2024 |
Stone J, Mitrofanis J, Johnstone DM, Robinson SR, 'The Catastrophe of Intracerebral Hemorrhage Drives the Capillary-Hemorrhage Dementias, Including Alzheimer's Disease.', J Alzheimers Dis, 97 1069-1081 (2024) [C1]
|
|
|
2023 |
Ting KK, Coleman P, Kim HJ, Zhao Y, Mulangala J, Cheng NC, et al., 'Vascular senescence and leak are features of the early breakdown of the blood-brain barrier in Alzheimer's disease models.', Geroscience, 45 3307-3331 (2023) [C1]
|
|
Nova |
2023 |
Johnstone DM, Mitrofanis J, Stone J, 'The brain s weakness in the face of trauma: How head trauma causes the destruction of the brain', Frontiers in Neuroscience, 17 (2023) [C1]
Of all our organs, the brain is perhaps the best protected from trauma. The skull has evolved to enclose it and, within the skull, the brain floats in a protective bath of cerebro... [more]
Of all our organs, the brain is perhaps the best protected from trauma. The skull has evolved to enclose it and, within the skull, the brain floats in a protective bath of cerebrospinal fluid. It is becoming evident, however, that head trauma experienced in young adult life can cause a dementia that appears decades later. The level of trauma that induces such destruction is still being assessed but includes levels well below that which cracks the skull or causes unconsciousness or concussion. Clinically this damage appears as dementia, in people who played body-contact sports in their youth or have survived accidents or the blasts of combat; and appears also, we argue, in old age, without a history of head trauma. The dementias have been given different names, including dementia pugilistica (affecting boxers), chronic traumatic encephalopathy (following certain sports, particularly football), traumatic brain injury (following accidents, combat) and Alzheimer¿s (following decades of life). They share common features of clinical presentation and neuropathology, and this conceptual analysis seeks to identify features common to these forms of brain injury and to identify where in the brain the damage common to them occurs; and how it occurs, despite the protection provided by the skull and cerebrospinal fluid. The analysis suggests that the brain¿s weak point in the face of trauma is its capillary bed, which is torn by the shock of trauma. This identification in turn allows discussion of ways of delaying, avoiding and even treating these trauma-induced degenerations.
|
|
Nova |
2023 |
Stone J, Mitrofanis J, Johnstone DM, Robinson SR, 'Twelve protections evolved for the brain, and their roles in extending its functional life', Frontiers in Neuroanatomy, 17 (2023) [C1]
As human longevity has increased, we have come to understand the ability of the brain to function into advanced age, but also its vulnerability with age, apparent in the age-relat... [more]
As human longevity has increased, we have come to understand the ability of the brain to function into advanced age, but also its vulnerability with age, apparent in the age-related dementias. Against that background of success and vulnerability, this essay reviews how the brain is protected by (by our count) 12 mechanisms, including: the cranium, a bony helmet; the hydraulic support given by the cerebrospinal fluid; the strategically located carotid body and sinus, which provide input to reflexes that protect the brain from blood-gas imbalance and extremes of blood pressure; the blood brain barrier, an essential sealing of cerebral vessels; the secretion of molecules such as haemopexin and (we argue) the peptide Aß to detoxify haemoglobin, at sites of a bleed; autoregulation of the capillary bed, which stabilises metabolites in extracellular fluid; fuel storage in the brain, as glycogen; oxygen storage, in the haemoprotein neuroglobin; the generation of new neurones, in the adult, to replace cells lost; acquired resilience, the stress-induced strengthening of cell membranes and energy production found in all body tissues; and cognitive reserve, the ability of the brain to maintain function despite damage. Of these 12 protections, we identify 5 as unique to the brain, 3 as protections shared with all body tissues, and another 4 as protections shared with other tissues but specialised for the brain. These protections are a measure of the brain¿s vulnerability, of its need for protection. They have evolved, we argue, to maintain cognitive function, the ability of the brain to function despite damage that accumulates during life. Several can be tools in the hands of the individual, and of the medical health professional, for the lifelong care of our brains.
