Therapeutic Effects of Aripiprazole in the 5xFAD Alzheimer's Disease Mouse Model
- Authors
- Jeong, Ye Ji; Son, Yeonghoon; Park, Hye-Jin; Oh, Se Jong; Choi, Jae Yong; Ko, Young-Gyu; Lee, Hae-June
- Issue Date
- 9월-2021
- Publisher
- MDPI
- Keywords
- Alzheimer' s disease mice; FDG-PET; aripiprazole; beta A pathology; therapeutic agent
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.22, no.17
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Volume
- 22
- Number
- 17
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/136459
- DOI
- 10.3390/ijms22179374
- ISSN
- 1661-6596
- Abstract
- Global aging has led to growing health concerns posed by Alzheimer's disease (AD), the most common type of dementia. Aripiprazole is an atypical FDA-approved anti-psychotic drug with potential against AD. To investigate its therapeutic effects on AD pathology, we administered aripiprazole to 5xFAD AD model mice and examined beta-amyloid (beta A)-induced AD-like phenotypes, including beta A production, neuroinflammation, and cerebral glucose metabolism. Aripiprazole administration significantly decreased beta A accumulation in the brains of 5xFAD AD mice. Aripiprazole significantly modified amyloid precursor protein processing, including carboxyl-terminal fragment beta and beta A, a disintegrin and metalloproteinase domain-containing protein 10, and beta-site APP cleaving enzyme 1, as determined by Western blotting. Neuroinflammation, as evidenced by ionized calcium binding adapter molecule 1 and glial fibrillary acidic protein upregulation was dramatically inhibited, and the neuron cell layer of the hippocampal CA1 region was preserved following aripiprazole administration. In 18F-fluorodeoxyglucose positron emission tomography, after receiving aripiprazole, 5xFAD mice showed a significant increase in glucose uptake in the striatum, thalamus, and hippocampus compared to vehicle-treated AD mice. Thus, aripiprazole effectively alleviated beta A lesions and prevented the decline of cerebral glucose metabolism in 5xFAD AD mice, suggesting its potential for beta A metabolic modification and highlighting its therapeutic effect over AD progression.
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