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- W2087451343 abstract "Central cholinergic system, as well as serotonin, noradrenaline and somatostatin neurotransmitter and modulator systems, is differentially altered in the brains of individuals with Alzheimer's disease (AD). This selective neuronal vulnerability during disease progression is poorly understood and unfortunately neuronal loss is a phenotype scarcely reproduced by transgenic mouse models of AD. However, we have previously reported in a PS1/APP model significant early pyramidal cell loss in entorhinal cortex and interneuron degeneration in both hippocampus and entorhinal cortex. Here we assessed the temporal course of cholinergic degeneration in this transgenic model in which plaque formation and neuronal loss started since early ages. Transgenic PS1M146L/APP751SL and non-transgenic mice were examined at 4-12 months of age. Cholinergic neurons were immunostained with an antiserum against choline-acetyltransferase (ChAT). Forebrain cholinergic neurons projecting to the hippocampus (medial septum and vertical limb of the diagonal band of Broca) and cortex (nucleus basalis of Meynert) and cortical ChAT-interneurons were stereologically counted. The amyloid deposition in the brain cholinergic system was analyzed by immunohistochemistry and Thioflavin-S or congo-red staining. Cortical and basal forebrain mRNA levels of ChAT were measured by quantitative RT-PCR. We found a significant decrease in the number of cholinergic neurons in basal forebrain nuclei in 12 month-old PS1/APP mice compared to age-matched control animals. This was confirmed by RT-PCR analysis. Cortical ChAT-interneurons were affected at 6 months. Abnormal swollen cholinergic neurites were seen in close association with amyloid plaques throughout the cortex and hippocampus at 4 months of age suggesting that amyloid peptides could induce cholinergic neurodegenerative changes. These PS1/APP mice developed early (3 months) amyloid plaques throughout the neocortex and hippocampus with only late (18 months) and modest amyloid deposition in the basal forebrain. The brain cholinergic neurons of these transgenic mice showed no intracellular amyloid pathology. This PS1/APP transgenic model recapitulates the robust basal forebrain cholinergic neurodegeneration as seen in human AD. Our results suggest that the early cortical and hippocampal amyloidosis causes severe disruption of the cholinergic fiber network. Amyloid-induced retrograde axonal degeneration might be responsible of the basal cholinergic neuron loss." @default.
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- W2087451343 date "2011-07-01" @default.
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- W2087451343 title "P3-047: Cholinergic degenerative pathology in ps1m146l/APP751sl alzheimer transgenic model" @default.
- W2087451343 doi "https://doi.org/10.1016/j.jalz.2011.05.1486" @default.
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