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@ARTICLE{Filser:137858,
author = {Filser, Severin and Ovsepian, Saak V and Masana, Mercè and
Blazquez-Llorca, Lidia and Brandt Elvang, Anders and
Volbracht, Christiane and Müller, Marianne B and Jung,
Christian K E and Herms, Jochen},
title = {{P}harmacological inhibition of {BACE}1 impairs synaptic
plasticity and cognitive functions.},
journal = {Biological psychiatry},
volume = {77},
number = {8},
issn = {0006-3223},
address = {Amsterdam [u.a.]},
publisher = {Elsevier Science},
reportid = {DZNE-2020-04180},
pages = {729-739},
year = {2015},
abstract = {BACE1 (beta site amyloid precursor protein cleaving enzyme
1) is the rate limiting protease in amyloid β production,
hence a promising drug target for the treatment of
Alzheimer's disease. Inhibition of BACE1, as the major
β-secretase in vivo with multiple substrates, however is
likely to have mechanism-based adverse effects. We explored
the impact of long-term pharmacological inhibition of BACE1
on dendritic spine dynamics, synaptic functions, and
cognitive performance of adult mice.Sandwich enzyme-linked
immunosorbent assay was used to assess Aβ40 levels in brain
and plasma after oral administration of BACE1 inhibitors
SCH1682496 or LY2811376. In vivo two-photon microscopy of
the somatosensory cortex was performed to monitor structural
dynamics of dendritic spines while synaptic functions and
plasticity were measured via electrophysiological recordings
of excitatory postsynaptic currents and hippocampal
long-term potentiation in brain slices. Finally, behavioral
tests were performed to analyze the impact of
pharmacological inhibition of BACE1 on cognitive
performance.Dose-dependent decrease of Aβ40 levels in vivo
confirmed suppression of BACE1 activity by both inhibitors.
Prolonged treatment caused a reduction in spine formation of
layer V pyramidal neurons, which recovered after withdrawal
of inhibitors. Congruently, the rate of spontaneous and
miniature excitatory postsynaptic currents in pyramidal
neurons and hippocampal long-term potentiation were reduced
in animals treated with BACE1 inhibitors. These effects were
not detected in Bace1(-/-) mice treated with SCH1682496,
confirming BACE1 as the pharmacological target. Described
structural and functional changes were associated with
cognitive deficits as revealed in behavioral tests.Our
findings indicate important functions to BACE1 in structural
and functional synaptic plasticity in the mature brain, with
implications for cognition.},
keywords = {Amyloid Precursor Protein Secretases: deficiency / Amyloid
Precursor Protein Secretases: genetics / Amyloid
beta-Peptides: metabolism / Animals / Aspartic Acid
Endopeptidases: deficiency / Aspartic Acid Endopeptidases:
genetics / Brain: anatomy $\&$ histology / Brain: drug
effects / Brain: metabolism / Cognition: physiology /
Cognitive Dysfunction: chemically induced / Cognitive
Dysfunction: metabolism / Dendritic Spines: drug effects /
Dendritic Spines: metabolism / Dose-Response Relationship,
Drug / Enzyme Inhibitors: chemistry / Enzyme Inhibitors:
pharmacology / Exploratory Behavior: drug effects / Humans /
Maze Learning: drug effects / Mice / Mice, Inbred C57BL /
Mice, Transgenic / Peptide Fragments: metabolism / Pyramidal
Cells: drug effects / Pyramidal Cells: physiology /
Pyrimidines: chemistry / Pyrimidines: pharmacology /
Pyrimidinones: pharmacology / Synaptic Potentials: drug
effects / Synaptic Potentials: physiology / Thiazines:
chemistry / Thiazines: pharmacology / Thiophenes:
pharmacology / Time Factors / Amyloid beta-Peptides (NLM
Chemicals) / Enzyme Inhibitors (NLM Chemicals) / LY2811376
(NLM Chemicals) / Peptide Fragments (NLM Chemicals) /
Pyrimidines (NLM Chemicals) / Pyrimidinones (NLM Chemicals)
/ SCH1682496 (NLM Chemicals) / Thiazines (NLM Chemicals) /
Thiophenes (NLM Chemicals) / amyloid beta-protein (1-40)
(NLM Chemicals) / Amyloid Precursor Protein Secretases (NLM
Chemicals) / Aspartic Acid Endopeptidases (NLM Chemicals) /
Bace1 protein, mouse (NLM Chemicals)},
cin = {AG Herms},
ddc = {610},
cid = {I:(DE-2719)1110001},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:25599931},
doi = {10.1016/j.biopsych.2014.10.013},
url = {https://pub.dzne.de/record/137858},
}