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Mechanical stress increases brain amyloid β, tau, and α-synuclein concentrations in wild-type mice
Marcel Levy Nogueira1, Minoo Hamraz2, Mohammad Abolhassani2
1Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A), Département de Neurologie, Hôpital de la Pitié-Salpêtrière, AP-HP, Paris, France; Institut de Recherche Translationnelle en Neurosciences (IHU-A-ICM), Institut du Cerveau et de la Moelle Epinière (ICM), Paris, France.
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 β 1-42 (Aβ1-42), total tau, and α-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 α-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.
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