Alpha-asarone Improves Cognitive Function of APP/PS1 Mice and Reducing Aβ42, P-tau and Neuroinflammation, and Promoting Neuron Survival in the Hippocampus
[Display omitted] •Alpha-asarone improves the cognitive function of APP/PS1 transgenic mice.•Alpha-asarone reduced Aβ42 and p-tau protein levels in the hippocampus.•Alpha-asarone reduced the brain GFAP expression and alleviated neuroinflammation.•Alpha-asarone decreased autophagosomes and promoted h...
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| Veröffentlicht in: | Neuroscience 2021-03, Vol.458, p.141-152 |
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| creator | Zeng, Lili Zhang, Di Liu, Qi Zhang, Jian Mu, Keman Gao, Xiaofeng Zhang, Kun Li, Hui Wang, Qiantao Zheng, Yongxiang Mao, Shengjun |
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•Alpha-asarone improves the cognitive function of APP/PS1 transgenic mice.•Alpha-asarone reduced Aβ42 and p-tau protein levels in the hippocampus.•Alpha-asarone reduced the brain GFAP expression and alleviated neuroinflammation.•Alpha-asarone decreased autophagosomes and promoted hippocampal neuron survival.•Alpha-asarone might be a promising drug candidate for the treatment of AD.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease most often characterized by memory impairment and cognitive decline. Alpha-asarone has been reported to have the potential to treat AD. Our previous studies have found that alpha-asarone improves aged rats’ cognitive function by alleviating neuronal excitotoxicity via type A gamma-aminobutyric acid (GABA) receptors. GABA level’s change, neuroinflammation, and dysfunctional autophagy are found to be associated with AD. However, the effect of alpha-asarone on cognitive function of APP/PS1 transgenic mice and its underlying mechanism in terms of aggregation of amyloid-β42 (Aβ42) and phosphorylated tau (p-tau), glutamic acid decarboxylase (GAD) level, neuroinflammation, and autophagy are unclear. Accordingly, we attempted to explore whether alpha-asarone improves AD mice’s cognitive function and alleviates pathological symptoms by regulating GAD level, inhibiting neuroinflammation, or restore autophagy. We found that alpha-asarone enhanced spatial learning memory and decreased Aβ42 and p-tau levels without influencing the GAD level in APP/PS1 transgenic mice. Also, it decreased the GFAP expression and reduced pro-inflammatory cytokines levels, thus alleviating neuroinflammation. Furthermore, alpha-asarone decreased the excess number of autophagosomes and promoted hippocampal neurons’ survival. In conclusion, the results confirmed the therapeutic effect of alpha-asarone on AD-related astrogliosis, dysfunctional autophagy, and neuronal damage, which indicates its great potential to treat AD. |
| doi_str_mv | 10.1016/j.neuroscience.2020.12.026 |
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•Alpha-asarone improves the cognitive function of APP/PS1 transgenic mice.•Alpha-asarone reduced Aβ42 and p-tau protein levels in the hippocampus.•Alpha-asarone reduced the brain GFAP expression and alleviated neuroinflammation.•Alpha-asarone decreased autophagosomes and promoted hippocampal neuron survival.•Alpha-asarone might be a promising drug candidate for the treatment of AD.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease most often characterized by memory impairment and cognitive decline. Alpha-asarone has been reported to have the potential to treat AD. Our previous studies have found that alpha-asarone improves aged rats’ cognitive function by alleviating neuronal excitotoxicity via type A gamma-aminobutyric acid (GABA) receptors. GABA level’s change, neuroinflammation, and dysfunctional autophagy are found to be associated with AD. However, the effect of alpha-asarone on cognitive function of APP/PS1 transgenic mice and its underlying mechanism in terms of aggregation of amyloid-β42 (Aβ42) and phosphorylated tau (p-tau), glutamic acid decarboxylase (GAD) level, neuroinflammation, and autophagy are unclear. Accordingly, we attempted to explore whether alpha-asarone improves AD mice’s cognitive function and alleviates pathological symptoms by regulating GAD level, inhibiting neuroinflammation, or restore autophagy. We found that alpha-asarone enhanced spatial learning memory and decreased Aβ42 and p-tau levels without influencing the GAD level in APP/PS1 transgenic mice. Also, it decreased the GFAP expression and reduced pro-inflammatory cytokines levels, thus alleviating neuroinflammation. Furthermore, alpha-asarone decreased the excess number of autophagosomes and promoted hippocampal neurons’ survival. In conclusion, the results confirmed the therapeutic effect of alpha-asarone on AD-related astrogliosis, dysfunctional autophagy, and neuronal damage, which indicates its great potential to treat AD.