A TELOscopic View of Neuroinflammation

Deterioration of physiological integrity that is observed with age is a primary risk factor for associated pathologies. Telomere shortening and chronic inflammation are two of such prominent cellular changes associated with ageing. Telomeres, the repeat sequences at chromosomal ends, are considered as one determinant of biological age. The ability of telomeres to predict cellular senescence has sparked a keen interest in understanding its role in age-related disorders. The highly interdependent relationship between telomere biology and inflammation has been comprehensively described in a recent review by Zhang and Rane, et al . A growing epidemic of chronic low grade inflammation seems to be a common denominator for many age-related diseases. Neuro-inflammation leading to neurodegeneration is considered as the primary cause of age-associated neurological disorders. An increasing number of studies indicate a link between telomere length (TL) and dementia or cognitive impairment, however, the role of telomeres in neurodegenerative disorder still remains ambiguous. The question of whether telomeres are cause or consequence of disease still remains. Nevertheless, in a recent report employing Mendelian randomization technique, TL has been causally linked to risk of Alzheimer’s disease. These results suggest that telomeres might be a part of an active mechanism leading to the development of the disease. Telomeres thus provide an entirely new dimension to the understanding neurodegenerative disorders.