|
|
Nova |
2023 |
Gordon LC, Martin KL, Torres N, Benabid A-L, Mitrofanis J, Stone J, et al., 'Remote photobiomodulation targeted at the abdomen or legs provides effective neuroprotection against parkinsonian MPTP insult.', Eur J Neurosci, 57 1611-1624 (2023) [C1]
|
|
Nova |
2023 |
Ting KK, Coleman P, Kim HJ, Zhao Y, Mulangala J, Cheng NC, et al., 'Vascular senescence and leak are features of the early breakdown of the blood-brain barrier in Alzheimer's disease models', GEROSCIENCE, [C1]
|
|
|
2021 |
Johnstone DM, Hamilton C, Gordon LC, Moro C, Torres N, Nicklason F, et al., 'Exploring the Use of Intracranial and Extracranial (Remote) Photobiomodulation Devices in Parkinson's Disease: A Comparison of Direct and Indirect Systemic Stimulations', JOURNAL OF ALZHEIMERS DISEASE, 83 1399-1413 (2021) [C1]
|
|
|
2021 |
Gomez HM, Pillar AL, Brown AC, Kim RY, Ali MK, Essilfie A-T, et al., 'Investigating the Links between Lower Iron Status in Pregnancy and Respiratory Disease in Offspring Using Murine Models', NUTRIENTS, 13 (2021) [C1]
|
|
Nova |
2020 |
Woods JJ, Skelding KA, Martin KL, Aryal R, Sontag E, Johnstone DM, et al., 'Assessment of evidence for or against contributions of Chlamydia pneumoniae infections to Alzheimer's disease etiology', Brain, Behavior, and Immunity, 83 22-32 (2020) [C1]
Alzheimer's disease, the most common form of dementia, was first formally described in 1907 yet its etiology has remained elusive. Recent proposals that Aß peptide may be par... [more]
Alzheimer's disease, the most common form of dementia, was first formally described in 1907 yet its etiology has remained elusive. Recent proposals that Aß peptide may be part of the brain immune response have revived longstanding contention about the possibility of causal relationships between brain pathogens and Alzheimer's disease. Research has focused on infectious pathogens that may colonize the brain such as herpes simplex type I. Some researchers have proposed the respiratory bacteria Chlamydia pneumoniae may also be implicated in Alzheimer's disease, however this remains controversial. This review aims to provide a balanced overview of the current evidence and its limitations and future approaches that may resolve controversies. We discuss the evidence from in vitro, animal and human studies proposed to implicate Chlamydia pneumoniae in Alzheimer's disease and other neurological conditions, the potential mechanisms by which the bacterium may contribute to pathogenesis and limitations of previous studies that may explain the inconsistencies in the literature.
|
|
Nova |
2020 |
Mo M, Jönsson ME, Mathews MA, Johnstone D, Ke YD, Ittner LM, et al., 'K369I Tau Mice Demonstrate a Shift Towards Striatal Neuron Burst Firing and Goal-directed Behaviour', Neuroscience, 449 46-62 (2020) [C1]
Pathological forms of the microtubule-associated protein tau are involved in a large group of neurodegenerative diseases named tauopathies, including frontotemporal lobar degenera... [more]
Pathological forms of the microtubule-associated protein tau are involved in a large group of neurodegenerative diseases named tauopathies, including frontotemporal lobar degeneration (FTLD-tau). K369I mutant tau transgenic mice (K3 mice) recapitulate neural and behavioural symptoms of FTLD, including tau aggregates in the cortex, alterations to nigrostriatum, memory deficits and parkinsonism. The aim of this study was to further characterise the K3 mouse model by examining functional alterations to the striatum. Whole-cell patch-clamp electrophysiology was used to investigate the properties of striatal neurons in K3 mice and wildtype controls. Additionally, striatal-based instrumental learning tasks were conducted to assess goal-directed versus habitual behaviours (i.e., by examining sensitivity to outcome devaluation and progressive ratios). The K3 model demonstrated significant alterations in the discharge properties of striatal neurons relative to wildtype mice, which manifested as a shift in neuronal output towards a burst firing state. K3 mice acquired goal-directed responding faster than control mice and were goal-directed at test unlike wildtype mice, which is likely to indicate reduced capacity to develop habitual behaviour. The observed pattern of behaviour in K3 mice is suggestive of deficits in dorsal lateral striatal function and this was supported by our electrophysiological findings. Thus, both the electrophysiological and behavioural alterations indicate that K3 mice have early deficits in striatal function. This finding adds to the growing literature which indicate that the striatum is impacted in tau-related neuropathies such as FTLD, and further suggests that the K3 model is a unique mouse model for investigating FTLD especially with striatal involvement.
