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@ARTICLE{Dsedau:279879,
author = {Düsedau, Henning Peter and Cangalaya, Carla and Stoyanov,
Stoyan Borislavov and Dityatev, Alexander and Dunay, Ildiko
Rita},
title = {{R}educed synaptic tagging by complement protein {C}3 is
associated with elevated extracellular matrix in the
middle-aged cerebellum of mice.},
journal = {Frontiers in aging neuroscience},
volume = {17},
issn = {1663-4365},
address = {Lausanne},
publisher = {Frontiers Research Foundation},
reportid = {DZNE-2025-00846},
pages = {1616390},
year = {2025},
abstract = {Aging of the brain is associated with cognitive decline and
recognized as a major risk factor for the development of
neurodegenerative diseases. On a cellular level, brain aging
is accompanied by a progressive increase of the basal
pro-inflammatory tonus, leading to the activation of
phagocytic pathways in brain-resident microglia and
disruptive effects on synaptic neurotransmission. While the
aging process affects all brain compartments at different
velocities and one of the particularly affected regions is
the cerebellum (CB), the underlying effects remain
elusive.In the present study, we harnessed a murine model of
natural aging in males combined with orthogonal experimental
approaches comprising of cytokine gene expression analysis,
flow cytometry, immunohistochemistry, and flow
synaptometry.We report age-dependent morphological and
phenotypic changes in microglia that are distinct in the
cortex (CTX) and CB. Furthermore, we show an increased
expression of cytokines and complement factors upon aging
and a decline of C3-tagged VGLUT1+ presynaptic puncta in the
CB. Using flow synaptometry to quantify the composition of
synapses in more detail, we validated the reduction of
C3b-labeled excitatory synaptosomes while the overall
frequency of glutamatergic synaptosomes remained unaffected
by aging. Notably, proteoglycans brevican and aggrecan, key
components of the neural extracellular matrix, were
significantly upregulated in the middle-aged CB.The data
presented herein suggests the ECM-mediated shielding of
synapses from complement-tagging and subsequent engulfment
by microglia. Thus, we provide novel insights into
mechanisms that may confer resilience in the brain by
modulating synapse removal in the context of aging.},
keywords = {aging (Other) / cerebellum (Other) / complement system
(Other) / extracellular matrix (Other) / microglia (Other) /
proteoglycans (Other) / synaptic pruning (Other) /
synaptosomes (Other)},
cin = {AG Dityatev},
ddc = {610},
cid = {I:(DE-2719)1310007},
pnm = {351 - Brain Function (POF4-351)},
pid = {G:(DE-HGF)POF4-351},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40641620},
pmc = {pmc:PMC12240999},
doi = {10.3389/fnagi.2025.1616390},
url = {https://pub.dzne.de/record/279879},
}