PMID- 29710724
OWN - NLM
STAT- MEDLINE
DCOM- 20190610
LR  - 20191210
IS  - 1875-8908 (Electronic)
IS  - 1387-2877 (Print)
IS  - 1387-2877 (Linking)
VI  - 63
IP  - 3
DP  - 2018
TI  - Moringa Oleifera Alleviates Homocysteine-Induced Alzheimer's Disease-Like 
      Pathology and Cognitive Impairments.
PG  - 1141-1159
LID - 10.3233/JAD-180091 [doi]
AB  - Alzheimer's disease (AD) is multifactorial with unclear etiopathology. Due to the 
      complexity of AD, many attempted single therapy treatments, like Abeta immunization, 
      have generally failed. Therefore, there is a need for drugs with multiple 
      benefits. Naturally occurring phytochemicals with neuroprotective, 
      anti-amyloidogenic, antioxidative, and anti-inflammatory properties could be a 
      possible way out. In this study, the effect of Moringa oleifera (MO), a naturally 
      occurring plant with high antioxidative, anti-inflammatory, and neuroprotective 
      effects, was evaluated on hyperhomocysteinemia (HHcy) induced AD-like pathology 
      in rats. Homocysteine (Hcy) injection for 14 days was used to induce AD-like 
      pathology. Simultaneous MO extract gavage followed the injection as a preventive 
      treatment or, after injection completion, MO gavage was performed for another 14 
      days as a curative treatment. MO was found to not only prevent but also rescue 
      the oxidative stress and cognitive impairments induced by Hcy treatment. 
      Moreover, MO recovered the decreased synaptic proteins PSD93, PSD95, Synapsin 1 
      and Synaptophysin, and improved neurodegeneration. Interestingly, MO decreased 
      the Hyc-induced tau hyperphosphorylation at different sites including S-199, 
      T-231, S-396, and S-404, and at the same time decreased Abeta production through 
      downregulation of BACE1. These effects in HHcy rats were accompanied by a 
      decrease in calpain activity under MO treatment, supporting that calpain 
      activation might be involved in AD pathogenesis in HHcy rats. Taken together, our 
      data, for the first time, provided evidence that MO alleviates tau 
      hyperphosphorylation and Abeta pathology in a HHcy AD rat model. This and previous 
      other studies support MO as a good candidate for, and could provide new insights 
      into, the treatment of AD and other tauopathies.
FAU - Mahaman, Yacoubou Abdoul Razak
AU  - Mahaman YAR
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Huang, Fang
AU  - Huang F
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Wu, Mengjuan
AU  - Wu M
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Wang, Yuman
AU  - Wang Y
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Wei, Zhen
AU  - Wei Z
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Bao, Jian
AU  - Bao J
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Salissou, Maibouge Tanko Mahamane
AU  - Salissou MTM
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Ke, Dan
AU  - Ke D
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Wang, Qun
AU  - Wang Q
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Liu, Rong
AU  - Liu R
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Wang, Jian-Zhi
AU  - Wang JZ
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
AD  - Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
FAU - Zhang, Bin
AU  - Zhang B
AD  - Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount 
      Sinai, New York, NY, USA.
FAU - Chen, Dan
AU  - Chen D
AD  - School of Public Health, Wuhan University of Science and Technology, Wuhan, 
      China.
FAU - Wang, Xiaochuan
AU  - Wang X
AD  - Department of Pathophysiology, School of Basic Medicine, Key Laboratory of 
      Education Ministry of China for Neurological Disorders, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
AD  - Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Alzheimers Dis
JT  - Journal of Alzheimer's disease : JAD
JID - 9814863
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Peptide Fragments)
RN  - 0 (Plant Extracts)
RN  - 0 (amyloid beta-protein (1-42))
RN  - 0 (tau Proteins)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - EC 3.4.- (Amyloid Precursor Protein Secretases)
RN  - EC 3.4.23.- (Aspartic Acid Endopeptidases)
RN  - EC 3.4.23.46 (Bace1 protein, rat)
SB  - IM
MH  - Alzheimer Disease/chemically induced/*drug therapy/*pathology
MH  - Amyloid Precursor Protein Secretases/metabolism
MH  - Amyloid beta-Peptides/metabolism
MH  - Amyloid beta-Protein Precursor/metabolism
MH  - Animals
MH  - Aspartic Acid Endopeptidases/metabolism
MH  - Brain/drug effects/metabolism
MH  - *Cognition Disorders/chemically induced/drug therapy
MH  - Disease Models, Animal
MH  - Homocysteine/*toxicity
MH  - Male
MH  - Maze Learning/drug effects
MH  - *Moringa oleifera
MH  - Nerve Tissue Proteins/metabolism
MH  - Neurons/pathology/ultrastructure
MH  - Oxidative Stress/drug effects
MH  - Peptide Fragments/metabolism
MH  - Phosphorylation/drug effects
MH  - Plant Extracts/*therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Silver Staining
MH  - tau Proteins/metabolism
PMC - PMC6004908
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - BACE1
OT  - Moringa oleifera (MO)
OT  - amyloid-beta
OT  - calpain
OT  - homocysteine
OT  - tau
EDAT- 2018/05/02 06:00
MHDA- 2019/06/14 06:00
PMCR- 2018/06/18
CRDT- 2018/05/02 06:00
PHST- 2018/05/02 06:00 [pubmed]
PHST- 2019/06/14 06:00 [medline]
PHST- 2018/05/02 06:00 [entrez]
PHST- 2018/06/18 00:00 [pmc-release]
AID - JAD180091 [pii]
AID - 10.3233/JAD-180091 [doi]
PST - ppublish
SO  - J Alzheimers Dis. 2018;63(3):1141-1159. doi: 10.3233/JAD-180091.