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Arundic acid ameliorates cerebral amyloidosis and gliosis in Alzheimer transgenic mice


Year of Publication:
Contact PI Name:
Takao Asano
Contact PI Affiliation:
Institute of Medical Science, Saitama Medical School, Kawagoe, Saitama, Japan
Takashi Mori, Terrence Town, Jun Tan, Nobumichi Yada, Yuko Horikoshi, Junki Yamamoto, Taiji Shimoda, Yoshihisa Kamanaka, Narito Tateishi
Primary Reference (PubMED ID):
Funding Source:
Maruki Memorial Research Foundation of Japan
NIH Ruth L Kirschstein National Research Service Award (NRSA)
Alzheimer's Association
Japanese Ministry of Scientific Research on Innovative Areas
Study Goal and Principal Findings:

Like microglia, reactive astrocytes produce a myriad of neurotoxic substances in various brain pathologies, such as Alzheimer’s disease (AD), trauma, and cerebral ischemia. Among the numerous products of reactive astrocytes, attention has recently been directed toward the possible detrimental role of S100B, because the protein has been shown to be highly expressed along with the progression of brain damage and to exert neurotoxic effects at high concentrations. The present study aimed to examine the possible role of astrocyte-derived S100B in the progression of cerebral amyloidosis and gliosis in transgenic mice overproducing mutant amyloid precursor protein (Tg APPsw mice, line 2576). For this purpose, arundic acid (Ono Pharmaceutical Co., Ltd., Mishima, Osaka, Japan), which is known to negatively regulate astrocyte synthesis of S100B, was orally administered to Tg APPsw mice for 6 months from 12 months of age, and the effects of the agent on the above parameters were examined. Here, we report that β-amyloid deposits along with amyloid-β peptide/S100B levels, as well as β-amyloid plaque-associated reactive gliosis (astrocytosis and microgliosis), were significantly ameliorated in arundic acid treated Tg APPsw mice relative to vehicle-treated Tg APPsw mice at 19 months of age. Based on the above results, arundic acid is considered to deserve further exploration as a promising therapeutic agent for AD.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Small Molecule
Therapeutic Agent:
Arundic Acid
Therapeutic Target:
S100 Calcium-Binding Protein B (S100B)

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest


Outcome Measured
Outcome Parameters
beta Amyloid Deposits
Activated Astrocytes
beta Amyloid Load
Dense-core/Compact Plaques
Activated Microglia
Glial Fibrillary Acidic Protein (GFAP)
S100 Calcium-Binding Protein B (S100B)
Brain-Detergent Soluble beta Amyloid Peptide 40
Brain-Detergent Soluble beta Amyloid Peptide 42
Microglial Activation Markers
Brain-beta Amyloid Deposits
beta Amyloid Load
Activated Microglia
Activated Astrocytes
Target Engagement (Inhibition S100 Calcium-Binding Protein B Expression)