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Mechanical stress increases brain amyloid β, tau, and α‐synuclein concentrations in wild‐type mice
Author(s) -
Levy Nogueira Marcel,
Hamraz Minoo,
Abolhassani Mohammad,
Bigan Erwan,
Lafitte Olivier,
Steyaert JeanMarc,
Dubois Bruno,
Schwartz Laurent
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.11.003
Subject(s) - amyloid (mycology) , amyloid β , neuroscience , stress (linguistics) , chemistry , medicine , psychology , pathology , disease , philosophy , linguistics
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 (Aβ 1–42 ), 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 Aβ 1–42 , tau, and α‐synuclein levels ( P < .001), and a significant interaction between impact energy and duration of exposure for Aβ 1–42 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.