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Chronic head injury promotes tau and amyloid‐beta pathology and accelerates cognitive decline in a humanized knock‐in model of Alzheimer's disease

Clinical manifestation of Alzheimer's disease (AD) symptoms is known to reflect interactions between environmental and genetic factors. Unfortunately, preclinical modeling of AD has been relying primarily on transgenic overexpression of rare dominant mutations, with little considerations to the role the environment might play in triggering the disease. Hence the disappointing results towards translational progress in disease modifying therapies. Mild traumatic brain injury (mTBI) is a well‐known environmental risk factor for dementia, including Alzheimer’s, yet there has been limited mechanistic analysis of mTBI contribution to AD pathology. Here, we investigate the interplay between mTBI and Aβ precursor protein (APP) gene mutation in AD pathogenesis.