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/j.neuroscience.2020.12.026</identifier><language>eng</language><publisher>Elsevier Ltd</publisher><subject>alpha-asarone ; Alzheimer’s disease ; APP/PS1 transgenic mice ; autophagy ; neuroinflammation</subject><ispartof>Neuroscience, 2021-03, Vol.458, p.141-152</ispartof><rights>2020 IBRO</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c272t-71be8291f0ff1355478dfa4d99b1ccd37942b6c4b7cbee67beee47c84260b9df3</citedby><cites>FETCH-LOGICAL-c272t-71be8291f0ff1355478dfa4d99b1ccd37942b6c4b7cbee67beee47c84260b9df3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0306452220308058$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids></links><search><creatorcontrib>Zeng, Lili</creatorcontrib><creatorcontrib>Zhang, Di</creatorcontrib><creatorcontrib>Liu, Qi</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Mu, Keman</creatorcontrib><creatorcontrib>Gao, Xiaofeng</creatorcontrib><creatorcontrib>Zhang, Kun</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Wang, Qiantao</creatorcontrib><creatorcontrib>Zheng, Yongxiang</creatorcontrib><creatorcontrib>Mao, Shengjun</creatorcontrib><title>Alpha-asarone Improves Cognitive Function of APP/PS1 Mice and Reducing Aβ42, P-tau and Neuroinflammation, and Promoting Neuron Survival in the Hippocampus</title><title>Neuroscience</title><description>[Display omitted]
•Alpha-asarone improves the cognitive function of APP/PS1 transgenic mice.•Alpha-asarone reduced Aβ42 and p-tau protein levels in the hippocampus.•Alpha-asarone reduced the brain GFAP expression and alleviated neuroinflammation.•Alpha-asarone decreased autophagosomes and promoted hippocampal neuron survival.•Alpha-asarone might be a promising drug candidate for the treatment of AD.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease most often characterized by memory impairment and cognitive decline. Alpha-asarone has been reported to have the potential to treat AD. Our previous studies have found that alpha-asarone improves aged rats’ cognitive function by alleviating neuronal excitotoxicity via type A gamma-aminobutyric acid (GABA) receptors. GABA level’s change, neuroinflammation, and dysfunctional autophagy are found to be associated with AD. However, the effect of alpha-asarone on cognitive function of APP/PS1 transgenic mice and its underlying mechanism in terms of aggregation of amyloid-β42 (Aβ42) and phosphorylated tau (p-tau), glutamic acid decarboxylase (GAD) level, neuroinflammation, and autophagy are unclear. Accordingly, we attempted to explore whether alpha-asarone improves AD mice’s cognitive function and alleviates pathological symptoms by regulating GAD level, inhibiting neuroinflammation, or restore autophagy. We found that alpha-asarone enhanced spatial learning memory and decreased Aβ42 and p-tau levels without influencing the GAD level in APP/PS1 transgenic mice. Also, it decreased the GFAP expression and reduced pro-inflammatory cytokines levels, thus alleviating neuroinflammation. Furthermore, alpha-asarone decreased the excess number of autophagosomes and promoted hippocampal neurons’ survival. In conclusion, the results confirmed the therapeutic effect of alpha-asarone on AD-related astrogliosis, dysfunctional autophagy, and neuronal damage, which indicates its great potential to treat AD.</description><subject>alpha-asarone</subject><subject>Alzheimer’s disease</subject><subject>APP/PS1 transgenic mice</subject><subject>autophagy</subject><subject>neuroinflammation</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNqNUcFu1DAQtRBILIV_sDhxaLa249gJt9XS0kotRBTOluNMWq8SO9hJJL6Fv-BD-Cac3R44dg4z0sx7TzPzEHpPyZYSKi4OWwdz8NFYcAa2jLA0YFvCxAu0oaXMM1lw_hJtSE5ExgvGXqM3MR5IioLnG_R714-POtNRB-8A3wxj8AtEvPcPzk52AXw1OzNZ77Dv8K6uL-p7iu-sAaxdi79BOxvrHvDu7x_OznGdTXo-Tr6se1nX9XoY9Mo_P7br4Ac_rYwjwOH7OSx20T22Dk-PgK_tOHqjh3GOb9GrTvcR3j3VM_Tj6vL7_jq7_fr5Zr-7zQyTbMokbaBkFe1I19G8KLgs207ztqoaakyby4qzRhjeSNMACJkScGlKzgRpqrbLz9CHk266_ecMcVKDjQb6Xjvwc1SMS1GIkgqeoB9PUJOeHgN0agx20OGXokStjqiD-t8RtTqiKFPJkUT-dCJDOmaxENQTqrUBzKRab58j8w-vtJ6F</recordid><startdate>20210315</startdate><enddate>20210315</enddate><creator>Zeng, Lili</creator><creator>Zhang, Di</creator><creator>Liu, Qi</creator><creator>Zhang, Jian</creator><creator>Mu, Keman</creator><creator>Gao, Xiaofeng</creator><creator>Zhang, Kun</creator><creator>Li, Hui</creator><creator>Wang, Qiantao</creator><creator>Zheng, Yongxiang</creator><creator>Mao, Shengjun</creator><general>Elsevier