Early-onset dysfunction of retrosplenial cortex precedes overt amyloid plaque formation in Tg2576 mice

Poirier, Guillaume L., Amin, Eman, Good, Mark Andrew ORCID: https://orcid.org/0000-0002-1824-1203 and Aggleton, John Patrick ORCID: https://orcid.org/0000-0002-5573-1308 2011. Early-onset dysfunction of retrosplenial cortex precedes overt amyloid plaque formation in Tg2576 mice. Neuroscience 174 , pp. 71-83. 10.1016/j.neuroscience.2010.11.025

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Abstract

A mouse model of amyloid pathology was used to first examine using a cross sectional design changes in retrosplenial cortex activity in transgenic mice aged 5, 11, 17, and 23 months. Attention focused on: (1) overt amyloid labeled with β-amyloid(1–42) and Congo Red staining, (2) metabolic function assessed by the enzyme, cytochrome oxidase, and (3) neuronal activity as assessed indirectly by the immediate-early gene (IEG), c-Fos. Changes in cytochrome oxidase and c-Fos activity were observed in the retrosplenial cortex in Tg2576 mice as early as 5 months of age, long before evidence of plaque formation. Subsequent analyses concentrating on this early dysfunction revealed at 5 months pervasive, amyloid precursor protein (APP)-derived peptide accumulation in the retrosplenial cortex and selective afferents (anterior thalamus, hippocampus), which was associated with the observed c-Fos hyporeactivity. These findings indicate that retrosplenial cortex dysfunction occurs during early stages of amyloid production in Tg2576 mice and may contribute to cognitive dysfunction.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Psychology Medicine Neuroscience and Mental Health Research Institute (NMHRI)
Subjects:	R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Uncontrolled Keywords:	Alzheimer's disease; posterior cingulate cortex; diaschisis; disconnection; connectivity; energy metabolism
Publisher:	Elsevier
ISSN:	0306-4522
Last Modified:	18 Oct 2022 12:49
URI:	https://orca.cardiff.ac.uk/id/eprint/11338

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