Alzheimer’s disease (AD) represents a cause of severe disability in old age people while aging is per se a risk factor for AD. Thus, the study and identification of pathways within the biology of aging may represent an important end for the development of novel and effective disease-modifying drugs to treat, delay or prevent AD. Telomeres, long sequences of nucleotides at the end of our chromosomes, preserve genome stability and lead a cell to correctly divide. Due to the end replication problem, at each cell division or replication event, telomeres lose some of their length and when they get too short, the cell is no longer able to divide becoming "senescent". However, very short and dysfunctional telomeres can be repaired by the enzyme“telomerase”, which working as a reverse transcriptase, adds nucleotides at the end of each chromosome promoting its maintenance. Recent evidences show that telomerase can be modulate in adult stem cells and potentially in other cells by many mechanisms including healthy diet. Interestingly, AD lymphocytes show an accelerated telomere dysfunction, which diet or single component may significantly slowing down. In this context, cellular senescence and telomere biology represent suitable and promising targets.