Neurodegenerative diseases are the most prevalent age-related pathologies, including Alzheimer’s disease (AD). Recent studies suggest that telomere attrition, the main trigger of cellular senescence and pathological ageing may contribute to brain dysfunction and neurodegeneration. Senescent brain cells have been observed in AD brains, and studies in a transgenic mouse model of tauopathy found that the elimination of senescent cells led to an improvement in neurodegeneration and cognitive decline. In this project, we aim to unravel the relationship between brain senescence and the onset and progression of tau-related pathology associated with AD.For this purpose, we crossed a mouse model of telomere attrition and premature ageing (TercKO) with the tauopathy mouse model Tau P301S (PS19). By taking advantage of brain sections and brain protein extracts, and using biochemical and molecular biology techniques, we examined the expression of tau-related neuropathological features in a senescent context.We observed that telomere attrition exacerbates tau phosphorylation at specific residues in primary neurons and hippocampal tissue, and this increase in phosphorylated tau seems to be accompanied by other post-translational modifications (PTMs) of tau. Finally, we found that the increase in tau phosphorylation is not caused by a hyperactivity of tau kinases.Our results suggest that telomere attrition-induced senescence might be an upstream regulator of tau pathology, aggravating it and triggering tau-related neurodegeneration. Elucidating this process in more detail could lead to the identification of suitable intervention targets for AD treatment.