This comprehensive review paper delves into the impact of senescent cells on neurodegenerative conditions. Throughout life, somatic cells become senescent due to various factors, leading to a state of chronic inflammation and tissue dysfunction. The accumulation of senescent cells contributes to the onset and progression of age-related diseases.
Cellular senescence is a common process characterized by irreversible cell cycle arrest, driven by stimuli like DNA damage and telomere dysfunction. Senescent cells release pro-inflammatory signals and are resistant to apoptosis, impacting neighboring cells.
Neurodegenerative diseases involve progressive brain changes, including neuronal death and protein aggregation. Evidence suggests that cellular senescence precedes disease symptoms, possibly triggered by stressors like DNA damage.
In Alzheimer’s disease, senescent cells contribute to toxic protein build-up. Recent studies link cellular senescence to tau protein aggregation and neuronal dysfunction, with clearance of senescent cells reducing pathological markers.
Parkinson’s disease is associated with midbrain inflammation, possibly induced by cellular senescence and the senescence-associated secretory phenotype. Senescence markers have been found in dopaminergic neurons of PD patients, with α-synuclein aggregates triggering stress-induced premature senescence.
Link: https://doi.org/10.3389/fragi.2023.1292053
