PMID- 32973490
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1663-4365 (Print)
IS  - 1663-4365 (Electronic)
IS  - 1663-4365 (Linking)
VI  - 12
DP  - 2020
TI  - alpha-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1alpha Signaling 
      Pathway in P301S Mice.
PG  - 262
LID - 10.3389/fnagi.2020.00262 [doi]
LID - 262
AB  - The microtubule-associated protein tau is closely correlated with hypometabolism 
      in Alzheimer's disease (AD). alpha-lipoic acid (LA), which is a naturally occurring 
      cofactor in mitochondrial, has been shown to have properties that can inhibit the 
      tau pathology and neuronal damage in our previous research. However, if LA 
      affects glucose metabolism when it reverses tau pathology remains unclear, 
      especially concerning the potential mechanism. Therefore, we make a further study 
      using the P301S mouse model (a tauopathy and AD mouse model which overexpressing 
      fibrillary tau) to gain a clear idea of the aforementioned problems. Here, we 
      found chronic LA administration significantly increased glucose availability by 
      elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth 
      factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level 
      in P301S mouse brains. Meanwhile, we found that LA also promoted glycolysis by 
      directly upregulating hexokinase (HK) activity, indirectly by increasing 
      proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) and DNA repair 
      enzymes (OGG1/2 and MTH1). Further, we found the underlying mechanism of restored 
      glucose metabolism might involve in the activation of brain-derived neurotrophic 
      factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1alpha 
      (HIF-1alpha) signaling pathway by LA treatment.
CI  - Copyright (c) 2020 Zhang, Yan, Xu, Pang, Li, Yang, Fan, Wang, Yu, Guo and Ao.
FAU - Zhang, Yan-Hui
AU  - Zhang YH
AD  - School of Fundamental Sciences, China Medical University, Shenyang, China.
FAU - Yan, Xin-Zhu
AU  - Yan XZ
AD  - School of Fundamental Sciences, China Medical University, Shenyang, China.
FAU - Xu, Shuang-Feng
AU  - Xu SF
AD  - College of Life and Health Sciences, Northeastern University, Shenyang, China.
FAU - Pang, Zhong-Qiu
AU  - Pang ZQ
AD  - College of Life and Health Sciences, Northeastern University, Shenyang, China.
FAU - Li, Lin-Bo
AU  - Li LB
AD  - College of Life and Health Sciences, Northeastern University, Shenyang, China.
FAU - Yang, Yang
AU  - Yang Y
AD  - College of Life and Health Sciences, Northeastern University, Shenyang, China.
FAU - Fan, Yong-Gang
AU  - Fan YG
AD  - Institute of Health Science, China Medical University, Shenyang, China.
FAU - Wang, Zhuo
AU  - Wang Z
AD  - Institute of Health Science, China Medical University, Shenyang, China.
FAU - Yu, Xin
AU  - Yu X
AD  - Institute of Health Science, China Medical University, Shenyang, China.
FAU - Guo, Chuang
AU  - Guo C
AD  - College of Life and Health Sciences, Northeastern University, Shenyang, China.
FAU - Ao, Qiang
AU  - Ao Q
AD  - School of Fundamental Sciences, China Medical University, Shenyang, China.
LA  - eng
PT  - Journal Article
DEP - 20200821
PL  - Switzerland
TA  - Front Aging Neurosci
JT  - Frontiers in aging neuroscience
JID - 101525824
PMC - PMC7471806
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - glucose metabolism
OT  - hypoxia-inducible factor-1alpha
OT  - tau phosphorylation
OT  - alpha-lipoic acid
EDAT- 2020/09/26 06:00
MHDA- 2020/09/26 06:01
PMCR- 2020/01/01
CRDT- 2020/09/25 06:00
PHST- 2020/03/06 00:00 [received]
PHST- 2020/07/31 00:00 [accepted]
PHST- 2020/09/25 06:00 [entrez]
PHST- 2020/09/26 06:00 [pubmed]
PHST- 2020/09/26 06:01 [medline]
PHST- 2020/01/01 00:00 [pmc-release]
AID - 10.3389/fnagi.2020.00262 [doi]
PST - epublish
SO  - Front Aging Neurosci. 2020 Aug 21;12:262. doi: 10.3389/fnagi.2020.00262. 
      eCollection 2020.