|
|
|
2020 |
Kim B, Mitrofanis J, Stone J, Johnstone DM, 'Remote tissue conditioning is neuroprotective against MPTP insult in mice (vol 4, pg 14, 2018)', IBRO REPORTS, 9 324-324 (2020)
|
|
|
2020 |
Ali MK, Kim RY, Brown AC, Donovan C, Vanka KS, Mayall JR, et al., 'Critical role for iron accumulation in the pathogenesis of fibrotic lung disease', JOURNAL OF PATHOLOGY, 251 49-62 (2020) [C1]
|
|
Nova |
2020 |
Ali MK, Kim RY, Brown AC, Mayall JR, Karim R, Pinkerton JW, et al., 'Crucial role for lung iron level and regulation in the pathogenesis and severity of asthma', EUROPEAN RESPIRATORY JOURNAL, 55 (2020) [C1]
|
|
Nova |
2020 |
Benson P, Kim JY, Riveros C, Camp A, Johnstone DM, 'Elucidating the time course of the transcriptomic response to photobiomodulation through gene co-expression analysis', JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY, 208 (2020) [C1]
|
|
Nova |
2019 |
Bicknell B, Liebert A, Johnstone D, Kiat H, 'Photobiomodulation of the microbiome: implications for metabolic and inflammatory diseases', LASERS IN MEDICAL SCIENCE, 34 317-327 (2019)
|
|
|
2019 |
Ganeshan V, Skladnev NV, Kim JY, Mitrofanis J, Stone J, Johnstone DM, 'Pre-conditioning with Remote Photobiomodulation Modulates the Brain Transcriptome and Protects Against MPTP Insult in Mice', NEUROSCIENCE, 400 85-97 (2019)
|
|
|
2019 |
Gordon LC, Johnstone DM, 'Remote photobiomodulation: an emerging strategy for neuroprotection', NEURAL REGENERATION RESEARCH, 14 2086-2087 (2019)
|
|
|
2019 |
Liebert A, Bicknell B, Johnstone DM, Gordon LC, Kiat H, Hamblin MR, '"Photobiomics": Can Light, Including Photobiomodulation, Alter the Microbiome?', PHOTOBIOMODULATION PHOTOMEDICINE AND LASER SURGERY, 37 681-693 (2019) [C1]
|
|
|
2019 |
San Miguel M, Martin KL, Stone J, Johnstone DM, 'Photobiomodulation mitigates cerebrovascular leakage induced by the parkinsonian neurotoxin MPTP', Biomolecules, 9 (2019)
|
|
|
2018 |
Stone J, Mitrofanis J, Johnstone DM, Falsini B, Bisti S, Adam P, et al., 'Acquired Resilience: An Evolved System of Tissue Protection in Mammals', DOSE-RESPONSE, 16 (2018)
|
|
|
2018 |
Kim B, Mitrofanis J, Stone J, Johnstone DM, 'Remote tissue conditioning is neuroprotective against MPTP insult in mice', IBRO Reports, 4 14-17 (2018) [C1]
Current treatments for Parkinson's disease (PD) are primarily symptomatic, leaving a need for treatments that mitigate disease progression. One emerging neuroprotective strat... [more]
Current treatments for Parkinson's disease (PD) are primarily symptomatic, leaving a need for treatments that mitigate disease progression. One emerging neuroprotective strategy is remote tissue conditioning, in which mild stress in a peripheral tissue (e.g. a limb) induces protection of life-critical organs such as the brain. We evaluated the potential of two remote tissue conditioning interventions ¿ mild ischemia and photobiomodulation ¿ in protecting the brain against the parkinsonian neurotoxin MPTP. Further, we sought to determine whether combining these two interventions provided any added benefit. Male C57BL/6 mice (n = 10/group) were pre-conditioned with either ischemia of the leg (4 × 5 min cycles of ischemia/reperfusion), or irradiation of the dorsum with 670 nm light (50 mW/cm2, 3 min), or both interventions, immediately prior to receiving two MPTP injections 24 hours apart (50 mg/kg total). Mice were sacrificed 6 days later and brains processed for tyrosine hydroxylase immunohistochemistry. Stereological counts of functional dopaminergic neurons in the substantia nigra pars compacta revealed that both remote ischemia and remote photobiomodulation rescued around half of the neurons that were compromised by MPTP (p < 0.001). Combining the two interventions provided no added benefit, rescuing only 40% of vulnerable neurons (p < 0.01). The present results suggest that remote tissue conditioning, whether ischemia of a limb or photobiomodulation of the torso, induces protection of brain centers critical in PD. The lack of additional benefit when combining these two interventions suggests they may share common mechanistic pathways. Further research is needed to identify these pathways and determine the conditioning doses that yield optimal neuroprotection.
