PMID- 23608100
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140219
LR  - 20130603
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 245
DP  - 2013 Aug 15
TI  - 1H-MRS can monitor metabolites changes of lateral intraventricular BDNF infusion 
      into a mouse model of Alzheimer's disease in vivo.
PG  - 40-9
LID - S0306-4522(13)00333-3 [pii]
LID - 10.1016/j.neuroscience.2013.04.015 [doi]
AB  - Proton magnetic resonance spectroscopy (1H-MRS) can provide noninvasive detection 
      of brain metabolite changes in vivo in Alzheimer's disease (AD). AD is a 
      prevalent neurodegenerative disorder characterized by deposition of beta-amyloid 
      peptides (Abeta) in multiple brain regions. Brain-derived neurotrophic factor (BDNF) 
      is a neurotrophic factor whose level has been shown to be decreased in AD. BDNF 
      supplementation can offer improvement in AD. However, the means of evaluation are 
      still relatively limited. In the present study, 1H-MRS was applied to evaluate 
      the therapeutic effects of bilateral intraventricular BDNF infusion into APP+PS1 
      (amyloid precursor protein+presenilin 1) transgenic mice. For comparison to the 
      1H-MRS changes in the prefrontal cortex, Morris water maze (MWM) test, 
      Fluoro-Jade B staining and immunofluorescence for Abeta, glial fibrillary acidic 
      protein and tropomyosin-related kinase B (TrkB) were also performed. Our results 
      showed that N-acetylaspartate (NAA) levels increased and myo-inositol levels 
      decreased in Tg-BDNF mice compared with Tg-PBS mice. But NAA level in Tg-BDNF 
      mice was still lower than that in wild-type mice at 6weeks after infusion. These 
      changes correlated with increased immunoreactivity of TrkB, reduced compact Abeta 
      peptide and FJB+ neurons in Tg-BDNF mice compared to Tg-PBS mice. However, 
      Tg-BDNF mice did not present obvious changes in behavior in the MWM. Taken 
      together, we suggest that 1H-MRS may be a sensitive means of evaluating metabolic 
      changes in response to therapeutic strategies in AD. Moreover, BDNF, may be a 
      viable means of offering trophic support during disease.
CI  - Copyright (c) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Zhang, W
AU  - Zhang W
AD  - Department of Radiology, Tongji Hospital, Medical School of Tongji University, 
      Shanghai, China.
FAU - Wang, P J
AU  - Wang PJ
FAU - Li, M H
AU  - Li MH
FAU - Gao, X L
AU  - Gao XL
FAU - Gu, G J
AU  - Gu GJ
FAU - Shao, Z H
AU  - Shao ZH
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20130420
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RIN - Neuroscience. 2013 Dec 19;254:477. PMID: 24527493
EDAT- 2013/04/24 06:00
MHDA- 2013/04/24 06:01
CRDT- 2013/04/24 06:00
PHST- 2012/12/27 00:00 [received]
PHST- 2013/04/02 00:00 [revised]
PHST- 2013/04/03 00:00 [accepted]
PHST- 2013/04/24 06:00 [entrez]
PHST- 2013/04/24 06:00 [pubmed]
PHST- 2013/04/24 06:01 [medline]
AID - S0306-4522(13)00333-3 [pii]
AID - 10.1016/j.neuroscience.2013.04.015 [doi]
PST - ppublish
SO  - Neuroscience. 2013 Aug 15;245:40-9. doi: 10.1016/j.neuroscience.2013.04.015. Epub 
      2013 Apr 20.