From cellular senescence to Alzheimer’s disease: The role of telomere shortening

• Cellular senescence in the brain contributes to AD pathogenesis and may represent a link between the aging process and disease progression.
• Telomere stability and maintenance is required for brain functions.
• Cellular senescence and short telomeres are associated with AD, while shorter telomeres also limit the amyloid accumulation in the brain of mouse models of AD.
• The contribution of LTL to AD, either as a biomarker for disease or as an indicator of the telomere length in brain cells is still unclear and under debate.
• Telomerase persists in neurons of the adult human brain, where it may have a protective role against tau pathology.

The old age population is increasing worldwide as well as age related diseases, including neurodegenerative disorders, such as Alzheimer’s disease (AD), which negatively impacts on the health care systems. Aging represents per se a risk factor for AD. Thus, the study and identification of pathways within the biology of aging represent an important end point for the development of novel and effective disease-modifying drugs to treat, delay, or prevent AD. Cellular senescence and telomere shortening represent suitable and promising targets. Several studies show that cellular senescence is tightly interconnected to aging and AD, while the role of telomere dynamic and stability in AD pathogenesis is still unclear. This review will focus on the linking mechanisms between cellular senescence, telomere shortening, and AD.