Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 109, Issue 34, Pages 13835-13840Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1201209109
Keywords
memory dysfunction; neural plasticity; aging; T-maze; hippocampus
Categories
Funding
- National Institutes of Health Fogarty International Research Collaboration [R03 TW007171-01A1, R01 AG034606]
- Chilean National Commission for Scientific and Technological Research Grant [ANR-47, PFB 12/2007, AT-24091109]
- Interdisciplinary Center for Neuroscience of Valparaiso Millenium Scientific Initiative [P09-022-F]
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Alzheimer's disease (AD) is an age-related neurodegenerative disorder associated with progressive memory loss, severe dementia, and hallmark neuropathological markers, such as deposition of amyloid-beta (A beta) peptides in senile plaques and accumulation of hyperphosphorylated tau proteins in neurofibrillary tangles. Recent evidence obtained from transgenic mouse models suggests that soluble, nonfibrillar A beta oligomers may induce synaptic failure early in AD. Despite their undoubted value, these transgenic models rely on genetic manipulations that represent the inherited and familial, but not the most abundant, sporadic form of AD. A nontransgenic animal model that still develops hallmarks of AD would be an important step toward understanding how sporadic AD is initiated. Here we show that starting between 12 and 36 mo of age, the rodent Octodon degus naturally develops neuropathological signs of AD, such as accumulation of A beta oligomers and phosphorylated tau proteins. Moreover, age-related changes in A beta oligomers and tau phosphorylation levels are correlated with decreases in spatial and object recognition memory, postsynaptic function, and synaptic plasticity. These findings validate O. degus as a suitable natural model for studying how sporadic AD may be initiated.
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