Ltd</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20210315</creationdate><title>Alpha-asarone Improves Cognitive Function of APP/PS1 Mice and Reducing Aβ42, P-tau and Neuroinflammation, and Promoting Neuron Survival in the Hippocampus</title><author>Zeng, Lili ; Zhang, Di ; Liu, Qi ; Zhang, Jian ; Mu, Keman ; Gao, Xiaofeng ; Zhang, Kun ; Li, Hui ; Wang, Qiantao ; Zheng, Yongxiang ; Mao, Shengjun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c272t-71be8291f0ff1355478dfa4d99b1ccd37942b6c4b7cbee67beee47c84260b9df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>alpha-asarone</topic><topic>Alzheimer’s disease</topic><topic>APP/PS1 transgenic mice</topic><topic>autophagy</topic><topic>neuroinflammation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Lili</creatorcontrib><creatorcontrib>Zhang, Di</creatorcontrib><creatorcontrib>Liu, Qi</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Mu, Keman</creatorcontrib><creatorcontrib>Gao, Xiaofeng</creatorcontrib><creatorcontrib>Zhang, Kun</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Wang, Qiantao</creatorcontrib><creatorcontrib>Zheng, Yongxiang</creatorcontrib><creatorcontrib>Mao, Shengjun</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Lili</au><au>Zhang, Di</au><au>Liu, Qi</au><au>Zhang, Jian</au><au>Mu, Keman</au><au>Gao, Xiaofeng</au><au>Zhang, Kun</au><au>Li, Hui</au><au>Wang, Qiantao</au><au>Zheng, Yongxiang</au><au>Mao, Shengjun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alpha-asarone Improves Cognitive Function of APP/PS1 Mice and Reducing Aβ42, P-tau and Neuroinflammation, and Promoting Neuron Survival in the Hippocampus</atitle><jtitle>Neuroscience</jtitle><date>2021-03-15</date><risdate>2021</risdate><volume>458</volume><spage>141</spage><epage>152</epage><pages>141-152</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><abstract>[Display omitted]
•Alpha-asarone improves the cognitive function of APP/PS1 transgenic mice.•Alpha-asarone reduced Aβ42 and p-tau protein levels in the hippocampus.•Alpha-asarone reduced the brain GFAP expression and alleviated neuroinflammation.•Alpha-asarone decreased autophagosomes and promoted hippocampal neuron survival.•Alpha-asarone might be a promising drug candidate for the treatment of AD.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease most often characterized by memory impairment and cognitive decline. Alpha-asarone has been reported to have the potential to treat AD. Our previous studies have found that alpha-asarone improves aged rats’ cognitive function by alleviating neuronal excitotoxicity via type A gamma-aminobutyric acid (GABA) receptors. GABA level’s change, neuroinflammation, and dysfunctional autophagy are found to be associated with AD. However, the effect of alpha-asarone on cognitive function of APP/PS1 transgenic mice and its underlying mechanism in terms of aggregation of amyloid-β42 (Aβ42) and phosphorylated tau (p-tau), glutamic acid decarboxylase (GAD) level, neuroinflammation, and autophagy are unclear. Accordingly, we attempted to explore whether alpha-asarone improves AD mice’s cognitive function and alleviates pathological symptoms by regulating GAD level, inhibiting neuroinflammation, or restore autophagy. We found that alpha-asarone enhanced spatial learning memory and decreased Aβ42 and p-tau levels without influencing the GAD level in APP/PS1 transgenic mice. Also, it decreased the GFAP expression and reduced pro-inflammatory cytokines levels, thus alleviating neuroinflammation. Furthermore, alpha-asarone decreased the excess number of autophagosomes and promoted hippocampal neurons’ survival. In conclusion, the results confirmed the therapeutic effect of alpha-asarone on AD-related astrogliosis, dysfunctional autophagy, and neuronal damage, which indicates its great potential to treat AD.</abstract><pub>Elsevier Ltd</pub><doi>10.1016/j.neuroscience.2020.12.026</doi><tpages>12</tpages></addata></record> |
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| subjects | alpha-asarone Alzheimer’s disease APP/PS1 transgenic mice autophagy neuroinflammation |
| title | Alpha-asarone Improves Cognitive Function of APP/PS1 Mice and Reducing Aβ42, P-tau and Neuroinflammation, and Promoting Neuron Survival in the Hippocampus |
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