In a recent study published within the journal Journal of Neurology, Neurosurgery, & Psychiatryresearchers examined the association between three clinical biomarker-based measures of biological age (BA) and the chance of age-related neurological disease amongst UK Biobank (UKBB) participants.
They compared the results of advanced biological age on time-to-event patterns in causal and systemic dementia, ischemic stroke, motor neurone disease (MND), and Parkinson’s disease (PD).
Test: Biomarker-driven clinical biological aging and future risk of neurological disease within the UK Biobank. Photo credit: Chinnapong/Shutterstock.com
Background
Aging increases the chance of assorted neurological disorders. Many common neurological diseases have been related to increasing chronological age (CA; nonetheless, their relationship to biological age (BA) is unknown. Biological age measures similar to epigenetic clocks, telomere length, and composite biomarkers have been developed to explain age-related events more sophisticated than CA.
Clinically relevant approaches to measuring BA use changes in routinely used clinical biomarker levels, and research indicates that when BA exceeds CA, anxiety, depression, cancer, and mortality risk increase.
Nevertheless, limited research has examined associations between measures of biological age and the likelihood of neurological disease, warranting further investigation.
In regards to the study
Researchers assessed the association between biological age and the incidence of neurological disease amongst UKBB participants in a prospective cohort study.
The team studied 325,870 UKBB participants aged 37 to 73, recruited between 2006 and 2010. At first of the study, the participants didn’t suffer from any neurological diseases.
Three previously described measures of biological age based on 18 frequently assessed biomarkers [Klemera-Doubal method age (KDMAge), PhenoAge, and homeostatic dysregulation age (HDAge)] were used for evaluation.
Individuals with incomplete data on biological age measures and covariates and individuals with a history of dementia, ischemic stroke, MND, or Parkinson’s disease were excluded. Data from the US National Health and Nutrition Examination Survey (US NHANES) were combined with biomarker information for training and validation of BA measures.
At baseline, participants accomplished questionnaires, accomplished functional and physical measurements, and provided biological samples.
The team assessed the impact of advanced biological age on recent neurological diagnoses, including causal and general dementia, ischemic stroke, MND and Parkinson’s disease, using survival models.
Neurologic diseases were diagnosed using International Classification of Diseases, Tenth Revision (ICD-10) codes obtained from inpatient hospital records and the death registry. Participants were followed until diagnosis, death, or study end, whichever got here first.
PhenoAge and KDMAge were regressed on chronological age in order that residual values could possibly be considered deviations between biological and chronological age. HDAge values were obtained from individual physiological variations from a disease-free reference sample and were log-transformed before evaluation because of skewed distribution.
A Cox proportional hazard regression model was performed to find out hazard ratios (HRs). Covariates adjusted for yr of birth, gender, body mass index (BMI), ethnicity, alcohol consumption, smoking, and deprivation.
Results
The typical age of the study participants was 56 years, of which 54% were women. Throughout the nine-year follow-up (mean), 1,397 cases, 2,515 cases, 679 cases, and 203 cases of dementia, ischemic stroke, Parkinson’s disease, and motor neurone disease were reported, respectively. KDMAge (HR, 1.3), PhenoAge (HR, 1.3), and HDAge (HR, 1.2) were significantly related to increased risk of dementia no matter cause.
All measures of biological age were strongly related to vascular dementia, but weaker associations were observed with the event of Alzheimer’s disease (AD).
Similarly, the team found a significantly increased risk of ischemic stroke as measured by biological age: KDMAge (HR, 1.4), PhenoAge (HR, 1.4), and HDAge (HR, 1.3). Weakly positive associations were observed between advanced biological age and the chance of MND, and only HDAge showed a big association with motor neuron disease (HR 1.2).
Similarly, non-significant relationships were found between biological age and the chance of Parkinson’s disease; nonetheless, unlike the opposite results, the HR values obtained for PD were below 1.0 (HR values were 0.96, 0.95, and 0.88 for KDMAge, PhenoAge, and HDAge, respectively).
Stratification by sex and age showed similar results, although biological age was more strongly related to dementia amongst young women under 60 years of age.
Increased forced expiratory volumes were related to a lower risk of ischemic stroke and dementia, while increased red blood cell counts were related to an increased risk of PD and dementia.
In a sensitivity evaluation, eliminating subjects diagnosed with a neurological disorder inside five years of their biological age assessment tended to indicate smaller effect sizes but similar effect directions, with significant associations remaining for vascular dementia and general dementia, ischemic stroke, and PhenoAge in AD.
Conclusions
Overall, the study results showed that increased biological aging is related to an increased risk of assorted age-related neurological diseases, including ischemic stroke, vascular dementia and all-cause dementia, having the best impact. Reversing your biological age can reduce your risk of dementia and stroke.
After controlling for key variables in disease-specific modeling (including smoking history and prevalence of diabetes, hypertension, and dyslipidemia), strong associations continued, indicating that these indicators of biological age have significance beyond simply estimating cardiovascular risk.