Alzheimer’s disease (AD) is the most common cause of dementia. Despite age being the main risk factor, previous studies have also reported that type 1 diabetes (T1D) may contribute to abnormal tau phosphorylation and worsen cognitive impairment in AD patients. However, the underlying mechanisms are not completely understood. Therefore, we have analyzed the effects of streptozotocin (STZ)-induced T1D in a mouse model of AD (APP/PS1) in terms of metabolic impairment, cortical tau phosphorylation and cognition at 26 weeks of age, when the pathology is fully established. When all groups under study (WT, APP/PS1, WT-STZ and APP/PS1-STZ) were considered, we observed positive correlations between phosphorylation at Thr217 and Thr231, Thr231 and Ser202/Thr205 and Ser396 and Ser202/Thr205, indicating specific tau phosphorylation patterns. Bivariate analyses between metabolic parameters and tau phosphorylation showed that blood glucose positively correlates with tau hyperphosphorylation at Ser199, indicating that hyperglycemia might be the trigger of tau pathology in T1D individuals. Cognition was also impaired in APP/PS1-STZ mice in both Morris Water Maze (MWM) and Novel Object Discrimination (NOD) tests, with inverse correlations between tau hyperphosphorylation at Thr 217 (in the MWM) and Ser199 (in the NOD) and cognitive performance.Overall our findings suggest that tau phosphorylation is an underlying mechanism involved in the high risk of cognitive impairment observed in T1D. Funding: RECOGNISED (Clinical Trials gov registration no. NCT04281186) European Commission (H2020-GA847749). Ministerio de Ciencia e Innovacion (PID2020-115499RB-I00). Proyectos I+D+i Sistema Andaluz del Conocimiento (P20-00928). Margarita Salas fellowship NextGenerationEU-Spanish Ministry of Universities (2022) (M.C.-G).