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Alzheimer’s disease (AD) is a neurocognitive disorder that affects over 40 million people worldwide and has become one of the main causes of death in developed countries. Its major neurobiological hallmarks are the extracellular Aβ plaques and the aggregation of hyperphosphorylated tau protein into intracellular neurofibrillary tangles (NFTs). The disease is characterized by a gradual onset and progressive decline of cognitive functions such as episodic memory, executive functions and language. Moreover, AD patients present behavioural and psychological signs and symptoms of dementia (BPSD), such as social withdrawal, apathy, depressive mood, aggression and diurnal rhythm disturbances. Currently, no cure exists for the disease. However, many authors have proposed that earlier intervention could improve AD prognosis and might even halt AD progression. Therefore, it is crucial to improve preclinical detection and diagnosis of AD based on biomarkers and behavioural markers. In order to identify robust preclinical cognitive and non-cognitive changes in AD, we assessed cognitive functions and social behaviour in 3-month-old wild-type and transgenic mice over a period of three months. All mice had a C57BL/6J background. Two transgenic mouse models were used: 1) the biAT mouse model (APP.V717I x Tau.P301L) expressing both Aβ plaques and NFTs and 2) the TPLH mouse model (Tau.P301L) which only expresses tau pathology. All mice performed a variety of behavioural tasks to evaluate cognitive and non-cognitive impairments. More specifically, the test battery included 12 tasks (Morris water maze (MWM), context- and cue-dependent fear conditioning (CFR), spontaneous activity, rotarod, marble burying, elevated plus maze, open field, SPSN, tail suspension, tail withdrawal, nesting, and nesting 2.0), designed to assess hippocampus-dependent memory, exploratory, anxiety-related, social, depressive and nociceptive behaviour, and activities of daily living (ADLs). We hypothesized that compared to age-matched controls, transgenic mice would show specific impairments in both cognitive and non-cognitive tasks. We expected significant differences in hippocampus-dependent memory function and anxiety-related, social and depressive behaviour, which are affected first in human patients. Furthermore, we expected little to no differences in exploratory behaviour, nociception and ADLs, since these functions are generally affected in later stages of the disease. Furthermore, we expected more severe impairments in the biAT than in the TPLH mouse model. In line with our expectations, transgenic mice showed decreased cognitive flexibility in the MWM. Moreover, transgenic mice displayed increased anxiety-related behaviour. However, transgenic mice also displayed decreased exploratory behaviour and reduced functioning in ADLs. Finally, there were no major differences in performance between the biAT and TPLH mouse models.