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Full-Text Articles in Medicine and Health Sciences
Beneficial Effects Of Increased Lysozyme Levels In Alzheimer's Disease Modelled In Drosophila Melanogaster, Linnea Sandin, Liza Bergkvist, Sangeeta Nath, Claudia Kielkopf, Camilla Janefjord, Linda Helmfors, Henrik Zetterberg, Kaj Blennow, Hongyun Li, Camilla Nilsberth, Brett Garner, Ann-Christin Brorsson, Katarina Kagedal
Beneficial Effects Of Increased Lysozyme Levels In Alzheimer's Disease Modelled In Drosophila Melanogaster, Linnea Sandin, Liza Bergkvist, Sangeeta Nath, Claudia Kielkopf, Camilla Janefjord, Linda Helmfors, Henrik Zetterberg, Kaj Blennow, Hongyun Li, Camilla Nilsberth, Brett Garner, Ann-Christin Brorsson, Katarina Kagedal
Illawarra Health and Medical Research Institute
Genetic polymorphisms of immune genes that associate with higher risk to develop Alzheimer's disease (AD) have led to an increased research interest on the involvement of the immune system in AD pathogenesis. A link between amyloid pathology and immune gene expression was suggested in a genome-wide gene expression study of transgenic amyloid mouse models. In this study, the gene expression of lysozyme, a major player in the innate immune system, was found to be increased in a comparable pattern as the amyloid pathology developed in transgenic mouse models of AD. A similar pattern was seen at protein levels of lysozyme …
Neurotrophin Signaling And Alzheimer's Disease Neurodegeneration - Focus On Bdnf/Trkb Signaling, Jenny Wong
Neurotrophin Signaling And Alzheimer's Disease Neurodegeneration - Focus On Bdnf/Trkb Signaling, Jenny Wong
Illawarra Health and Medical Research Institute
Neurotrophins are small proteins vital for neuronal growth, differentiation, survival, and plasticity. Members of the mammalian neurotrophin family include nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin- 4/5 (NT-4/5). Their neurotrophic effects are mediated by the tropomyosin receptor kinase (Trk) receptors, membrane-bound receptor tyrosine kinases (NGF for TrkA, BDNF and NT4/5 for TrkB, and NT-3 for TrkC) which activate various cell signaling pathways linked to growth, differentiation, and survival. The importance of neurotrophin signaling in brain development is highlighted by findings showing that knockout mice for any one of the neurotrophins or their receptors are fatal …
Novel Behavioural Characteristics Of The Appswe/Ps1Δe9 Transgenic Mouse Model Of Alzheimer's Disease, David Cheng, Warren Logge, Jac Kee Low, Brett Garner, Tim Karl
Novel Behavioural Characteristics Of The Appswe/Ps1Δe9 Transgenic Mouse Model Of Alzheimer's Disease, David Cheng, Warren Logge, Jac Kee Low, Brett Garner, Tim Karl
Illawarra Health and Medical Research Institute
In order to better understand animal models of Alzheimer's disease, novel phenotyping strategies have been established for transgenic mouse models. In line with this, the current study characterised male APPxPS1 transgenic mice on mixed C57BL/6JxC3H/HeJ background for the first time for social recognition memory, sensorimotor gating, and spatial memory using the cheeseboard test as an alternative to the Morris water maze. Furthermore, locomotion, anxiety, and fear conditioning were evaluated in transgenic and wild type-like animals. APPxPS1 males displayed task-dependent hyperlocomotion and anxiety behaviours and exhibited social recognition memory impairments compared to wild type-like littermates. Spatial learning and memory, fear conditioning, …
Amyloid Beta Selectively Modulates Neuronal Trkb Alternative Transcript Expression With Implications For Alzheimer's Disease, J Wong, M Higgins, G Halliday, B Garner
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
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 …