PMID- 22086139
OWN - NLM
STAT- MEDLINE
DCOM- 20120928
LR  - 20211021
IS  - 1435-1463 (Electronic)
IS  - 0300-9564 (Linking)
VI  - 119
IP  - 2
DP  - 2012 Feb
TI  - Recent rodent models for Alzheimer's disease: clinical implications and basic 
      research.
PG  - 173-95
LID - 10.1007/s00702-011-0731-5 [doi]
AB  - Alzheimer's disease (AD) is the most common origin of dementia in the elderly. 
      Although the cause of AD remains unknown, several factors have been identified 
      that appear to play a critical role in the development of this debilitating 
      disorder. In particular, amyloid precursor protein (APP), tau 
      hyperphosphorylation, and the secretase enzymes, have become the focal point of 
      recent research. Over the last two decades, several transgenic and non-transgenic 
      animal models have been developed to elucidate the mechanistic aspects of AD and 
      to validate potential therapeutic targets. Transgenic rodent models 
      over-expressing human beta-amyloid precursor protein (beta-APP) and mutant forms of tau 
      have become precious tools to study and understand the pathogenesis of AD at the 
      molecular, cellular and behavioural levels, and to test new therapeutic agents. 
      Nevertheless, none of the transgenic models of AD recapitulate fully all of the 
      pathological features of the disease. Octodon degu, a South American rodent has 
      been recently found to spontaneously develop neuropathological signs of AD in old 
      age. This review aims to address the limitations and clinical relevance of 
      transgenic rodent models in AD, and to highlight the potential for O. degu as a 
      natural model for the study of AD neuropathology.
FAU - Braidy, Nady
AU  - Braidy N
AD  - Department of Pharmacology, University of New South Wales, Sydney, NSW, 2052, 
      Australia.
FAU - Munoz, Pablo
AU  - Munoz P
FAU - Palacios, Adrian G
AU  - Palacios AG
FAU - Castellano-Gonzalez, Gloria
AU  - Castellano-Gonzalez G
FAU - Inestrosa, Nibaldo C
AU  - Inestrosa NC
FAU - Chung, Roger S
AU  - Chung RS
FAU - Sachdev, Perminder
AU  - Sachdev P
FAU - Guillemin, Gilles J
AU  - Guillemin GJ
LA  - eng
GR  - 1 R03TW007171-01/TW/FIC NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20111116
PL  - Austria
TA  - J Neural Transm (Vienna)
JT  - Journal of neural transmission (Vienna, Austria : 1996)
JID - 9702341
SB  - IM
MH  - Alzheimer Disease/*genetics/*pathology/therapy
MH  - Animals
MH  - Animals, Genetically Modified
MH  - Biomedical Research/methods/*trends
MH  - *Disease Models, Animal
MH  - Humans
MH  - Mice
MH  - Octodon/genetics/physiology
MH  - Species Specificity
EDAT- 2011/11/17 06:00
MHDA- 2012/09/29 06:00
CRDT- 2011/11/17 06:00
PHST- 2011/05/26 00:00 [received]
PHST- 2011/10/24 00:00 [accepted]
PHST- 2011/11/17 06:00 [entrez]
PHST- 2011/11/17 06:00 [pubmed]
PHST- 2012/09/29 06:00 [medline]
AID - 10.1007/s00702-011-0731-5 [doi]
PST - ppublish
SO  - J Neural Transm (Vienna). 2012 Feb;119(2):173-95. doi: 10.1007/s00702-011-0731-5. 
      Epub 2011 Nov 16.