2. Academic Validation
  3. Avenanthramide-C Restores Impaired Plasticity and Cognition in Alzheimer's Disease Model Mice

Avenanthramide-C Restores Impaired Plasticity and Cognition in Alzheimer's Disease Model Mice

  • Mol Neurobiol. 2020 Jan;57(1):315-330. doi: 10.1007/s12035-019-01707-5.
Vijay Sankar Ramasamy 1 2,  Manikandan Samidurai 1 2,  Hyung Joon Park 3,  Ming Wang 1 2,  Ra Young Park 4,  Seon Young Yu 5,  Hee Kyung Kang 1,  Semi Hong 3,  Won-Seok Choi 6,  Yu Young Lee 7,  Hyung-Seok Kim 8 9,  Jihoon Jo 10 11 12 13
Affiliations

Affiliations

  • 1 NeuroMedical Convergence Laboratory, Biomedical Research Institute, Chonnam National University Hospital, Jebong-ro, Gwangju, 501-757, Republic of Korea.
  • 2 Department of Biomedical Sciences, BK21 PLUS Center for Creative Biomedical Scientists at Chonnam National University, Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, 501-757, Republic of Korea.
  • 3 School of Biological Sciences and Technology, College of Natural Sciences, Chonnam National University, Gwangju, 500-757, Republic of Korea.
  • 4 Bio-Medical treatment technology development projects, Institute for Biomedical Science, Chonnam National University Hwasun Hospital, Gwangju, Republic of Korea.
  • 5 Forensic Medicine Division, National Forensic Service Daegu Institute, Daegu, 39872, Republic of Korea.
  • 6 School of Biological Sciences and Technology, College of Natural Sciences, Chonnam National University, Gwangju, 500-757, Republic of Korea. choiw@chonnam.ac.kr.
  • 7 Department of Central Area, National Institute of Crop Science, Rural Development Administration, Suwon, 16429, Republic of Korea. leeyy260@korea.kr.
  • 8 Department of Forensic Medicine, Chonnam National University Medical School, Gwangju, South Korea. veritas@chonnam.ac.kr.
  • 9 Center for Creative Biomedical Scientists, Chonnam National University Medical School, Gwangju, 501-757, Republic of Korea. veritas@chonnam.ac.kr.
  • 10 NeuroMedical Convergence Laboratory, Biomedical Research Institute, Chonnam National University Hospital, Jebong-ro, Gwangju, 501-757, Republic of Korea. Jihoon.Jo@chonnam.ac.kr.
  • 11 Department of Biomedical Sciences, BK21 PLUS Center for Creative Biomedical Scientists at Chonnam National University, Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, 501-757, Republic of Korea. Jihoon.Jo@chonnam.ac.kr.
  • 12 Department of Neurology, Chonnam National University Medical School, Gwangju, 501-757, Republic of Korea. Jihoon.Jo@chonnam.ac.kr.
  • 13 NeuroMedical Convergence Laboratory, Department of Biomedical Sciences and Neurology, Chonnam National University Medical School, Gwangju, 501-746, Republic of Korea. Jihoon.Jo@chonnam.ac.kr.
PMID: 31332763 DOI: 10.1007/s12035-019-01707-5
Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline and dementia with no effective treatment. Here, we investigated a novel compound from oats named avenanthramide-C (Avn-C), on AD-related memory impairment and behavioral deficits in transgenic mouse models. Acute hippocampal slices of wild-type or AD transgenic mice were treated with Avn-C in the presence or absence of oligomeric Aβ42. LTP analyses and immunoblotting were performed to assess the effect of Avn-C on Aβ-induced memory impairment. To further investigate the effect of Avn-C on impaired memory and Aβ pathology, two different AD transgenic mice (Tg2576 and 5XFAD) models were orally treated with either Avn-C or vehicle for 2 weeks. They were then assessed for the effect of the treatment on neuropathologies and behavioral impairments. Avn-C reversed impaired LTP in both ex vivo- and in vivo-treated AD mice hippocampus. Oral administration (6 mg/kg per day) for 2 weeks in AD mice leads to improved recognition and spatial memory, reduced Caspase-3 cleavage, reversed neuroinflammation, and to accelerated glycogen synthase kinase-3β (pS9GSK-3β) and interleukin (IL-10) levels. Avn-C exerts its beneficial effects by binding to α1A adrenergic receptors to stimulate adenosine monophosphate-activated kinase (AMPK). All of the beneficial effects of Avn-C on LTP retrieval could be blocked by prazosin hydrochloride, a specific inhibitor of α1A adrenergic receptors. Our findings provide evidence, for the first time, that oats' Avn-C reverses the AD-related memory and behavioral impairments, and establish it as a potential candidate for Alzheimer's disease drug development.

Keywords

Alzheimer’s disease; Amyloid-β; Avn-C; LTP; Memory; Mouse model; Oats.

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