|
|
|
2017 |
Reinhart F, El Massri N, Torres N, Chabrol C, Molet J, Johnstone DM, et al., 'The behavioural and neuroprotective outcomes when 670 nm and 810 nm near infrared light are applied together in MPTP-treated mice', NEUROSCIENCE RESEARCH, 117 42-47 (2017)
|
|
|
2017 |
Kim B, Brandli A, Mitrofanis J, Stone J, Purushothuman S, Johnstone DM, 'Remote tissue conditioning - An emerging approach for inducing body-wide protection against diseases of ageing', AGEING RESEARCH REVIEWS, 37 69-78 (2017)
|
|
|
2017 |
Skladnev NV, Johnstone DM, 'Neuroprotective properties of dietary saffron: more than just a chemical scavenger?', NEURAL REGENERATION RESEARCH, 12 210-211 (2017)
|
|
|
2017 |
Fitzsimmons C, Johnstone D, Conant K, St Hillaire C, Parsons CH, Stins M, et al., 'Soluble lipoprotein receptor-related protein immunoreactive species in cell culture media and serum replacement supplements', Analytical Methods, 9 110-116 (2017) [C1]
The low-density lipoprotein receptor-related protein (LRP) is a large multifunctional cell surface membrane receptor capable of binding over 50 ligands. These include molecules im... [more]
The low-density lipoprotein receptor-related protein (LRP) is a large multifunctional cell surface membrane receptor capable of binding over 50 ligands. These include molecules important in Alzheimer's disease such as the amyloid ß-protein precursor (AßPP), the ß-amyloid (Aß) peptide and apolipoprotein E (ApoE). Full length LRP consists of a 515 kDa extracellular ligand binding a-chain and an 85 kDa membrane spanning ß-chain. A soluble form of LRP (sLRP) present in human plasma retains the ability to bind ligands, including Aß. This soluble form is an ectodomain fragment generated from the membrane bound form of the receptor by proteolytic cleavage. Here we report data demonstrating that some commercial 'serum-free' supplements and 'serum-free' media contain unlisted sLRP immunoreactive species that may reflect the presence of undefined serum protein extracts in these 'serum-free' preparations. This has the potential to interfere with experimental results and interpretation in a range of cell culture studies involving LRP or any of its ligands and possibly also other serum proteins.
