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PTU-induced hypothyroidism in rats leads to several early neuropathological signs of Alzheimer's disease in the hippocampus and spatial memory impairments.

Authors: Chaalal, Amina  Poirier, Roseline  Blum, David  Gillet, Brigitte  Le Blanc, Pascale  Basquin, Marie  Buée, Luc  Laroche, Serge  Enderlin, Valérie 
Citation: Chaalal A, etal., Hippocampus. 2014 Nov;24(11):1381-93. doi: 10.1002/hipo.22319. Epub 2014 Jul 22.
Pubmed: (View Article at PubMed) PMID:24978200
DOI: Full-text: DOI:10.1002/hipo.22319

The multifactorial causes impacting the risk of developing sporadic forms of Alzheimer's disease (AD) remain to date poorly understood. Epidemiologic studies in humans and research in rodents have suggested that hypothyroidism could participate in the etiology of AD. Recently, we reported that adult-onset hypothyroidism in rats favors ß-amyloid peptide production in the hippocampus. Here, using the same hypothyroidism model with the antithyroid molecule propythiouracyl (PTU), we further explored AD-related features, dysfunctional cell-signaling mechanisms and hippocampal-dependent learning and memory. In vivo MRI revealed a progressive decrease in cerebral volume of PTU-treated rats. In the hippocampus, hypothyroidism resulted in tau hyperphosphorylation and increases in several proinflammatory cytokines. These modifications were associated with impaired spatial memory and reduced hippocampal expression of signaling molecules important for synaptic plasticity and memory, including neurogranin, CaMKII, ERK, GSK3ß, CREB, and expression of the transcription factor EGR1/Zif268. These data strengthen the idea that hypothyroidism represents an important factor influencing the risk of developing sporadic forms of AD.


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RGD Object Information
RGD ID: 13800922
Created: 2018-10-23
Species: All species
Last Modified: 2018-10-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.