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• W2158713023 endingPage "10087" @default.
• W2158713023 startingPage "10083" @default.
• W2158713023 abstract "The ε4 allele of apolipoprotein E (<i>APOE</i>) and traumatic brain injury (TBI) are both risk factors for the development of Alzheimer9s disease (AD). These factors may act synergistically, in that <i>APOE4</i>+ individuals are more likely to develop dementia after TBI. Because the mechanism underlying these effects is unclear, we questioned whether<i>APOE4</i> and TBI interact either through effects on amyloid-β (Aβ) or by enhancing cell death/tissue injury. We assessed the effects of TBI in PDAPP mice (transgenic mice that develop AD-like pathology) expressing human <i>APOE3</i>(PDAPP:E3), human <i>APOE4</i> (PDAPP:E4), or no<i>APOE</i> (PDAPP:E−/−). Mice were subjected to a unilateral cortical impact injury at 9–10 months of age and allowed to survive for 3 months. Aβ load, hippocampal/cortical volumes, and hippocampal CA3 cell loss were quantified using stereological methods. All of the groups contained mice with Aβ-immunoreactive deposits (56% PDAPP:E4, 20% PDAPP:E3, 75% PDAPP:E−/−), but thioflavine-S-positive Aβ (amyloid) was present only in the molecular layer of the dentate gyrus in the PDAPP:E4 mice (44%). In contrast, our previous studies showed that in the absence of TBI, PDAPP:E3 and PDAPP:E4 mice have little to no Aβ deposition at this age. After TBI, all of the Aβ deposits present in PDAPP:E3 and PDAPP:E−/− mice were diffuse plaques. In contrast to the effect of <i>APOE4</i> on amyloid, PDAPP:E3, PDAPP:E4, and PDAPP:E−/− mice did not differ in the amount of brain tissue or cell loss. These data support the hypothesis that<i>APOE4</i> influences the neurodegenerative cascade after TBI via an effect on Aβ." @default.
• W2158713023 created "2016-06-24" @default.
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• W2158713023 date "2002-12-01" @default.
• W2158713023 modified "2023-10-11" @default.
• W2158713023 title "Apolipoprotein E4 Influences Amyloid Deposition But Not Cell Loss after Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease" @default.
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• W2158713023 doi "https://doi.org/10.1523/jneurosci.22-23-10083.2002" @default.
• W2158713023 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6758744" @default.
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