Ailanthus altissima Extract Ameliorates Cognitive Decline and Neurodegeneration in an Aluminum Chloride–Induced Rat Model of Alzheimer's Disease.

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Title: Ailanthus altissima Extract Ameliorates Cognitive Decline and Neurodegeneration in an Aluminum Chloride–Induced Rat Model of Alzheimer's Disease.
Authors: Gravandi, Mohammad Mehdi1,2 (AUTHOR), Elieh-Ali-Komi, Daniel3,4 (AUTHOR), Amirian, Roshanak2 (AUTHOR), Hosseini, Seyede Zahra1 (AUTHOR), Alavi, Seyede Darya1 (AUTHOR), Shirooie, Samira1 (AUTHOR), Kiani, Amir1 (AUTHOR) akiani@kums.ac.ir, Farzaei, Mohammad Hosein1 (AUTHOR) mh_farzaei@kums.ac.ir, Bose, Anupama (AUTHOR) abose@wiley.com
Source: Journal of Food Biochemistry. 4/3/2026, Vol. 2026, p1-10. 10p.
Subjects: Alzheimer's disease, Neurodegeneration, Amyloid beta-protein, Neuroprotective agents, Aluminum chloride, Animal disease models, Cognition disorders
Abstract: Background: The extract of Ailanthus altissima possesses anti‐inflammatory and neuroprotective properties. We aimed to investigate its effectiveness in mitigating the AlCl3‐induced Alzheimer's disease in a rat model. Methods: A total of 32 adult male Wistar rats were divided into 4 groups each consisting of 8 rats. The control group received saline and the AlCl3 group received AlCl3 (0.2 cc 100 mg/kg, intraperitoneal) for 14 days. Two other groups received either 50 or 100 mg/kg of Ailanthus altissima after AlCl3 treatment. Behavioral tests including open field test (OFT), elevated plus maze, and passive avoidance tests were performed. Nuclear factor kappa B (NF‐κB), glial filamentous acidic protein (GFAP), and amyloid beta were stained using immunohistochemistry (IHC) in the hippocampus. Results: AlCl3 administration caused significant memory impairment, and treatment with Ailanthus altissima extract effectively mitigated these deficits in a dose‐dependent manner. The effects were dose‐dependent, and the group receiving 100 mg/kg extract presented the most significant results in the conducted behavioral tests. The IHC results for NF‐κB showed that treatment with 50 mg/kg of extract significantly reduced NF‐κB expression compared with the AlCl3 group (6.64% vs. 13.3%, respectively, p < 0.05). A higher dose of 100 mg/kg resulted in an even greater reduction (4.45% vs. 13.3%, p < 0.01). Extract treatment reduced GFAP positivity in a dose‐dependent manner, with the 50 mg/kg group showing a significant decrease to 11.8% (p < 0.05). The 100 mg/kg group demonstrated an even more substantial reduction to 7.7% (p < 0.01) compared with the AlCl3 group (18.65%). Amyloid beta positivity was critically reduced in the 100 mg/kg‐receiving group. Conclusions: Ailanthus altissima extract shows potential as a neuroprotective extract. It counteracts AlCl3‐induced behavioral and neuropathological changes, suggesting promising therapeutic applications. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Food Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Label: Title
  Group: Ti
  Data: Ailanthus altissima Extract Ameliorates Cognitive Decline and Neurodegeneration in an Aluminum Chloride–Induced Rat Model of Alzheimer&#39;s Disease.
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  Data: &lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Gravandi%2C+Mohammad+Mehdi%22&quot;&gt;Gravandi, Mohammad Mehdi&lt;/searchLink&gt;&lt;relatesTo&gt;1,2&lt;/relatesTo&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Elieh-Ali-Komi%2C+Daniel%22&quot;&gt;Elieh-Ali-Komi, Daniel&lt;/searchLink&gt;&lt;relatesTo&gt;3,4&lt;/relatesTo&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Amirian%2C+Roshanak%22&quot;&gt;Amirian, Roshanak&lt;/searchLink&gt;&lt;relatesTo&gt;2&lt;/relatesTo&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Hosseini%2C+Seyede+Zahra%22&quot;&gt;Hosseini, Seyede Zahra&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Alavi%2C+Seyede+Darya%22&quot;&gt;Alavi, Seyede Darya&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Shirooie%2C+Samira%22&quot;&gt;Shirooie, Samira&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Kiani%2C+Amir%22&quot;&gt;Kiani, Amir&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt; (AUTHOR)&lt;i&gt; akiani@kums.ac.ir&lt;/i&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Farzaei%2C+Mohammad+Hosein%22&quot;&gt;Farzaei, Mohammad Hosein&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt; (AUTHOR)&lt;i&gt; mh_farzaei@kums.ac.ir&lt;/i&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Bose%2C+Anupama%22&quot;&gt;Bose, Anupama&lt;/searchLink&gt; (AUTHOR)&lt;i&gt; abose@wiley.com&lt;/i&gt;
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22Journal+of+Food+Biochemistry%22&quot;&gt;Journal of Food Biochemistry&lt;/searchLink&gt;. 4/3/2026, Vol. 2026, p1-10. 10p.
