Quantification of Vocal Fold Atrophy in Age-Related and Parkinson's Disease-Related Vocal Atrophy.

OBJECTIVE: Vocal fold atrophy (VFA) is associated with aging and Parkinson's disease (PD). Clinical diagnosis of VFA depends on several visual-perceptual laryngostroboscopy findings that are inherently subjective. The purpose of this study was to use quantitative measurements to; (1) examine the relationships between VFA and dysphonia severity and (2) evaluate differences in VFA in patients with age-related VFA versus PD. METHODS: Thirty-six patients >60 years of age with VFA were included in this retrospective cohort study. Demographic information, medical history, Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V), Voice Handicap Index-10 (VHI-10), and still images from the stroboscopic exam were obtained. Image J™ was used to measure VFA, including bowing index (BI), normalized glottal gap area, and normalized mucosal wave amplitude. Pearson's correlation was used to evaluate the relationship between VFA, CAPE-V, and VHI-10. t-Tests and multivariate linear regression were used to compare VFA measures by dysphonia severity (CAPE-V <30 vs. >30) and diagnosis (age-related vocal atrophy [ARVA] and PD). RESULTS: BI was positively correlated with CAPE-V. Patients with CAPE-V >30 had a significantly larger BI compared to those with CAPE-V <30. Patients with PD had significantly larger BI than those with ARVA. Diagnosis of PD also predicted a larger BI after controlling for age and CAPE-V. CONCLUSION: Quantitative measures supported an association between bowing severity and dysphonia severity in patients with PD and ARVA. A PD diagnosis significantly predicted more severe BI. These findings demonstrate the potential utility of BI. Quantitative VFA measures might also provide insight into the mechanisms of ARVA and dysphonia. LEVEL OF EVIDENCE: 3 Laryngoscope, 133:1462-1469, 2023.

Loss of foxo rescues stem cell aging in Drosophila germ line.

Aging stem cells lose the capacity to properly respond to injury and regenerate their residing tissues. Here, we utilized the ability of Drosophila melanogaster germline stem cells (GSCs) to survive exposure to low doses of ionizing radiation (IR) as a model of adult stem cell injury and identified a regeneration defect in aging GSCs: while aging GSCs survive exposure to IR, they fail to reenter the cell cycle and regenerate the germline in a timely manner. Mechanistically, we identify foxo and mTOR homologue, Tor as important regulators of GSC quiescence following exposure to ionizing radiation. foxo is required for entry in quiescence, while Tor is essential for cell cycle reentry. Importantly, we further show that the lack of regeneration in aging germ line stem cells after IR can be rescued by loss of foxo.