|
|
Nova |
2017 |
Ali MK, Kim RY, Karim R, Mayall JR, Martin KL, Shahandeh A, et al., 'Role of iron in the pathogenesis of respiratory disease', INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 88 181-195 (2017) [C1]
|
|
Nova |
2016 |
Heidari M, Gerami SH, Bassett B, Graham RM, Chua ACG, Aryal R, et al., 'Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases', RARE DISEASES, 4 (2016) [C1]
|
|
Nova |
2016 |
Shahandeh A, Johnstone DM, Atkins JR, Sontag J-M, Heidari M, Daneshi N, et al., 'Advantages of Array-Based Technologies for Pre-Emptive Pharmacogenomics Testing.', Microarrays (Basel), 5 (2016) [C1]
|
|
Nova |
2016 |
Moro C, El Massri N, Darlot F, Torres N, Chabrol C, Agay D, et al., 'Effects of a higher dose of near-infrared light on clinical signs and neuroprotection in a monkey model of Parkinson's disease', BRAIN RESEARCH, 1648 19-26 (2016)
|
|
|
2016 |
Reinhart F, El Massri N, Johnstone DM, Stone J, Mitrofanis J, Benabid A-L, Moro C, 'Near-infrared light (670 nm) reduces MPTP-induced parkinsonism within a broad therapeutic time window', EXPERIMENTAL BRAIN RESEARCH, 234 1787-1794 (2016)
|
|
|
2016 |
El Massri N, Moro C, Torres N, Darlot F, Agay D, Chabrol C, et al., 'Near-infrared light treatment reduces astrogliosis in MPTP-treated monkeys', EXPERIMENTAL BRAIN RESEARCH, 234 3225-3232 (2016)
|
|
|
2016 |
El Massri N, Johnstone DM, Peoples CL, Moro C, Reinhart F, Torres N, et al., 'The effect of different doses of near infrared light on dopaminergic cell survival and gliosis in MPTP-treated mice', INTERNATIONAL JOURNAL OF NEUROSCIENCE, 126 76-87 (2016)
|
|
|
2016 |
Skladnev NV, Ganeshan V, Kim JY, Burton TJ, Mitrofanis J, Stone J, Johnstone DM, 'Widespread brain transcriptome alterations underlie the neuroprotective actions of dietary saffron', JOURNAL OF NEUROCHEMISTRY, 139 858-871 (2016)
|
|
|
2016 |
Reinhart F, El Massri N, Chabrol C, Cretallaz C, Johnstone DM, Torres N, et al., 'Intracranial application of near-infrared light in a hemi-parkinsonian rat model: the impact on behavior and cell survival', JOURNAL OF NEUROSURGERY, 124 1829-1841 (2016)
|
|
|
2016 |
Brandli A, Johnstone DM, Stone J, 'Remote Ischemic Preconditioning Protects Retinal Photoreceptors: Evidence From a Rat Model of Light-Induced Photoreceptor Degeneration', INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 57 5302-5313 (2016)
|
|
|
2016 |
Darlot F, Moro C, El Massri N, Chabrol C, Johnstone DM, Reinhart F, et al., 'Near-Infrared Light Is Neuroprotective in a Monkey Model of Parkinson Disease', ANNALS OF NEUROLOGY, 79 59-75 (2016)
|
|
|
2016 |
Johnstone DM, Moro C, Stone J, Benabid A-L, Mitrofanis J, 'Turning On Lights to Stop Neurodegeneration: The Potential of Near Infrared Light Therapy in Alzheimer's and Parkinson's Disease', FRONTIERS IN NEUROSCIENCE, 9 (2016)
|
|
|
2016 |
Woods JJ, Martin KL, Freeman-Acquah E, Smith M, Hansbro P, Horvat J, Johnstone D, 'Cigarette Smoking: A Causal Factor for Alzheimers Disease?', Journal of Gerontology & Geriatric Research, 05 (2016)
|
|
|
2016 |
Bettencourt C, Forabosco P, Wiethoff S, Heidari M, Johnstone DM, Botía JA, et al., 'Gene co-expression networks shed light into diseases of brain iron accumulation', Neurobiology of Disease, 87 59-68 (2016) [C1]
Aberrant brain iron deposition is observed in both common and rare neurodegenerative disorders, including those categorized as Neurodegeneration with Brain Iron Accumulation (NBIA... [more]
Aberrant brain iron deposition is observed in both common and rare neurodegenerative disorders, including those categorized as Neurodegeneration with Brain Iron Accumulation (NBIA), which are characterized by focal iron accumulation in the basal ganglia. Two NBIA genes are directly involved in iron metabolism, but whether other NBIA-related genes also regulate iron homeostasis in the human brain, and whether aberrant iron deposition contributes to neurodegenerative processes remains largely unknown. This study aims to expand our understanding of these iron overload diseases and identify relationships between known NBIA genes and their main interacting partners by using a systems biology approach.We used whole-transcriptome gene expression data from human brain samples originating from 101 neuropathologically normal individuals (10 brain regions) to generate weighted gene co-expression networks and cluster the 10 known NBIA genes in an unsupervised manner. We investigated NBIA-enriched networks for relevant cell types and pathways, and whether they are disrupted by iron loading in NBIA diseased tissue and in an in vivo mouse model.We identified two basal ganglia gene co-expression modules significantly enriched for NBIA genes, which resemble neuronal and oligodendrocytic signatures. These NBIA gene networks are enriched for iron-related genes, and implicate synapse and lipid metabolism related pathways. Our data also indicates that these networks are disrupted by excessive brain iron loading.We identified multiple cell types in the origin of NBIA disorders. We also found unforeseen links between NBIA networks and iron-related processes, and demonstrate convergent pathways connecting NBIAs and phenotypically overlapping diseases. Our results are of further relevance for these diseases by providing candidates for new causative genes and possible points for therapeutic intervention.
