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Thomas, J. ; Martinez-Reza, M.F. ; Thorwirth, M. ; Zarb, Y. ; Conzelmann, K.K.* ; Hauck, S.M. ; Grade, S. ; Götz, M.

Excessive local host-graft connectivity in aging and amyloid-loaded brain.

Sci. Adv. 8:eabg9287 (2022)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Transplantation is a clinically relevant approach for brain repair, but much remains to be understood about influences of the disease environment on transplant connectivity. To explore the effect of amyloid pathology in Alzheimer's disease (AD) and aging, we examined graft connectivity using monosynaptic rabies virus tracing in APP/PS1 mice and in 16- to 18-month-old wild-type (WT) mice. Transplanted neurons differentiated within 4 weeks and integrated well into the host visual cortex, receiving input from the appropriate brain regions for this area. Unexpectedly, we found a prominent several-fold increase in local inputs, in both amyloid-loaded and aged environments. State-of-the-art deep proteome analysis using mass spectrometry highlights complement system activation as a common denominator of environments promoting excessive local input connectivity. These data therefore reveal the key role of the host pathology in shaping the input connectome, calling for caution in extrapolating results from one pathological condition to another.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 2375-2548
e-ISSN 2375-2548
Zeitschrift Science Advances
Quellenangaben Band: 8, Heft: 23, Seiten: , Artikelnummer: eabg9287 Supplement: ,
Verlag American Association for the Advancement of Science (AAAS)
Verlagsort Washington, DC [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Stem Cell Research (ISF)
CF Metabolomics & Proteomics (CF-MPC)
POF Topic(s) 30204 - Cell Programming and Repair
30203 - Molecular Targets and Therapies
Forschungsfeld(er) Stem Cell and Neuroscience
Enabling and Novel Technologies
PSP-Element(e) G-500800-001
G-505700-001
A-630700-001
DOI 10.1126/sciadv.abg9287
WOS ID WOS:000852717800001
Scopus ID 85131904143
PubMed ID 35687689
Erfassungsdatum 2022-07-08
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