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@ARTICLE{Bachmann:878454,
author = {Bachmann, Claudia and Tetzlaff, Tom and Duarte, Renato and
Morrison, Abigail},
title = {{F}iring rate homeostasis counteracts changes in stability
of recurrent neural networks caused by synapse loss in
{A}lzheimer’s disease},
journal = {PLoS Computational Biology},
volume = {16},
number = {8},
issn = {1553-734X},
address = {San Francisco, Calif.},
publisher = {Public Library of Science},
reportid = {FZJ-2020-02860},
pages = {e1007790 -},
year = {2020},
note = {Additional grants: Helmholtz Association Initiative and
Networking Fund (project no. SO-092 [Advanced Computing
Architectures] and Helmholtz Portfolio Theme "Supercomputing
and Modeling for the Human Brain"),},
abstract = {The impairment of cognitive function in Alzheimer’s
disease is clearly correlated to synapse loss. However, the
mechanisms underlying this correlation are only poorly
understood. Here, we investigate how the loss of excitatory
synapses in sparsely connected random networks of spiking
excitatory and inhibitory neurons alters their dynamical
characteristics. Beyond the effects on the activity
statistics, we find that the loss of excitatory synapses on
excitatory neurons reduces the network’s sensitivity to
small perturbations. This decrease in sensitivity can be
considered as an indication of a reduction of computational
capacity. A full recovery of the network’s dynamical
characteristics and sensitivity can be achieved by firing
rate homeostasis, here implemented by an up-scaling of the
remaining excitatory-excitatory synapses. Mean-field
analysis reveals that the stability of the linearised
network dynamics is, in good approximation, uniquely
determined by the firing rate, and thereby explains why
firing rate homeostasis preserves not only the firing rate
but also the network’s sensitivity to small
perturbations.},
cin = {INM-6 / IAS-6 / INM-10 / JARA-HPC / JSC},
ddc = {610},
cid = {I:(DE-Juel1)INM-6-20090406 / I:(DE-Juel1)IAS-6-20130828 /
I:(DE-Juel1)INM-10-20170113 / $I:(DE-82)080012_20140620$ /
I:(DE-Juel1)JSC-20090406},
pnm = {571 - Connectivity and Activity (POF3-571) / 572 -
(Dys-)function and Plasticity (POF3-572) / 574 - Theory,
modelling and simulation (POF3-574) / HBP SGA1 - Human Brain
Project Specific Grant Agreement 1 (720270) / HBP SGA2 -
Human Brain Project Specific Grant Agreement 2 (785907) /
DFG project 233510988 - Mathematische Modellierung der
Entstehung und Suppression pathologischer
Aktivitätszustände in den Basalganglien-Kortex-Schleifen
(233510988) / Advanced Computing Architectures
$(aca_20190115)$ / Functional Neural Architectures
$(jinm60_20190501)$},
pid = {G:(DE-HGF)POF3-571 / G:(DE-HGF)POF3-572 /
G:(DE-HGF)POF3-574 / G:(EU-Grant)720270 / G:(EU-Grant)785907
/ G:(GEPRIS)233510988 / $G:(DE-Juel1)aca_20190115$ /
$G:(DE-Juel1)jinm60_20190501$},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:32841234},
UT = {WOS:000565612000002},
doi = {10.1371/journal.pcbi.1007790},
url = {https://juser.fz-juelich.de/record/878454},
}