PMID- 22750275
OWN - NLM
STAT- MEDLINE
DCOM- 20130729
LR  - 20121016
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 61
IP  - 5
DP  - 2012 Oct
TI  - Effects of prenatal stress exposure on soluble Abeta and brain-derived neurotrophic 
      factor signaling in male and female APPswe/PS1dE9 mice.
PG  - 697-701
LID - S0197-0186(12)00219-7 [pii]
LID - 10.1016/j.neuint.2012.06.022 [doi]
AB  - Chronic stress and stress-related disorders, such as major depression (MD), have 
      been shown to increase the risk for developing Alzheimer's disease (AD). 
      Brain-derived neurotrophic factor (BDNF) has been postulated as a 
      neurophysiological link between these illnesses. Our previous research has 
      indicated that exposing the APPswe/PS1dE9 mouse model of AD to prenatal maternal 
      stress (PS) induced a depressive-like phenotype, specifically in female mice. 
      Considering the role of BDNF in depressive-like behavior and its interactions 
      with amyloid-beta (Abeta), our aim was to explore whether these mice would also exhibit 
      alterations in soluble Abeta, mature BDNF (mBDNF), proBDNF, and the receptors TrkB 
      and p75(NTR) in comparison to non-stressed animals. Our results demonstrate that 
      female APPswe/PS1dE9 mice have higher levels of hippocampal proBDNF and soluble 
      Abeta as compared to their male littermates. Additionally, a tendency was observed 
      for PS to lower mBDNF protein levels in the hippocampus, but only in female mice, 
      while receptor levels remained unaltered by sex or PS exposure. Given that female 
      mice both have higher proBDNF and Abeta levels, these findings suggest an underlying 
      role for BDNF signaling and Abeta production in the selective vulnerability of women 
      for MD and AD development.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Sierksma, Annerieke S R
AU  - Sierksma AS
AD  - Department of Psychiatry and Neuropsychology, Faculty of Health, Medicine and 
      Life Science, School for Mental Health and Neuroscience (MHeNS), Maastricht 
      University, Maastricht, The Netherlands.
FAU - Vanmierlo, Tim
AU  - Vanmierlo T
FAU - De Vry, Jochen
AU  - De Vry J
FAU - Raijmakers, Marjolein E A
AU  - Raijmakers ME
FAU - Steinbusch, Harry W M
AU  - Steinbusch HW
FAU - van den Hove, Daniel L A
AU  - van den Hove DL
FAU - Prickaerts, Jos
AU  - Prickaerts J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120629
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Peptide Fragments)
RN  - 0 (Presenilin-1)
RN  - 0 (amyloid beta-protein (1-40))
RN  - 0 (amyloid beta-protein (1-42))
SB  - IM
MH  - Amyloid beta-Peptides/genetics/metabolism/*physiology
MH  - Amyloid beta-Protein Precursor/genetics
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Female
MH  - Hippocampus/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Peptide Fragments/genetics/*metabolism
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/genetics/*metabolism
MH  - Presenilin-1/genetics
MH  - *Sex Characteristics
MH  - Solubility
MH  - Stress, Psychological/genetics/*metabolism
EDAT- 2012/07/04 06:00
MHDA- 2013/07/31 06:00
CRDT- 2012/07/04 06:00
PHST- 2012/02/24 00:00 [received]
PHST- 2012/06/04 00:00 [revised]
PHST- 2012/06/25 00:00 [accepted]
PHST- 2012/07/04 06:00 [entrez]
PHST- 2012/07/04 06:00 [pubmed]
PHST- 2013/07/31 06:00 [medline]
AID - S0197-0186(12)00219-7 [pii]
AID - 10.1016/j.neuint.2012.06.022 [doi]
PST - ppublish
SO  - Neurochem Int. 2012 Oct;61(5):697-701. doi: 10.1016/j.neuint.2012.06.022. Epub 
      2012 Jun 29.