. Postsynaptic dysfunction is associated with spatial and object recognition memory loss in a natural model of Alzheimer's disease. Proc Natl Acad Sci U S A. 2012 Aug 21;109(34):13835-40. PubMed.

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  1. A most interesting model for AD, but why specifically for the "sporadic" form? Chilean degus manifest "AD" beginning at about three years of age, whereas their "relatives," the Chilean guinea pigs, do not; Calabrian carriers of M146L in PS1 manifest AD at about 45 years of age, whereas their non-carrier relatives do not. The difference between Chilean degus and guinea pigs is, by definition, genetic, the same as the difference between Calabrian people. In the absence of demonstrated environmental causes, the null hypothesis is that late-onset "sporadic," i.e., apparently non-familial, human AD, is genetic with a large stochastic dispersion of the age at onset, as we observed for familial early-onset AD. The absence of apparent familiality in late-onset AD is due to "statistical censorship," the theoretical, genetically determined, median age at onset of AD being older than the mean age of death from other causes (1).

    References:

    . Alzheimer's disease: a model from the quantitative study of a large kindred. J Geriatr Psychiatry Neurol. 1992 Jul-Sep;5(3):126-31. PubMed.

    View all comments by Jean-François Foncin
  2. A most interesting animal model of AD, not only with the Aβ peptide, intracellular and extracellular accumulations of tau protein, and ubiquitin, but also demonstrating strong astrocytic responses and acetylcholinesterase (AChE)-rich pyramidal neurons (Inestrosa et al., 2005). Analysis of different regions from the cerebral cortex (frontal, parietal, temporal, and entorhinal) and hippocampus of young and aged wild-type degus with anti-human Aβ peptide (1-40) antibodies found prominent Aβ deposited in both cerebral cortex and hippocampus of the aged degus (Hardy and Higgins 1992).

    Increased GFAP-positive astrocytes have also been seen in the aged degu brain, as well as in the human brain, with age, and in older rats. This phenomenon does not appear to reflect astrocyte gliosis that occurs in association with neurofibrillary tangles and senile plaques, but rather as an astrocyte reaction in the whole brain related to an accumulation of GFAP (Nichols et al., 1993).

    Ardiles and associates in Chile found that during aging, degus display a significant reduction in synaptic memory; object recognition memory, tested using an alternance T-maze task; and object recognition in an open-field arena (Ardiles et al., 2011).

    We can only hope that Dr. Kirkwood’s Octodon degus colony will be large enough to allow other Alzheimer’s disease researchers here in the United States to conduct research with this animal model of AD.

    See also:

    Ardiles A, et al., β-Amyloid dodecamers and hyperphosphorylated Tau correlates with synaptic and cognitive impairments in aged Octodon degus. 2011. Paper presented at Reunion Annual Sociedad Chilena de Neuroscienca, Las Cruces, Chile.

    References:

    . Human-like rodent amyloid-beta-peptide determines Alzheimer pathology in aged wild-type Octodon degu. Neurobiol Aging. 2005 Jul;26(7):1023-8. PubMed.

    . Alzheimer's disease: the amyloid cascade hypothesis. Science. 1992 Apr 10;256(5054):184-5. PubMed.

    . GFAP mRNA increases with age in rat and human brain. Neurobiol Aging. 1993 Sep-Oct;14(5):421-9. PubMed.

    View all comments by Trent Nichols

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  1. Degu Debut—The New Face of Sporadic Alzheimer’s Research?