• Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors – “The results show a consistent biological age increase in the post-COVID-19 population, determining a DeltaAge acceleration of 10.45 ± 7.29 years (+5.25 years above the range of normality).”
  • Shorter telomere lengths in patients with severe COVID-19 disease – “Critically short telomeres impair the regenerative capacity of tissues and trigger loss of tissue homeostasis and disease.”
  • Acceleration of Biological Aging and Underestimation of Subjective Age Are Risk Factors for Severe COVID-19 – “Indicators of individual relative biological and subjective aging affect the probability of getting COVID-19 and its severity. The combination of high indicators of biological aging and underestimated indicators of subjective aging is associated with increased chances of developing severe forms of the disease.”
  • Accelerated biological aging in COVID-19 patients – “We also find the increasing acceleration of epigenetic aging and telomere attrition in the sequential blood samples from healthy individuals and infected patients developing non-severe and severe COVID-19”
  • Severe COVID-19 is associated with molecular signatures of aging in the human brain – “As coronavirus disease 2019 (COVID-19) and aging are both accompanied by cognitive decline, we hypothesized that COVID-19 might lead to molecular signatures similar to aging. We performed whole-transcriptome analysis of the frontal cortex, a critical area for cognitive function, in individuals with COVID-19, age-matched and sex-matched uninfected controls, and uninfected individuals with intensive care unit/ventilator treatment. Our findings indicate that COVID-19 is associated with molecular signatures of brain aging and emphasize the value of neurological follow-up in recovered individuals.”
  • Causal association of epigenetic aging and COVID-19 severity and susceptibility: A bidirectional Mendelian randomization study – “Our findings suggest that there is may no clear association between aging and susceptibility to COVID-19, and that COVID-19 severity is may not be associated with changes in age. Severe COVID-19 could lead to accelerated telomere wear and shorter telomere lengths. At the same time, severe COVID-19 could also slow the acceleration of GrimAge clocks, which is not significantly related to other epigenetic clocks. The fly in the ointment is that our study lacks observational studies, and existing observational studies differ from some of our findings. We conclude the above possible arguments through the Mendelian randomization approach. More research is needed to demonstrate the link between aging and adverse COVID-19 and the underlying mechanism by which this genetic predictive effect occurs.”
  • SARS-CoV-2 and the central nervous system: Emerging insights into hemorrhage-associated neurological consequences and therapeutic considerations – “In conclusion, SARS-CoV-2 infection-induced microhemorrhages in crucial brain regions have the potential to accelerate brain aging in COVID-19 survivors and can also lead to complex and irreversible neurodegenerative conditions, a risk factor for both cognitive and motor functions. Loss of neuronal cells in COVID-19 patient-affected brain areas may be attributed to a combination of senescence and ferroptosis along with acute inflammation-induced oxidative stress-mediated cell death.”