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Disruptions in transposable elements and gene networks occur before the onset of tauopathy in a humanized mouse model of AD

Alzheimer’s Disease (AD) is an age‐related neurodegenerative disorder culminating in dementia with additional non‐cognitive behavioral and metabolic symptomatology such as hyperactivity and altered sleep/wake patterns, which promote weight loss. In demented patients weight loss is associated with adverse outcomes, including accelerated AD progression and higher institutionalization. Mouse models of tau deposition, such as Tg4510 mice, also have negative energy balance. Tg4510 mice, which express a P301L mutant variant of human tau, develop both cognitive and non‐cognitive symptoms. To identify early pre‐symptomatic factors affecting AD, we analyzed RNA‐seq data from young, pre‐tauopathic Tg4510 mice to identify gene and transposable elements (TE) expression changes that may initiate the behavioral and metabolic derangements in AD.