TY - JOUR
T1 - Recent rodent models for Alzheimer's disease
T2 - Clinical implications and basic research
AU - Braidy, Nady
AU - Muñoz, Pablo
AU - Palacios, Adrian G.
AU - Castellano-Gonzalez, Gloria
AU - Inestrosa, Nibaldo C.
AU - Chung, Roger S.
AU - Sachdev, Perminder
AU - Guillemin, Gilles J.
PY - 2012/2
Y1 - 2012/2
N2 - 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 β-amyloid precursor protein (β-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.
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 β-amyloid precursor protein (β-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.
UR - http://www.scopus.com/inward/record.url?scp=84857629109&partnerID=8YFLogxK
U2 - 10.1007/s00702-011-0731-5
DO - 10.1007/s00702-011-0731-5
M3 - Review article
C2 - 22086139
AN - SCOPUS:84857629109
SN - 0300-9564
VL - 119
SP - 173
EP - 195
JO - Journal of Neural Transmission
JF - Journal of Neural Transmission
IS - 2
ER -