Reference code: | PT/FB/BL-2012-217.05 |
Location: | Arquivo PCA - Pasta 27/2012
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Title:
| Type I and II interferon responses are altered in the choroid plexus and in the hippocampus of a mouse model of Alzheimer's disease
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Publication year: | 2015
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URL:
| http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=39a4fbb4-5832-4414-987b-ad4983496059&cKey=c87de13a-c64a-47e9-bcab-3c3370065c32&mKey=d0ff4555-8574-4fbb-b9d4-04eec8ba0c84
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Abstract/Results: | ABSTRACT:
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a marked decline in cognition and memory function. One of the major pathological hallmarks of AD is the progressive accumulation and deposition of amyloid beta (Aß) peptides in the brain. Importantly, increased Aß toxicity and pathology is accompanied by alterations in parallel mechanisms and responses that regulate brain homeostasis and function. Increasing evidence highlights the essential role of neuroinflammatory and immune-related molecules, including those produced at the brain barriers, on brain immune surveillance, decreased Aß clearance from the brain and increased brain cell dysfunction and pathology in AD. Therefore, understanding the response at the brain barriers may unravel novel pathways of relevance for the pathophysiology of AD. Herein, we focused on the study of the choroid plexus (CP), which constitutes the blood-cerebrospinal fluid barrier, in aging and in AD. Specifically, we used the PDGFB-APPSwInd (J20) transgenic mouse model of AD, which presents early memory decline and progressive Aß accumulation in the brain, and littermate age-matched wild-type (WT) mice, to characterize the CP transcriptome at 3, 5-6 and 11-12 months of age. The most striking observation was that the CP of J20 mice displayed an overall overexpression of type I interferon (IFN) response genes at all ages. Moreover, J20 mice presented a high expression of type II IFN genes in the CP at 3 months, which became lower than WT at 5-6 and 11-12 months. Importantly, along with a marked memory impairment and increased glial activation, J20 mice also presented a similar overexpression of type I IFN genes in the dorsal hippocampus at 3 months. Altogether, these findings provide new insights on a possible interplay between type I and type II IFN responses in AD and point to IFNs as targets for modulation in cognitive decline.
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Accessibility: | Document does not exist in file
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Author:
| Mesquita, S. D.
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Secondary author(s):
| Ferreira, A. C., Rodrigues, A., Gao, F., Coppola, G., Geschwind, D. H., Sousa, J. C., Correia-Neves, M., Sousa, N., Palha, J., Marques, F.
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Document type:
| Online abstract
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Number of reproductions:
| 1
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Reference:
| Mesquita, S. D., Ferreira, A. C., Rodrigues, A., Gao, F., Coppola, G., Geschwind, D. H., Sousa, J. C., Correia-Neves, M., Sousa, N., Palha, J., & Marques, F. (2015, November). Type I and II interferon responses are altered in the choroid plexus and in the hippocampus of a mouse model of Alzheimer's disease. Paper presented at the Society for Neuroscience (SFN), Chicago, USA. Abstract available at http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=39a4fbb4-5832-4414-987b-ad4983496059&cKey=c87de13a-c64a-47e9-bcab-3c3370065c32&mKey=d0ff4555-8574-4fbb-b9d4-04eec8ba0c84
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Indexed document: | No
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Keywords: | Alzheimer's disease / Inflammation / Cognition
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