|
|
Nova |
2016 |
Heidari M, Johnstone DM, Bassett B, Graham RM, Chua ACG, House MJ, et al., 'Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features', Molecular Psychiatry, 21 1599-1607 (2016) [C1]
The 'neurodegeneration with brain iron accumulation' (NBIA) disease family entails movement or cognitive impairment, often with psychiatric features. To understand how i... [more]
The 'neurodegeneration with brain iron accumulation' (NBIA) disease family entails movement or cognitive impairment, often with psychiatric features. To understand how iron loading affects the brain, we studied mice with disruption of two iron regulatory genes, hemochromatosis (Hfe) and transferrin receptor 2 (Tfr2). Inductively coupled plasma atomic emission spectroscopy demonstrated increased iron in the Hfe -/- × Tfr2 mut brain (P=0.002, n =5/group), primarily localized by Perls' staining to myelinated structures. Western immunoblotting showed increases of the iron storage protein ferritin light polypeptide and microarray and real-time reverse transcription-PCR revealed decreased transcript levels (P<0.04, n =5/group) for five other NBIA genes, phospholipase A2 group VI, fatty acid 2-hydroxylase, ceruloplasmin, chromosome 19 open reading frame 12 and ATPase type 13A2. Apart from the ferroxidase ceruloplasmin, all are involved in myelin homeostasis; 16 other myelin-related genes also showed reduced expression (P<0.05), although gross myelin structure and integrity appear unaffected (P>0.05). Overlap (P<0.0001) of differentially expressed genes in Hfe -/- × Tfr2 mut brain with human gene co-expression networks suggests iron loading influences expression of NBIA-related and myelin-related genes co-expressed in normal human basal ganglia. There was overlap (P<0.0001) of genes differentially expressed in Hfe -/- × Tfr2 mut brain and post-mortem NBIA basal ganglia. Hfe -/- × Tfr2 mut mice were hyperactive (P<0.0112) without apparent cognitive impairment by IntelliCage testing (P>0.05). These results implicate myelin-related systems involved in NBIA neuropathogenesis in early responses to iron loading. This may contribute to behavioral symptoms in NBIA and hemochromatosis and is relevant to patients with abnormal iron status and psychiatric disorders involving myelin abnormalities or resistant to conventional treatments.
