Medicine and Health Sciences Commons^™

Novel Implications Of Lingo-1 And Its Signaling Partners In Schizophrenia, F Fernandez-Enright, J L. Andrews, K A. Newell, C Pantelis, Xu-Feng Huang

Illawarra Health and Medical Research Institute

Myelination and neurite outgrowth both occur during brain development, and their disturbance has been previously been implicated in the pathophysiology of schizophrenia. Leucine-rich repeat and immunoglobulin domain-containing protein (Lingo-1) is a potent negative regulator of axonal myelination and neurite extension. As co-factors of Lingo-1 signaling (Nogo receptor (NgR), With No Lysine (K) (WNK1) and Myelin transcription factor 1 (Myt1)) have been implicated in the genetics of schizophrenia, we explored for the first time the role of Lingo-1 signaling pathways in this disorder. Lingo-1 protein, together with its co-receptor and co-factor proteins NgR, tumor necrosis factor (TNF) receptor orphan Y (TROY), …

Preventing Help-Negation For Suicidal Ideation: Implications For Thwarted Belongingness, Social Network Size And Frequency Of Social Interaction, Alexander Svenson, Coralie J. Wilson, Peter Caputi

Illawarra Health and Medical Research Institute

Poster presented at the National Suicide Prevention Conference, Melbourne Australia, July 2013

Help-negation is seen when the severity of an individual's suicidal ideation increases and they become less likely to seek help as a result of their condition. Research has implicated distorted affect regulation and perceptual processes related to social support in the development of help-negation among suicidal individuals (Wilson et al., 2013). Future research needs to focus on psycho-social factors that can be linked to neurological processes that differentiate suicidal individuals from controls and are directly implicated in the help-negation processes associated with suicidal ideation. As suicidal individuals have …

Novel Implications Of Lingo-1 And Its Signalling Partners In The Dorsolateral Prefrontal Cortex In Schizophrenia, Jessica L. Andrews, Kelly A. Newell, Xu-Feng Huang, Francesca Fernandez-Enright

Illawarra Health and Medical Research Institute

No abstract provided.

Amyloid Beta Selectively Modulates Neuronal Trkb Alternative Transcript Expression With Implications For Alzheimer's Disease, J Wong, M Higgins, G Halliday, B Garner

Illawarra Health and Medical Research Institute

Dysregulation in brain-derived neurotrophic factor (BDNF)/full-length TrkB (TrkB-TK+) signaling is implicated in promoting neurodegeneration in Alzheimer's disease (AD). BDNF/TrkB-TK+ signaling can be modulated by the presence of truncated TrkB isoforms (TrkB-TK-, TrkB-Shc). All TrkB isoforms are encoded by different alternative transcripts. In this study, we assessed if expression of the three main TrkB alternative transcripts, TrkB-TK+, TrkB-TK-, and TrkB-Shc are altered in AD. Using a cohort of control and AD brains (n=29), we surveyed the hippocampus, temporal cortex, occipital cortex, and cerebellum and found specific increases in TrkB-Shc, a neuron-specific transcript, in the AD hippocampus. No significant changes were detected …

Srp20 Regulates Trkb Pre-Mrna Splicing To Generate Trkb-Shc Transcripts With Implications For Alzheimer's Disease, Jenny Wong, Brett Garner, Glenda M. Halliday, John B.J Kwok

Illawarra Health and Medical Research Institute

Previously, we reported elevated levels of the neuronspecific tropomyosin receptor kinase B (TrkB) transcript, TrkB- sarc homology containing (Shc) in the hippocampus of Alzheimer’s disease (AD) brains. In this study, we determined how TrkB-Shc transcripts are increased in AD. Utilizing a TrkB minigene transiently transfected into SHSY5Y cells, we found increased exon 19 inclusion in TrkB minigene transcripts (to generate TrkB-Shc) following cellular exposure to amyloid beta 1–42 (Ab42). As this suggested altered TrkB pre-mRNA splicing in AD, we conducted an in silico screening for putative splice regulatory protein-binding sites in the intron/exon splice regulatory regions of exons 18 and …