A house is not a home: a network model perspective on the dynamics between subjective quality of living conditions, social support, and mental health of refugees and asylum seekers.

BACKGROUND: Providing adequate living conditions for forcibly displaced people represents a significant challenge for host countries such as Germany. This study explores refugee mental health's reciprocal, dynamic relationship with post-migration living conditions and social support. METHODS: The study sample included 325 Arabic- or Farsi-speaking asylum seekers and refugees residing in Germany since 2014 and seeking mental health treatment. Associations between reported symptoms of post-traumatic stress and depression and the subjective quality of living conditions and perceived social support were analyzed using a two-level approach including multiple linear regression and network analyses. RESULTS: Post-migration quality of living conditions and perceived social support were significantly associated with negative mental health outcomes on both levels. In the network, both post-migration factors were negatively connected with overlapping symptoms of psychiatric disorders, representing potential target symptoms for psychological treatment. CONCLUSION: Post-migration quality of living conditions and social support are important factors for refugee mental health and should be targeted by various actors fostering mental well-being and integration.

Seed-induced Aß deposition alters neuronal function and impairs olfaction in a mouse model of Alzheimer's disease.

Alzheimer's disease (AD) is characterized by the accumulation of amyloid-ß (Aß) which ultimately forms plaques. These Aß deposits can be induced in APP transgenic mouse models by prion-like seeding. It has been widely accepted that anosmia and hyposmia occur during the early stages of AD, even before cognitive deficits are present. In order to determine the impact of seed-induced Aß deposits on olfaction, we performed intracerebral injections of seed-competent brain homogenate into the olfactory bulb of young pre-depositing APP transgenic mice. Remarkably, we observed a dramatic olfactory impairment in those mice. Furthermore, the number of newborn neurons as well as the activity of cells in the mitral cell layer was decreased. Notably, exposure to an enriched environment reduced Aß seeding, vivified neurogenesis and most importantly reversed olfactory deficits. Based on our findings, we conclude that altered neuronal function as a result of induced Aß pathology might contribute to olfactory dysfunction in AD.