|
|
Nova |
2015 |
Reinhart F, El Massri N, Darlot F, Torres N, Johnstone DM, Chabrol C, et al., '810 nm near-infrared light offers neuroprotection and improves locomotor activity in MPTP-treated mice', NEUROSCIENCE RESEARCH, 92 86-90 (2015)
|
|
|
2015 |
Purushothurnan S, Johnstone DM, Nandasena C, van Eersel J, Ittner LM, Mitrofanis J, Stone J, 'Near infrared light mitigates cerebellar pathology in transgenic mouse models of dementia', NEUROSCIENCE LETTERS, 591 155-159 (2015)
|
|
|
2015 |
Stone J, Johnstone DM, Mitrofanis J, O'Rourke M, 'The Mechanical Cause of Age-Related Dementia (Alzheimer's Disease): The Brain is Destroyed by the Pulse', JOURNAL OF ALZHEIMERS DISEASE, 44 355-373 (2015)
|
|
|
2015 |
Johnstone DM, Mitrofanis J, Stone J, 'Targeting the body to protect the brain: inducing neuroprotection with remotely-applied near infrared light', NEURAL REGENERATION RESEARCH, 10 349-351 (2015)
|
|
|
2014 |
Moro C, El Massri N, Torres N, Ratel D, De Jaeger X, Chabrol C, et al., 'Photobiomodulation inside the brain: a novel method of applying near-infrared light intracranially and its impact on dopaminergic cell survival in MPTP-treated mice', JOURNAL OF NEUROSURGERY, 120 670-683 (2014)
|
|
|
2014 |
Johnstone DM, El Massri N, Moro C, Spana S, Wang XS, Torres N, et al., 'INDIRECT APPLICATION OF NEAR INFRARED LIGHT INDUCES NEUROPROTECTION IN A MOUSE MODEL OF PARKINSONISM - AN ABSCOPAL NEUROPROTECTIVE EFFECT', NEUROSCIENCE, 274 93-101 (2014)
|
|
|
2014 |
Purushothuman S, Johnstone DM, Nandasena C, Mitrofanis J, Stone J, 'Photobiomodulation with near infrared light mitigates Alzheimer's disease-related pathology in cerebral cortex - evidence from two transgenic mouse models', ALZHEIMERS RESEARCH & THERAPY, 6 (2014)
|
|
|
2014 |
Shahandeh A, Purushothuman S, Martin K, Graham M, Johnstone DM, Milward EA, 'Anti-oxidant Phytochemicals As Potential Treatments For Age-Related Macular Degeneration.', Journal of Antioxidant Activity, 1 29-41 (2014)
|
|
|
2014 |
Johnstone D, Coleman K, Moro C, Torres N, Eells J, Baker G, et al., 'The potential of light therapy in Parkinson's disease', ChronoPhysiology and Therapy, 1-1 (2014)
|
|
|
2014 |
Aryal R, Woods J, Johnstone DM, Horvat J, Milward E, 'Is the A-beta peptide of Alzheimer s Disease an Antimicrobial Peptide?', Journal of Gerontology & Geriatric Research, 03 (2014)
|
|
|
2014 |
Milward EA, Moscato P, Riveros C, Johnstone DM, 'Beyond Statistics: A New Combinatorial Approach to Identifying Biomarker Panels for the Early Detection and Diagnosis of Alzheimer's Disease', JOURNAL OF ALZHEIMERS DISEASE, 39 211-217 (2014) [C1]
|
|
Nova |
2014 |
Mate K, Riveros C, Weidenhofer J, Goldie B, Scott J, Moscato P, et al., 'Strategies for Enhancing Communication between Students, Academics and Researchers participating in Large-Scale Undergraduate Research Projects', International Journal of Innovation in Science and Mathematics Education, 22 14-29 (2014) [C1]
|
|
Nova |
2013 |
Purushothuman S, Nandasena C, Johnstone DM, Stone J, Mitrofanis J, 'The impact of near-infrared light on dopaminergic cell survival in a transgenic mouse model of parkinsonism', BRAIN RESEARCH, 1535 61-70 (2013)
|
|
|
2013 |
Moro C, Torres N, El Massri N, Ratel D, Johnstone DM, Stone J, et al., 'Photobiomodulation preserves behaviour and midbrain dopaminergic cells from MPTP toxicity: evidence from two mouse strains', BMC NEUROSCIENCE, 14 (2013)
|
|
|
2013 |
Purushothuman S, Nandasena C, Peoples CL, El Massri N, Johnstone DM, Mitrofanis J, Stone J, 'Saffron Pre-Treatment Offers Neuroprotection to Nigral and Retinal Dopaminergic Cells of MPTP-Treated mice', JOURNAL OF PARKINSONS DISEASE, 3 77-83 (2013)
