PMID- 18786162
OWN - NLM
STAT- MEDLINE
DCOM- 20090511
LR  - 20090217
IS  - 1601-183X (Electronic)
IS  - 1601-183X (Linking)
VI  - 8
IP  - 1
DP  - 2009 Feb
TI  - Effect of the brain-derived neurotrophic factor and the apolipoprotein E 
      polymorphisms on disease progression in preclinical Alzheimer's disease.
PG  - 43-52
LID - 10.1111/j.1601-183X.2008.00440.x [doi]
AB  - Genetic factors, such as apolipoprotein E (ApoE) polymorphisms, are thought to 
      play an important role in the etiology of Alzheimer's disease (AD). Recent 
      association studies have suggested that the Val66Met polymorphism in the 
      brain-derived neurotrophic factor (BDNF) gene could play a role in the 
      development of AD. To identify genotypic effects of the BDNF and the ApoE genes 
      on disease progression in preclinical AD, we assessed morphological changes using 
      serial magnetic resonance imaging during the preclinical period of AD in 35 
      individuals. When all subjects were analyzed as one group, progressive atrophy 
      was noted in the limbic, paralimbic and neocortical areas. Individuals of the 
      BDNF Val/Val genotype showed progressive atrophy in the left medial temporal 
      areas, whereas the BDNF Met allele carriers showed additional changes in the 
      anterior cingulate cortex (ACC), posterior cingulate cortex (PCC) and the 
      precuneus. An interaction between the BDNF genotype and progressive morphological 
      changes was found in the PCC. The noncarriers for the ApoE epsilon4 allele showed 
      progressive atrophy in the bilateral medial temporal areas. In addition to 
      changes in the medial temporal areas, epsilon4 carriers showed progressive 
      atrophy in the PCC, ACC and precuneus. An interaction between the ApoE genotype 
      and progressive morphological change was noted in the right medial temporal area. 
      The present preliminary study indicates that polymorphisms of the ApoE and the 
      BDNF genes could affect disease progression in preclinical AD and implies that 
      the Met-BDNF polymorphism could be an additional risk factor for rapid disease 
      progression in preclinical AD.
FAU - Hashimoto, R
AU  - Hashimoto R
AD  - Department of Clinical Disorder Research, The Osaka-Hamamatsu Joint Research 
      Center For Child Mental Development, Osaka University Graduate School of 
      Medicine, Suita, Osaka, Japan. hashimor@psy.med.osaka-u.ac.jp
FAU - Hirata, Y
AU  - Hirata Y
FAU - Asada, T
AU  - Asada T
FAU - Yamashita, F
AU  - Yamashita F
FAU - Nemoto, K
AU  - Nemoto K
FAU - Mori, T
AU  - Mori T
FAU - Moriguchi, Y
AU  - Moriguchi Y
FAU - Kunugi, H
AU  - Kunugi H
FAU - Arima, K
AU  - Arima K
FAU - Ohnishi, T
AU  - Ohnishi T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080911
PL  - England
TA  - Genes Brain Behav
JT  - Genes, brain, and behavior
JID - 101129617
RN  - 0 (Apolipoproteins E)
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Aged
MH  - Alzheimer Disease/*genetics/pathology/*psychology
MH  - Apolipoproteins E/*genetics
MH  - Atrophy
MH  - Brain/pathology
MH  - Brain-Derived Neurotrophic Factor/*genetics
MH  - Disease Progression
MH  - Female
MH  - Follow-Up Studies
MH  - Genotype
MH  - Humans
MH  - Image Processing, Computer-Assisted
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Middle Aged
MH  - Neuropsychological Tests
MH  - Polymorphism, Genetic/genetics
EDAT- 2008/09/13 09:00
MHDA- 2009/05/12 09:00
CRDT- 2008/09/13 09:00
PHST- 2008/09/13 09:00 [pubmed]
PHST- 2009/05/12 09:00 [medline]
PHST- 2008/09/13 09:00 [entrez]
AID - GBB440 [pii]
AID - 10.1111/j.1601-183X.2008.00440.x [doi]
PST - ppublish
SO  - Genes Brain Behav. 2009 Feb;8(1):43-52. doi: 10.1111/j.1601-183X.2008.00440.x. 
      Epub 2008 Sep 11.