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Stereological estimation of neuron number and plaque load in the hippocampal region of a transgenic rat model of A lzheimer's disease
Author(s) -
Heggland Ingrid,
Storkaas Inge S.,
Soligard Hanne T.,
KobroFlatmoen Asgeir,
Witter Menno P.
Publication year - 2015
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12876
Subject(s) - subiculum , entorhinal cortex , senile plaques , hippocampal formation , pathology , hippocampus , genetically modified mouse , stereology , neuroscience , parahippocampal gyrus , alzheimer's disease , biology , medicine , transgene , dentate gyrus , disease , temporal lobe , biochemistry , gene , epilepsy
The main hallmarks of Alzheimer's disease ( AD ) are senile plaques, neurofibrillary tangles and neuronal death. The McGill‐R‐Thy1‐ APP rat is one of the few transgenic rat models of AD that displays progressive amyloid pathology. This study aimed to further characterise this rat model, focusing on the pathological changes in the hippocampal formation and the parahippocampal region. These structures, that are important for episodic memory and spatial navigation, are affected in the early stages of the disease. This study used unbiased stereology to investigate possible neuronal loss in the CA 1, subiculum and entorhinal cortex of 18‐month‐old homozygous McGill‐R‐Thy1‐ APP rats, and also quantified the plaque load in all the areas of the hippocampal formation and parahippocampal region from 9 to 18 months old. A significant reduction of neurons at 18 months was only seen in the subiculum. The first plaque pathology was seen at 9 months in the subiculum. Although the quantified plaque load was variable between animals, the pattern of spatiotemporal progression was similar for all animals. The spread of plaque pathology mainly affected anatomically connected regions. Overall, the plaque pathology observed in the transgenic rats was similar to the early phases of amyloid beta (Aβ)‐deposition described in human patients. The findings here thus indicate that the McGill‐R‐Thy1‐ APP rat could be a good model of the Aβ pathology in AD , but less so with respect to neuron loss.