Browsing by Author "Cerpa, W"

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    Acetylcholinesterase-Aβ complexes are more toxic than Aβ fibrils in rat hippocampus -: Effect on rat β-amyloid aggregation, laminin expression, reactive astrocytosis, and neuronal cell loss
    (2004) Reyes, AE; Chacón, MA; Dinamarca, MC; Cerpa, W; Morgan, C; Inestrosa, NC
    Neuropathological changes generated by human amyloid-beta peptide (Abeta) fibrils and Abeta-acetylcholinesterase (Abeta-AChE) complexes were compared in rat hippocampus in vivo. Results showed that Abeta-AChE complexes trigger a more dramatic response in situ than Abeta fibrils alone as characterized by the following features observed 8 weeks after treatment: 1) amyloid deposits were larger than those produced in the absence of AChE. In fact, AChE strongly stimulates rat Abeta aggregation in vitro as shown by turbidity measurements, Congo Red binding, as well as electron microscopy, suggesting that Abeta-AChE deposits observed in vivo probably recruited endogenous Abeta peptide; 2) the appearance of laminin expressing neurons surrounding Abeta-AChE deposits (such deposits are resistant to disaggregation by laminin in vitro); 3) an extensive astrocytosis revealed by both glial fibrillary acidic protein immunoreactivity and number counting of reactive hypertrophic astrocytes; and 4) a stronger neuronal cell loss in comparison with Abeta-injected animals. We conclude that the hippocampal injection of Abeta-AChE complexes results in the appearance of some features reminiscent of Alzheimer-like lesions in rat brain. Our studies are consistent with the notion that Abeta-AChE complexes are more toxic than Abeta fibrils and that AChE triggered some of the neurodegenerative changes observed in Alzheimer's disease brains.
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    Human-like rodent amyloid-β-peptide determines Alzheimer pathology in aged wild-type Octodon degu
    (2005) Inestrosa, NC; Reyes, AE; Chacón, MA; Cerpa, W; Villalón, A; Montiel, J; Merabachvili, G; Aldunate, R; Bozinovic, F; Aboitiz, F
    It is generally accepted that human Alzheimer's 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 beta-amyloid precursor protein (beta-APP695) displaying both intracellular and extracellular deposits of amyloid-beta-peptide (A beta), 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 deguA beta and humanA beta sequences is probably a major factor in the appearance of AD markers in this aged rodent. Our results indicate that aged 0. degu constitutes the first wild-type rodent model for neurodegenerative processes associated to AD. (c) 2004 Elsevier Inc. All rights reserved.