Title of article
Human-like rodent amyloid-β-peptide determines Alzheimer pathology in aged wild-type Octodon degu
Author/Authors
Nibaldo C. Inestrosaa، نويسنده , , ?، نويسنده , , Ariel E. Reyesa، نويسنده , , Marcelo A. Chac´ona، نويسنده , , Waldo Cerpaa، نويسنده , , Aldo Villal´onb، نويسنده , , Juan Montielb، نويسنده , , Genevieve Merabachvilia، نويسنده , , Rebeca Aldunatea، نويسنده , , Francisco Bozinovicc، نويسنده , , Francisco Aboitiz، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2005
Pages
6
From page
1023
To page
1028
Abstract
It is generally accepted that human Alzheimerʹs disease (AD) neuropathology markers are completely absent in rodent brains. We report here that an aged wild-type South American rodent, Octodon degu, expresses neuronal β-amyloid precursor protein (β-APP695) displaying both intracellular and extracellular deposits of amyloid-β-peptide (Aβ), intracellular accumulations of tau-protein and ubiquitin, a strong astrocytic response and acetylcholinesterase (AChE)-rich pyramidal neurons. The high amino acid homology (97.5%) between deguAβ and humanAβ sequences is probably a major factor in the appearance of AD markers in this aged rodent. Our results indicate that aged O. degu constitutes the first wild-type rodent model for neurodegenerative processes associated to AD.
Keywords
neuropathology , Amyloid- -peptide , APP , Octodon degu , Alzheimer’s Disease , Alzheimer model
Journal title
Neurobiology of Aging
Serial Year
2005
Journal title
Neurobiology of Aging
Record number
820659
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