Journal Article

DZNE-2020-01297

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Memory trace interference impairs recall in a mouse model of Alzheimer's disease.

Poll, S. (First author)DZNE* ; Mittag, M.DZNE* ; Musacchio, F.DZNE* ; Justus, L. C.DZNE* ; Giovannetti, E. A.DZNE* ; Steffen, J.DZNE* ; Wagner, J.DZNE* ; Zohren, L. ; Schoch, S. ; Schmidt, B. ; Jackson, W. S.DZNE* ; Ehninger, D.DZNE* ; Fuhrmann, M. (Last author)DZNE*

2020
Nature America New York, NY

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Please use a persistent id in citations: doi:10.1038/s41593-020-0652-4  doi:10.60944/dzne-2020-01297

Abstract: In Alzheimer's disease (AD), hippocampus-dependent memories underlie an extensive decline. The neuronal ensemble encoding a memory, termed engram, is partially recapitulated during memory recall. Artificial activation of an engram can restore memory in a mouse model of early AD, but its fate and the factors that render the engram nonfunctional are yet to be revealed. Here, we used repeated two-photon in vivo imaging to analyze fosGFP transgenic mice (which express enhanced GFP under the Fos promoter) performing a hippocampus-dependent memory task. We found that partial reactivation of the CA1 engram during recall is preserved under AD-like conditions. However, we identified a novelty-like ensemble that interfered with the engram and thus compromised recall. Mimicking a novelty-like ensemble in healthy mice was sufficient to affect memory recall. In turn, reducing the novelty-like signal rescued the recall impairment under AD-like conditions. These findings suggest a novel mechanistic process that contributes to the deterioration of memories in AD.

Keyword(s): Alzheimer Disease: genetics (MeSH) ; Alzheimer Disease: metabolism (MeSH) ; Alzheimer Disease: physiopathology (MeSH) ; Amyloid beta-Protein Precursor: genetics (MeSH) ; Amyloid beta-Protein Precursor: metabolism (MeSH) ; Animals (MeSH) ; Disease Models, Animal (MeSH) ; Female (MeSH) ; Hippocampus: physiology (MeSH) ; Male (MeSH) ; Mental Recall: physiology (MeSH) ; Mice (MeSH) ; Mice, Transgenic (MeSH) ; Neurons: physiology (MeSH) ; Optogenetics (MeSH) ; Proto-Oncogene Proteins c-fos: genetics (MeSH) ; Proto-Oncogene Proteins c-fos: metabolism (MeSH) ; Amyloid beta-Protein Precursor ; Proto-Oncogene Proteins c-fos

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Contributing Institute(s):

1. Neuroimmunology and Imaging (AG Fuhrmann)
2. Selective Vulnerability of Neurodegenerative Diseases (AG Jackson)
3. Translational Biogerontology (AG Ehninger)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2020

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Database coverage:
; ; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; Essential Science Indicators ; Green Open Access ; IF >= 25 ; JCR ; Nationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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