Paranode length in the prefrontal cortex of subjects with major depression and rats under chronic unpredictable stress.

Experimental studies of major depressive disorder (MDD) and stress reveal connectivity disturbances of the prefrontal cortex (PFC) that may involve molecular and morphological changes in myelin and the axons it enwraps. These alterations may also affect the nodes of Ranvier (NR), myelin-bare axon stretches along myelin sheaths necessary for action potential propagation, as well as the paranodes, specialized regions of the myelin sheath flanking NRs. Thus, we investigated whether paranode length and the labeling of paranode marker CASPR in PFC white matter (WM) differed in MDD subjects and chronic stress-exposed rats, as compared to their respective controls.

Reduced length of nodes of Ranvier and altered proteoglycan immunoreactivity in prefrontal white matter in major depressive disorder and chronically stressed rats.

Major depressive disorder (MDD) and chronic unpredictable stress (CUS) in animals feature comparable cellular and molecular disturbances that involve neurons and glial cells in gray and white matter (WM) in prefrontal brain areas. These same areas demonstrate disturbed connectivity with other brain regions in MDD and stress-related disorders. Functional connectivity ultimately depends on signal propagation along WM myelinated axons, and thus on the integrity of nodes of Ranvier (NRs) and their environment.

Working with private hospital midwives in Victoria, Australia to identify practice change priorities: Outcomes of a Delphi study.

Objective/aim: In this study, we invited midwives working at one metropolitan private hospital in Victoria, Australia to identify their workplace change needs and priorities for research.

Methods: In this two-round Delphi study, all midwifery staff within the maternity unit of a private hospital in Melbourne, Australia were invited to participate. In round one, participants joined face-to-face focus groups to put forward their ideas for workplace change and research ideas, and these data were developed into themes.

Synapsin-caveolin-1 gene therapy preserves neuronal and synaptic morphology and prevents neurodegeneration in a mouse model of AD.

Alzheimer's disease (AD) is the most common form of neurodegeneration and cognitive dysfunction in the elderly. Identifying molecular signals that mitigate and reverse neurodegeneration in AD may be exploited therapeutically. Transgenic AD mice (PSAPP) exhibit learning and memory deficits at 9 and 11 months, respectively, with associated decreased expression of caveolin-1 (Cav-1), a membrane/lipid raft (MLR) scaffolding protein necessary for synaptic and neuroplasticity.