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Purpose The adverse impact of hearing loss (HL) extends beyond auditory impairment and may affect the individuals' psychosocial wellbeing. We aimed to examine whether there exists a causal psychosocial pathway between HL and depression in later life, via socioeconomic factors and quality of life, and whether hearing aids usage alleviates depressive symptoms over time. Methods We examined the longitudinal relationship between HL and depressive symptoms (CES-D) applying dynamic cross-lagged mediation path models. We used the full dataset of participants aged 50–89 years (74,908 person-years), from all eight Waves of the English Longitudinal Study of Ageing (ELSA). Their quality of life (CASP-19) and their wealth were examined as the mediator and moderator of this relationship, respectively. Subgroup analyses investigated differences among those with hearing aids within different models of subjectively and objectively identified HL. All models were adjusted for age, sex, retirement status and social engagement. Results Socioeconomic position (SEP) influenced the strength of the relationship between HL and depression, which was stronger in the lowest versus the highest wealth quintiles. The use of hearing aids was beneficial for alleviating depressive symptoms. Those in the lowest wealth quintiles experienced a lower risk for depression after the use of hearing aids compared to those in the highest wealth quintiles. Conclusion HL poses a substantial risk for depressive symptoms in older adults, especially those who experience socioeconomic inequalities. The early detection of HL and provision of hearing aids may not only promote better-hearing health but could also enhance the psychosocial wellbeing of older adults, particularly those in a lower SEP.

Heterogeneous nuclear ribonucleoproteins (HnRNPs) are a group of ubiquitously expressed RNA-binding proteins implicated in the regulation of all aspects of nucleic acid metabolism. HnRNP K is a member of this highly versatile hnRNP family. Pathological redistribution of hnRNP K to the cytoplasm has been linked to the pathogenesis of several malignancies but, until now, has been underexplored in the context of neurodegenerative disease. Here we show hnRNP K mislocalisation in pyramidal neurons of the frontal cortex to be a novel neuropathological feature that is associated with both frontotemporal lobar degeneration and ageing. HnRNP K mislocalisation is mutually exclusive to TDP-43 and tau pathological inclusions in neurons and was not observed to colocalise with mitochondrial, autophagosomal or stress granule markers. De-repression of cryptic exons in RNA targets following TDP-43 nuclear depletion is an emerging mechanism of potential neurotoxicity in frontotemporal lobar degeneration and the mechanistically overlapping disorder amyotrophic lateral sclerosis. We silenced hnRNP K in neuronal cells to identify the transcriptomic consequences of hnRNP K nuclear depletion. Intriguingly, by performing RNA-seq analysis we find that depletion of hnRNP K induces 101 novel cryptic exon events. We validated cryptic exon inclusion in an SH-SY5Y hnRNP K knockdown and in FTLD brain exhibiting hnRNP K nuclear depletion. We, therefore, present evidence for hnRNP K mislocalisation to be associated with FTLD and for this to induce widespread changes in splicing. Supplementary Information The online version contains supplementary material available at 10.1007/s00401-021-02340-0.

Some researchers claim that health care expenditures for older people are growing faster than for the rest of the population. This process is referred to as steepening. The aim of this paper is to test steepening, applying new data and revised methods. Furthermore, we explain the connection between the terms red herring hypothesis, i.e., that time to death and not age per se drives the health care expenditures, and steepening. We also present the mechanisms that may induce steepening, as presented in the literature. When testing steepening, we apply data from all inpatient stays in somatic hospitals in Norway in the period 1998–2009, i.e., the data has no self-selection and covers the entire population of Norway (5 million). Our analysis does not reject steepening, with the exception of the 0-year-olds. The results also hold when controlling for mortality-related expenditures. Furthermore, we observe an increase in expenditures for the 0-year-olds. Finally, we find increasing mortality-related expenditures over time. We find the link between steepening and the red herring hypothesis to be vague, and we find steepening and the red herring hypothesis to be independent.