|
|
|
2013 |
Purushothuman S, Marotte L, Stowe S, Johnstone DM, Stone J, 'The Response of Cerebral Cortex to Haemorrhagic Damage: Experimental Evidence from a Penetrating Injury Model', PLOS ONE, 8 (2013)
|
|
|
2013 |
Acikyol B, Graham RM, Trinder D, House MJ, Olynyk JK, Scott RJ, et al., 'Brain transcriptome perturbations in the transferrin receptor 2 mutant mouse support the case for brain changes in iron loading disorders, including effects relating to long-term depression and long-term potentiation', Neuroscience, 235 119-128 (2013) [C1]
|
|
Nova |
2013 |
Johnstone DM, Riveros C, Heidari M, Graham RM, Trinder D, Berretta R, et al., 'Evaluation of Different Normalization and Analysis Procedures for Illumina Gene Expression Microarray Data Involving Small Changes', Microarrays, 2 131-152 (2013) [C1]
|
|
Nova |
2012 |
Johnstone DM, Graham RM, Trinder D, Delima RD, Riveros RC, Olynyk JK, et al., 'Brain transcriptome perturbations in the Hfe(-/-) mouse model of genetic iron loading', Brain Research, 1448 144-152 (2012) [C1]
|
|
Nova |
2012 |
Milward AE, Daneshi N, Johnstone DM, 'Emerging real-time technologies in molecular medicine and the evolution of integrated 'pharmacomics' approaches to personalized medicine and drug discovery', Pharmacology and Therapeutics, 136 295-304 (2012) [C1]
|
|
Nova |
2012 |
De Bock CE, Ardjmand Ghahestani A, Molloy TJ, Bone SM, Johnstone DM, Campbell DM, et al., 'The Fat1 cadherin is overexpressed and an independent prognostic factor for survival in paired diagnosis-relapse samples of precursor B-cell acute lymphoblastic leukemia', Leukemia, 26 918-926 (2012) [C1]
|
|
Nova |
2012 |
Johnstone DM, Graham RM, Trinder D, Riveros RC, Olynyk JK, Scott R, et al., 'Changes in brain transcripts related to Alzheimer's disease in a model of HFE hemochromatosis are not consistent with increased Alzheimer's disease risk', Journal of Alzheimers Disease, 30 791-803 (2012) [C1]
|
|
Nova |
2012 |
Arefin AS, Mathieson L, Johnstone DM, Berretta RE, Moscato PA, 'Unveiling clusters of RNA transcript pairs associated with markers of Alzheimer's disease progression', PLOS One, 7 1-25 (2012) [C1]
|
|
Nova |
2012 |
Johnstone DM, Milward AE, Berretta RE, Moscato PA, 'Multivariate protein signatures of pre-clinical Alzheimer's disease in the Alzheimer's disease meuroimaging initiative (ADNI) plasma proteome dataset', PLoS One, 7 (2012) [C1]
|
|
Nova |
2010 |
Johnstone DM, Milward AE, 'Molecular genetic approaches to understanding the roles and regulation of iron in brain health and disease', Journal of Neurochemistry, 113 1387-1402 (2010) [C1]
|
|
Nova |
2010 |
Johnstone DM, Milward AE, 'Genome-wide microarray analysis of brain gene expression in mice on a short-term high iron diet', Neurochemistry International, 56 856-863 (2010) [C1]
|
|
Nova |
2010 |
Graham RM, Chua ACG, Carter KW, Delima RD, Johnstone DM, Herbison CE, et al., 'Hepatic iron loading in mice increases cholesterol biosynthesis', Hepatology, 52 462-471 (2010) [C1]
|
|
Nova |
2009 |
Shi Z, Johnstone DM, Talseth-Palmer B, Evans T-J, Spigelman AD, Groombridge C, et al., 'Haemochromatosis HFE gene polymorphisms as potential modifiers of hereditary nonpolyposis colorectal cancer risk and onset age', International Journal of Cancer, 125 78-83 (2009) [C1]
|
|
Nova |
2007 |
Milward AE, Johnstone DM, Trinder D, Ramm G, Olynyk J, 'The Nexus of iron and inflammation in hepcidin regulation: SMADs, STATs, and ECSIT', Hepatology, 45 253-256 (2007) [C1]
|
|
|