Altruistic behaviour, but not volunteering, has been associated with cognitive performance in community-dwelling older persons.

AIM: Studies have indicated that altruistic behaviour may be associated with better health. Nevertheless, it has not been determined if volunteering acts as a protective factor against cognitive decline or if a person's altruistic character does so. This study aims to evaluate whether altruistic behaviour and volunteering are associated with better cognitive function in active community-dwelling older persons. METHODS: This was a cross-sectional study in healthy older persons. Sociodemographics, altruistic behaviour (self-report altruism scale), volunteering (days volunteered), cognitive state (cognitive assessment battery), and factors associated with cognition (e.g. depression, social support, functional status, and religiosity) were evaluated. Adjusted and non-adjusted models were created in order to understand the relationship of altruistic behaviour and volunteering with cognitive performance. RESULTS: A total of 312 older adults were evaluated; 89.4% were women, and the mean age was 69.6 years. In the linear regression models, greater altruistic behaviour was associated with higher scores on the Mini-Mental State Examination (ß = 0.148, P < 0.05) and the verbal fluency test (ß = 0.219, P < 0.001), even after adjustments. In contrast, volunteering was not associated with any of the cognitive tests used. CONCLUSION: Altruistic behaviour seems to have a role in older persons' cognition, with more altruistic people tending to have greater cognitive performance. These findings can assist in developing mechanisms that can help keep older people more cognitively active and serve as the foundation for future interventions and studies in this area.

Human retinal ganglion cell neurons generated by synchronous BMP inhibition and transcription factor mediated reprogramming.

In optic neuropathies, including glaucoma, retinal ganglion cells (RGCs) die. Cell transplantation and endogenous regeneration offer strategies for retinal repair, however, developmental programs required for this to succeed are incompletely understood. To address this, we explored cellular reprogramming with transcription factor (TF) regulators of RGC development which were integrated into human pluripotent stem cells (PSCs) as inducible gene cassettes. When the pioneer factor NEUROG2 was combined with RGC-expressed TFs (ATOH7, ISL1, and POU4F2) some conversion was observed and when pre-patterned by BMP inhibition, RGC-like induced neurons (RGC-iNs) were generated with high efficiency in just under a week. These exhibited transcriptional profiles that were reminiscent of RGCs and exhibited electrophysiological properties, including AMPA-mediated synaptic transmission. Additionally, we demonstrated that small molecule inhibitors of DLK/LZK and GCK-IV can block neuronal death in two pharmacological axon injury models. Combining developmental patterning with RGC-specific TFs thus provided valuable insight into strategies for cell replacement and neuroprotection.