Recent evidence highlights the protective role of reelin against amyloid β (Aβ)-induced synaptic dysfunction and cognitive impairment in Alzheimer disease (AD). In this study, exploiting TgCRND8 mice that overexpress a mutant form of amyloid β precursor protein (AβPP) and display an early onset of AD neuropathological signs, we addressed the question whether changes of reelin expression eventually precede the appearance of Aβ-plaques in a sex-dependent manner. We show that sex-associated and brain region-specific differences in reelin expression appear long before Aβ-plaque formation. However, in spite of a downregulation of reelin expression compared to males, TgCRND8 females display fewer Aβ-plaques, suggesting that additional factors, other than sex and reelin level, influence amyloidosis in this mouse model.
Sexually Dimorphic Expression of Reelin in the Brain of a Mouse Model of Alzheimer Disease / Palladino, G.; Nicolia, V.; Kovacs, G. G.; Canterini, S.; Ciraci, V.; Fuso, A.; Mangia, F.; Scarpa, S.; Fiorenza, M. T.. - In: JOURNAL OF MOLECULAR NEUROSCIENCE. - ISSN 0895-8696. - 61:3(2017), pp. 359-367. [10.1007/s12031-016-0865-x]
Sexually Dimorphic Expression of Reelin in the Brain of a Mouse Model of Alzheimer Disease
Ciraci V.;
2017-01-01
Abstract
Recent evidence highlights the protective role of reelin against amyloid β (Aβ)-induced synaptic dysfunction and cognitive impairment in Alzheimer disease (AD). In this study, exploiting TgCRND8 mice that overexpress a mutant form of amyloid β precursor protein (AβPP) and display an early onset of AD neuropathological signs, we addressed the question whether changes of reelin expression eventually precede the appearance of Aβ-plaques in a sex-dependent manner. We show that sex-associated and brain region-specific differences in reelin expression appear long before Aβ-plaque formation. However, in spite of a downregulation of reelin expression compared to males, TgCRND8 females display fewer Aβ-plaques, suggesting that additional factors, other than sex and reelin level, influence amyloidosis in this mouse model.Pubblicazioni consigliate
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