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Mechanical stress increases brain amyloid β, tau, and α-synuclein
concentrations in wild-type mice
Marcel Levy Nogueiraa,b,c,e,* , Minoo Hamrazd,e, Mohammad Abolhassanid,e, Erwan Biganc,e,
Olivier Lafitted,e, Jean-Marc Steyaertc,e, Bruno Duboisa,b,e,f, Laurent Schwartzc,e

aInstitut de la Mémoire et de la Maladie d’Alzheimer (IM2A), Département de Neurologie, Hôpital de la Pitié-Salpêtrière, AP-HP, Paris, France
bInstitut de Recherche Translationnelle en Neurosciences (IHU-A-ICM), Institut du Cerveau et de la Moelle Épinière (ICM), Paris, France
cLaboratoire d’informatique (LIX), UMR 7161, École Polytechnique, Université Paris-Saclay, Palaiseau, France
dNosco Pharmaceuticals, Paris, France
eLAGA, UMR 7539, Université Paris 13, Sorbonne Paris Cité, Villetaneuse, France
fINSERM, CNRS, UMR-S975, Institut du Cerveau et de la Moelle Épinière (ICM), Paris, France

Abstract

 

 

 

 

 

 

 

  

Introduction:  Exposure to traumatic brain injury is a core risk factor that predisposes an individual to sporadic neurodegenerative diseases. We provide evidence that mechanical stress increases brain
levels of hallmark proteins associated with neurodegeneration.
Methods: Wild-type mice were exposed to multiple regimens of repetitive mild traumatic brain injury, generating a range of combinations of impact energies, frequencies, and durations of exposure. Brain concentrations of amyloid b 1–42 (Aβ1–42), total tau, and a-synuclein were measured by sandwich enzyme-linked immunosorbent assay.
Results: There was a highly significant main effect of impact energy, frequency, and duration of exposure on Aβ1–42, tau, and α-synuclein levels (P , .001), and a significant interaction between impact energy and duration of exposure for Aβ1–42 and tau (P , .001), but not for a-synuclein.
Discussion: Dose-dependent  and cumulative influence  of  repetitive mild  traumatic  brain injury induced mechanical stress may trigger and/or accelerate neurodegeneration by pushing protein concentration over the disease threshold.
© 2017 Published by Elsevier Inc. on behalf of the  Alzheimer’s Association.

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