bioRxiv Science⌕ Search

Biology subjects

Puhlmann, L. M.

Publications and source records attributed to Puhlmann, L. M..

2 recordsLinked to original sources

Cross-Modal Organization of Facial and Vocal Behavior Revealed by Coordination Metrics Derived from Temporal Alignment

Facial and vocal behaviors jointly convey affective and communicative information, yet their cross-modal organization remains difficult to characterize quantitatively. We propose a framework for characterizing facial-vocal organization by aligning facial and vocal dynamics using canonical time warping. Multivariate facial action unit trajectories and vocal prosodic trajectories were extracted from recordings of spontaneous speech and aligned in a shared latent space. From the alignment process, we derived three cross-modal coordination metrics: "scaling factor", reflecting the relative scaling between modalities; "time shift ratio", reflecting the frequency of temporal shifts; and "time shift magnitude", reflecting their size. We evaluated these metrics in verbally fluent adults with autism spectrum disorder (ASD; N = 35) and controls (N = 44). The proposed metrics did not differ significantly between diagnostic groups but showed associations with individual differences in communication and anxiety. Scaling factor was linked to trait anxiety in ASD, whereas time shift ratio was associated with communication characteristics across participants. The proposed metrics also showed little association with conventional vocal pitch variability, suggesting that they capture aspects of expressive organization not reflected by vocal variability alone. Our findings support alignment-derived metrics as a complementary approach for characterizing individual variability in facial-vocal expressive behavior.

neuroscience↗

Mapping Pathways to Neuronal Atrophy in Healthy, Mid-aged Adults: From Chronic Stress to Systemic Inflammation to Neurodegeneration?

Growing evidence implicates systemic inflammation in the loss of structural brain integrity in natural ageing and disorder development. Chronic stress and glucocorticoid exposure can potentiate inflammatory processes and have also been linked to neuronal atrophy, particularly in the hippocampus and the human neocortex. To improve understanding of emerging maladaptive interactions between stress and inflammation, this study examined evidence for glucocorticoid- and inflammation-mediated neurodegeneration in healthy mid-aged adults. N=169 healthy adults (mean age = 39.4, 64.5% female) were sampled from the general population in the context of the ReSource Project. Stress, inflammation and neuronal atrophy were quantified using physiological indices of chronic stress (hair cortisol and cortisone concentration), systemic inflammation (interleukin-6, high-sensitive C-reactive protein), the systemic inflammation index (SII), hippocampal volume (HCV) and cortical thickness (CT) in regions of interest. Structural equation models were used to examined evidence for pathways from stress and inflammation to neuronal atrophy. Model fit indices indicated good representation of stress, inflammation, and neurological data through the constructed models (CT model: robust RMSEA = 0.041, robust{chi} 2= 910.90; HCV model: robust RMSEA < 0.001, robust{chi} 2 = 40.95). We replicated typical negative age-cortical thickness associations (Anterior cingulate cortex ({beta} =-0.51, p < .001), Parahippocampal Cortex ({beta} = -0.50, p = .012), Frontal Lobe ({beta} = -0.56, p < .001) and Temporal Lobe ({beta} = -0.61, p < .001). Among inflammatory indices, only the SII was positively associated with hair cortisol as one indicator of chronic stress ({beta} = 0.18, p<.05). Direct and indirect pathways from chronic stress and systemic inflammation to cortical thickness or hippocampal volume were non-significant. We identify the SII as a potential marker of systemic inflammation in human psychobiological studies. More generally, these data suggest that neurophysiological associations found in at-risk populations are not detectable in healthy, mid-aged populations. We conclude that inflammation and glucocorticoid-mediated neurodegeneration may only emerge during advanced ageing and disorder processes and may thus have limited use as early risk markers. Future work should examine these pathways in prospective longitudinal designs, for which the present investigation serves as a baseline.

neuroscience↗