A5037199575- Alzheimer's disease research and treatments
- Fluoride Effects and Removal
- Nerve injury and regeneration
- Neuroinflammation and Neurodegeneration Mechanisms
- Cholesterol and Lipid Metabolism
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Cellular transport and secretion
- Drug Transport and Resistance Mechanisms
- Peroxisome Proliferator-Activated Receptors
- S100 Proteins and Annexins
- Amino Acid Enzymes and Metabolism
- Arsenic contamination and mitigation
- Erythrocyte Function and Pathophysiology
- Blood properties and coagulation
- Blood Coagulation and Thrombosis Mechanisms
- Prion Diseases and Protein Misfolding
- Peripheral Neuropathies and Disorders
- Cellular Mechanics and Interactions
- MicroRNA in disease regulation
- Infectious Encephalopathies and Encephalitis
- Neuroscience and Neuropharmacology Research
- Neurogenesis and neuroplasticity mechanisms
- Protease and Inhibitor Mechanisms
- Immunotoxicology and immune responses
- Autoimmune Neurological Disorders and Treatments
Flinders University
2020-2023
University of South Australia
2014-2020
Kyoto University
2012-2017
Background The molecular changes involved in Alzheimer's disease (AD) progression remain unclear since we cannot easily access antemortem human brains. Some non-mammalian vertebrates such as the zebrafish preserve AD-relevant transcript isoforms of PRESENILIN genes lost from mice and rats. One example is PS2V, alternative isoform PSEN2 gene. PS2V induced by hypoxia/oxidative stress shows increased expression late onset, sporadic AD A unique, early onset familial mutation PSEN2, K115fs,...
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive deposition of amyloid beta (Aβ) and dysregulation neurotrophic signaling, causing synaptic dysfunction, loss memory, cell death. The expression p75 neurotrophin receptor elevated in the brain AD patients, suggesting its involvement this disease. However, exact mechanism action not yet clear. Here, we show that interacts with beta-site precursor protein cleaving enzyme-1 (BACE1), interaction enhanced...
p75 neurotrophin receptor (p75 NTR ) has been implicated in Alzheimer's disease (AD).However, whether is involved Tau hyperphosphorylation, one of the pathologies observed AD, remains unclear.In our previous study, extracellular domain blocked amyloid beta (Aβ) toxicity and attenuated Aβ-induced hyperphosphorylation.Here we show that, absence Aβ, regulates phosphorylation transgenic mice with P301L human mutation (pR5).The knockout pR5 Tau.In addition, elevated activity kinases responsible...
Plasminogen activator inhibitor type-2 (PAI-2), a member of the serpin family, is dramatically upregulated during pregnancy and in response to inflammation. Although PAI-2 exists glycosylated non-glycosylated forms vivo, majority vitro studies have exclusively involved intracellular form. This study shows that exposure inflammation-associated hypochlorite induces oligomerisation via mechanism involving dityrosine formation. Compared plasminogen type-1 (PAI-1), both are more resistant...
Fibrinogen, a major constituent of blood plasma, is highly susceptible to reaction with biological oxidants. It has been proposed that fibrinogen plays role in antioxidant defence, but oxidation also known disrupt normal clotting and implicated the pathology atherosclerosis. In present study, we show oxidant hypochlorite promotes formation soluble high molecular weight assemblies ≥40 × 106 Da, do not accumulate when induced aggregate by other stresses such as heating or hydroxyl-mediated...
Exacerbated hypochlorite (OCl−) production is linked to neurodegenerative processes, but there growing evidence that lower levels of activity are important protein homeostasis. In this study we characterise the effects on aggregation and toxicity amyloid beta peptide 1–42 (Aβ1-42), a major component plaques form in brain Alzheimer's disease. Our results demonstrate treatment with promotes formation Aβ1-42 assemblies ≥100 kDa have reduced surface exposed hydrophobicity compared untreated...
Exacerbated hypochlorite (OCl-) production during inflammation promotes tissue damage, but there is growing evidence that lower levels of activity may be important to protein homeostasis. In this study we characterise the effects on aggregation and toxicity amyloid beta peptide 1-42 (Aβ1-42), a major component plaques form in brain Alzheimer’s disease. Our results demonstrate treatment with formation Aβ1-42 assemblies ≥ 100 kDa have reduced surface exposed hydrophobicity compared untreated...
Endogeneous phosphorylarted form of APP (pAPP) was investigated in WT and p75KO neurons to elucidate whether phosphorylation is mediated by p75. In addition, (wild type) mutant (T668A) will be co-transfected with different forms p75 identify the interaction pAPP vitro. Mouse primary cortical neuron cultures from wild type mice were treated amyloid beta 42 level phosphorylated measured Western Blotting. The cololalization pAPP/p75, BACE1/p75 also immunohistochemistry. AD models knocked out...
p75NTR, a neurotrophin receptor is found to be involved in amyloid beta pathology and tau hyperphosphorylation patients animal model with Alzheimer’s disease (AD). However, the mechanism on how p75NTR phosphorylation remains unclear. The extracellular domain (ECD) of was block toxicity attenuate hyperphosphorylation. ligand-binding region knocked out pR5 (P301L) mice determine its function by cross-breeding ExonIII -/- (p75KO) generate new pR75KO mice. 3 6 months-old (n=10) were subjected...