PMID- 20005283
OWN - NLM
STAT- MEDLINE
DCOM- 20100504
LR  - 20211020
IS  - 1873-6815 (Electronic)
IS  - 0531-5565 (Print)
IS  - 0531-5565 (Linking)
VI  - 45
IP  - 3
DP  - 2010 Mar
TI  - Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a 
      folate, vitamin B6 and B12-deficient diet.
PG  - 195-201
LID - 10.1016/j.exger.2009.12.005 [doi]
AB  - Epidemiological and clinical studies indicate that elevated circulating level of 
      homocysteine (Hcy) is a risk factor for developing Alzheimer's disease (AD). 
      Dietary deficiency of folate, vitamin B6 and B12 results in a significant 
      increase of Hcy levels, a condition also known as hyperhomocysteinemia (HHcy). In 
      the present study we tested the hypothesis that a diet deficient for these three 
      important factors when administered to a mouse model of AD, i.e. Tg2576, will 
      result in HHcy and in an acceleration of their amylodotic phenotype. Compared 
      with Tg2576 mice on regular chow, the ones receiving the diet deficient for 
      folate, B6 and B12 developed HHcy. This condition was associated with a 
      significant increase in Abeta levels in the cortex and hippocampus, and an 
      elevation of Abeta deposits in the same regions. No significant changes were 
      observed for steady-state levels of total APP, BACE-1, ADAM-10, PS1 and nicastrin 
      in the brains of mice with HHcy. No differences were observed for the main Abeta 
      catabolic pathways, i.e. IDE and neprilysin proteins, or the Abeta chaperone 
      apolipoprotein E. Our findings demonstrate that a dietary condition which leads 
      to HHcy may also result in increased Abeta levels and deposition in a transgenic 
      mouse model of AD-like amylodosis. They further support the concept that dietary 
      factors can contribute to the development of AD neuropathology.
CI  - Copyright 2009 Elsevier Inc. All rights reserved.
FAU - Zhuo, Jia-Min
AU  - Zhuo JM
AD  - Temple University, School of Medicine, Department of Pharmacology, Philadelphia, 
      PA 19140, USA.
FAU - Pratico, Domenico
AU  - Pratico D
LA  - eng
GR  - R01 AG022512-03/AG/NIA NIH HHS/United States
GR  - R01 AG022512-06/AG/NIA NIH HHS/United States
GR  - R01 AG022512/AG/NIA NIH HHS/United States
GR  - R01 AG022512-05/AG/NIA NIH HHS/United States
GR  - R01 AG022512-04/AG/NIA NIH HHS/United States
GR  - AG-22512/AG/NIA NIH HHS/United States
GR  - R01 AG022512-02/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20091211
PL  - England
TA  - Exp Gerontol
JT  - Experimental gerontology
JID - 0047061
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
SB  - IM
MH  - Alzheimer Disease/*etiology/metabolism
MH  - Amyloid beta-Peptides/metabolism
MH  - Amyloid beta-Protein Precursor/metabolism
MH  - Amyloidosis/*etiology
MH  - Animals
MH  - Brain/*metabolism
MH  - Disease Models, Animal
MH  - Female
MH  - Folic Acid Deficiency/*complications
MH  - Humans
MH  - Hyperhomocysteinemia/complications
MH  - Mice
MH  - Mice, Transgenic
MH  - Vitamin B 12 Deficiency/*complications
MH  - Vitamin B 6 Deficiency/*complications
PMC - PMC2826592
MID - NIHMS169259
EDAT- 2009/12/17 06:00
MHDA- 2010/05/05 06:00
PMCR- 2011/03/01
CRDT- 2009/12/17 06:00
PHST- 2009/09/09 00:00 [received]
PHST- 2009/11/03 00:00 [revised]
PHST- 2009/12/04 00:00 [accepted]
PHST- 2009/12/17 06:00 [entrez]
PHST- 2009/12/17 06:00 [pubmed]
PHST- 2010/05/05 06:00 [medline]
PHST- 2011/03/01 00:00 [pmc-release]
AID - S0531-5565(09)00298-8 [pii]
AID - 10.1016/j.exger.2009.12.005 [doi]
PST - ppublish
SO  - Exp Gerontol. 2010 Mar;45(3):195-201. doi: 10.1016/j.exger.2009.12.005. Epub 2009 
      Dec 11.