
Evidence suggests that curcumin, the phytochemical agent in the spice turmeric, might be a potential therapy for Alzheimer's disease (AD). Its antioxidant, anti‐inflammatory properties have been investigated extensively. Studies have also shown that curcumin can reduce amyloid pathology in AD. The underlying mechanism, however, is complex and is still being explored. In this study, we used the APPswe/PS1dE9 double transgenic mice, an AD model, to investigate the effects and mechanisms of curcumin in the prevention and treatment of AD. The water maze test indicated that curcumin can improve spatial learning and memory ability in mice. Immunohistochemical staining and Western blot analysis were used to test major proteins in β‐amyloid aggregation, β‐amyloid production, and β‐amyloid clearance. Data showed that, 3 months after administration, curcumin treatment reduced Aβ 40 , Aβ 42 , and aggregation of Aβ‐derived diffusible ligands in the mouse hippocampal CA1 area; reduced the expression of the γ‐secretase component presenilin‐2; and increased the expression of β‐amyloid‐degrading enzymes, including insulin‐degrading enzymes and neprilysin. This evidence suggests that curcumin, as a potential AD therapeutic method, can reduce β‐amyloid pathological aggregation, possibly through mechanisms that prevent its production by inhibiting presenilin‐2 and/or by accelerating its clearance by increasing degrading enzymes such as insulin‐degrading enzyme and neprilysin. © 2013 Wiley Periodicals, Inc.