PMID- 23157378
OWN - NLM
STAT- MEDLINE
DCOM- 20130312
LR  - 20220318
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 124
IP  - 3
DP  - 2013 Feb
TI  - Betaine attenuates Alzheimer-like pathological changes and memory deficits 
      induced by homocysteine.
PG  - 388-96
LID - 10.1111/jnc.12094 [doi]
AB  - Hyperhomocysteinemia (Hhcy) may induce memory deficits with beta-amyloid (Abeta) 
      accumulation and tau hyperphosphorylation. Simultaneous supplement of folate and 
      vitamin B12 partially restored the plasma homocysteine level and attenuated tau 
      hyperphosphorylation, Abeta accumulation and memory impairments induced by Hhcy. 
      However, folate and vitamin B12 treatment have no effects on Hhcy which has the 
      methylenetetrahydrofolate reductase genotype mutation. In this study, we 
      investigated the effects of simultaneous supplement of betaine on Alzheimer-like 
      pathological changes and memory deficits in hyperhomocysteinemic rats after a 
      2-week induction by vena caudalis injection of homocysteine (Hcy). We found that 
      supplementation of betaine could ameliorate the Hcy-induced memory deficits, 
      enhance long-term potentiation (LTP) and increase dendritic branches numbers and 
      the density of the dendritic spines, with up-regulation of NR1, NR2A, 
      synaptotagmin, synaptophysin, and phosphorylated synapsin I protein levels. 
      Supplementation of betaine also attenuated the Hcy-induced tau 
      hyperphosphorylation at multiple AD-related sites through activation protein 
      phosphatase-2A (PP2A) with decreased inhibitory demethylated PP2A(C) at Leu309 
      and phosphorylated PP2A(C) at Tyr307. In addition, supplementation of betaine 
      also decreased Abeta production with decreased presenilin-1 protein levels. Our data 
      suggest that betaine could be a promising candidate for arresting Hcy-induced 
      AD-like pathological changes and memory deficits.
CI  - (c) 2012 International Society for Neurochemistry.
FAU - Chai, Gao-Shang
AU  - Chai GS
AD  - Department of Pathophysiology, Key Laboratory of Neurological Diseases of Chinese 
      Ministry of Education, Tongji Medical College, Huazhong University of Science and 
      Technology, Wuhan, China.
FAU - Jiang, Xia
AU  - Jiang X
FAU - Ni, Zhong-Fei
AU  - Ni ZF
FAU - Ma, Zhi-Wei
AU  - Ma ZW
FAU - Xie, Ao-Ji
AU  - Xie AJ
FAU - Cheng, Xiang-Shu
AU  - Cheng XS
FAU - Wang, Qun
AU  - Wang Q
FAU - Wang, Jian-Zhi
AU  - Wang JZ
FAU - Liu, Gong-Ping
AU  - Liu GP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Lipotropic Agents)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 3SCV180C9W (Betaine)
SB  - IM
MH  - Alzheimer Disease/blood/*drug therapy/*pathology
MH  - Animals
MH  - Betaine/*toxicity
MH  - Disease Models, Animal
MH  - Homocysteine/blood/*toxicity
MH  - Hyperhomocysteinemia/chemically induced/*drug therapy
MH  - Lipotropic Agents/pharmacology
MH  - Male
MH  - Memory Disorders/chemically induced/*drug therapy
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2012/11/20 06:00
MHDA- 2013/03/13 06:00
CRDT- 2012/11/20 06:00
PHST- 2012/09/04 00:00 [received]
PHST- 2012/11/06 00:00 [revised]
PHST- 2012/11/06 00:00 [accepted]
PHST- 2012/11/20 06:00 [entrez]
PHST- 2012/11/20 06:00 [pubmed]
PHST- 2013/03/13 06:00 [medline]
AID - 10.1111/jnc.12094 [doi]
PST - ppublish
SO  - J Neurochem. 2013 Feb;124(3):388-96. doi: 10.1111/jnc.12094.