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  Data: &lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Alzheimer&#39;s+disease%22&quot;&gt;Alzheimer&#39;s disease&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Neurodegeneration%22&quot;&gt;Neurodegeneration&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Amyloid+beta-protein%22&quot;&gt;Amyloid beta-protein&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Neuroprotective+agents%22&quot;&gt;Neuroprotective agents&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Aluminum+chloride%22&quot;&gt;Aluminum chloride&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Animal+disease+models%22&quot;&gt;Animal disease models&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Cognition+disorders%22&quot;&gt;Cognition disorders&lt;/searchLink&gt;
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background: The extract of Ailanthus altissima possesses anti‐inflammatory and neuroprotective properties. We aimed to investigate its effectiveness in mitigating the AlCl3‐induced Alzheimer&#39;s disease in a rat model. Methods: A total of 32 adult male Wistar rats were divided into 4 groups each consisting of 8 rats. The control group received saline and the AlCl3 group received AlCl3 (0.2 cc 100 mg/kg, intraperitoneal) for 14 days. Two other groups received either 50 or 100 mg/kg of Ailanthus altissima after AlCl3 treatment. Behavioral tests including open field test (OFT), elevated plus maze, and passive avoidance tests were performed. Nuclear factor kappa B (NF‐κB), glial filamentous acidic protein (GFAP), and amyloid beta were stained using immunohistochemistry (IHC) in the hippocampus. Results: AlCl3 administration caused significant memory impairment, and treatment with Ailanthus altissima extract effectively mitigated these deficits in a dose‐dependent manner. The effects were dose‐dependent, and the group receiving 100 mg/kg extract presented the most significant results in the conducted behavioral tests. The IHC results for NF‐κB showed that treatment with 50 mg/kg of extract significantly reduced NF‐κB expression compared with the AlCl3 group (6.64% vs. 13.3%, respectively, p &lt; 0.05). A higher dose of 100 mg/kg resulted in an even greater reduction (4.45% vs. 13.3%, p &lt; 0.01). Extract treatment reduced GFAP positivity in a dose‐dependent manner, with the 50 mg/kg group showing a significant decrease to 11.8% (p &lt; 0.05). The 100 mg/kg group demonstrated an even more substantial reduction to 7.7% (p &lt; 0.01) compared with the AlCl3 group (18.65%). Amyloid beta positivity was critically reduced in the 100 mg/kg‐receiving group. Conclusions: Ailanthus altissima extract shows potential as a neuroprotective extract. It counteracts AlCl3‐induced behavioral and neuropathological changes, suggesting promising therapeutic applications. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: &lt;i&gt;Copyright of Journal of Food Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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    Identifiers:
      – Type: doi
        Value: 10.1155/jfbc/7471140
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 10
        StartPage: 1
    Subjects:
      – SubjectFull: Alzheimer's disease
        Type: general
      – SubjectFull: Neurodegeneration
        Type: general
      – SubjectFull: Amyloid beta-protein
        Type: general
      – SubjectFull: Neuroprotective agents
        Type: general
      – SubjectFull: Aluminum chloride
        Type: general
      – SubjectFull: Animal disease models
        Type: general
      – SubjectFull: Cognition disorders
        Type: general
    Titles:
      – TitleFull: Ailanthus altissima Extract Ameliorates Cognitive Decline and Neurodegeneration in an Aluminum Chloride–Induced Rat Model of Alzheimer's Disease.
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            – D: 03
              M: 04
              Text: 4/3/2026
              Type: published
              Y: 2026
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