A5039639173- Neurogenesis and neuroplasticity mechanisms
- Neuroinflammation and Neurodegeneration Mechanisms
- Genetic Neurodegenerative Diseases
- Alzheimer's disease research and treatments
- Mitochondrial Function and Pathology
- Neuroscience and Neuropharmacology Research
- Amyotrophic Lateral Sclerosis Research
- Parkinson's Disease Mechanisms and Treatments
- Neurological disorders and treatments
- RNA Research and Splicing
- Barrier Structure and Function Studies
- Olfactory and Sensory Function Studies
- Immune cells in cancer
- Axon Guidance and Neuronal Signaling
- Glioma Diagnosis and Treatment
- Neurogenetic and Muscular Disorders Research
- Nerve injury and regeneration
- Traumatic Brain Injury and Neurovascular Disturbances
- Immune Response and Inflammation
- Intracerebral and Subarachnoid Hemorrhage Research
- MicroRNA in disease regulation
- Epigenetics and DNA Methylation
- Prion Diseases and Protein Misfolding
- Cerebrospinal fluid and hydrocephalus
- Caveolin-1 and cellular processes
University of Auckland
2016-2025
Brain Research New Zealand
2015-2023
Janssen (United Kingdom)
2023
John Wiley & Sons (United States)
2023
Liechtenstein Institute
2023
Hudson Institute
2023
Texas Christian University
2019
University Radiology
2015
University of Gothenburg
2006-2013
Centers for Disease Control and Prevention
1998-2011
Gingipains from Porphyromonas gingivalis drive Alzheimer’s pathology and can be blocked with small-molecule inhibitors.
The rostral migratory stream (RMS) is the main pathway by which newly born subventricular zone cells reach olfactory bulb (OB) in rodents. However, RMS adult human brain has been elusive. We demonstrate presence of a RMS, unexpectedly organized around lateral ventricular extension reaching OB, and illustrate neuroblasts it. ensheathing extension, as seen magnetic resonance imaging, cell-specific markers, electron microscopy, contains progenitor with characteristics that incorporate...
Germline mutations in the tumour suppressor gene PTEN have been implicated two hamartoma syndromes that exhibit some clinical overlap, Cowden syndrome (CS) and Bannayan-Riley-Ruvalcaba (BRR). maps to 10q23 encodes a dual specificity phosphatase, substrate of which is phosphatidylinositol 3,4,5-triphosphate, phospholipid 3-kinase pathway. CS characterized by multiple hamartomas an increased risk benign malignant disease breast, thyroid central nervous system, whilst presence cancer has not...
Neurogenesis has recently been observed in the adult human brain, suggesting possibility of endogenous neural repair. However, augmentation neurogenesis brain response to neuronal cell loss not demonstrated. This study was undertaken investigate whether occurs subependymal layer (SEL) adjacent caudate nucleus neurodegeneration Huntington's disease (HD). Postmortem control and HD tissue were examined by using cycle marker proliferating nuclear antigen (PCNA), βIII-tubulin, glial fibrillary...
Stem cells generate neurons in discrete regions the postnatal mammalian brain. However, extent of neurogenesis adult human brain has been difficult to establish. We have taken advantage integration (14)C, generated by nuclear bomb tests during Cold War, DNA establish age major areas cerebral neocortex. Together with analysis neocortex from patients who received BrdU, which integrates dividing cells, our results demonstrate that, whereas nonneuronal turn over, are not adulthood at detectable...
Papertrinucleotide repeat expansion resulting in an elongated polyglutamine stretch near the N-terminus of huntingtin (HTT) protein [2].HD patients have CAG lengths greater than 36 on one HTT alleles.Although HD affects a number brain regions such as cortex, thalamus, and subthalamic nucleus, www.impactaging.com
Transforming growth factor beta 1 (TGFβ1) is strongly induced following brain injury and polarises microglia to an anti-inflammatory phenotype. Augmentation of TGFβ1 responses may therefore be beneficial in preventing inflammation neurological disorders including stroke neurodegenerative diseases. However, several other cell types display immunogenic potential identifying the effect on these cells required more fully understand its effects inflammation. Pericytes are multifunctional which...
Neutrophil accumulation is a well-established feature of Alzheimer's disease (AD) and has been linked to cognitive impairment by modulating disease-relevant neuroinflammatory vascular pathways. Neutrophils express high levels the oxidant-generating enzyme myeloperoxidase (MPO), however there controversy regarding cellular source localisation MPO in AD brain.We used immunostaining immunoassays quantify neutrophils human tissue microarrays brains APP/PS1 mice. We also multiplexed...
Abstract In Parkinson’s disease (PD), and other α-synucleinopathies, α-synuclein (α-Syn) aggregates form a myriad of conformational truncational variants. Most antibodies used to detect quantify α-Syn in the human brain target epitopes within C-terminus (residues 96–140) 140 amino acid protein may fail capture diversity variants present PD. We sought investigate heterogeneity conformations aggregation states PD by labelling with multiple that along entire length α-Syn. multiplex...
Abstract Myelin loss is frequently observed in human Alzheimer's disease (AD) and may constitute to AD‐related cognitive decline. A potential source repair myelin defects are the oligodendrocyte progenitor cells (OPCs) present an adult brain. However, until now, little known about reaction of these toward amyloid plaque deposition neither AD patients nor appropriate mouse models. Therefore, we analyzed lineage a model with chronic (APPPS1 mice) samples from patients. In APPPS1 mice integrity...
Alzheimer's disease (AD) is an age-related neurodegenerative disorder that displays pathological characteristics including senile plaques and neurofibrillary tangles. Metabolic defects are also present in AD-brain: for example, signs of deficient cerebral glucose uptake may occur decades before onset cognitive dysfunction tissue damage. There have been few systematic studies the metabolite content AD human brain, possibly due to scarcity high-quality brain and/or lack reliable experimental...
Abstract Parkinson’s disease (PD) is characterized by the presence of inclusions known as Lewy bodies, which mainly consist α-synuclein (α-syn) aggregates. There growing evidence that α-syn self-propagates in non-neuronal cells, thereby contributing to progression and spread PD pathology brain. Tunneling nanotubes (TNTs) are long, thin, F-actin-based membranous channels connect cells have been proposed act conduits for transfer between cells. SH-SY5Y primary human brain pericytes, derived...
Summary A main neurogenic niche in the adult human brain is subventricular zone (SVZ). Recent data suggest that progenitors are born SVZ migrate via rostral migratory stream (RMS) towards olfactory bulb (OB), similar to what has been observed other mammals. subpopulation of astrocytes specifically expresses an assembly‐compromised isoform intermediate filament protein glial fibrillary acidic (GFAP‐δ). To further define phenotype these GFAP‐δ expressing cells and determine whether present...
Microglia play critical roles in the brain during homeostasis and pathological conditions. Understanding molecular events underpinning microglial functions activation states will further enable us to target these cells for treatment of neurological disorders. The transcription factor PU.1 is development myeloid a major regulator gene expression. In brain, specifically expressed microglia recent evidence from genome-wide association studies suggests that reductions contribute delayed onset...
Pericytes and endothelial cells are critical cellular components of the blood-brain barrier (BBB) play an important role in neuroinflammation. To date, majority inflammation-related studies endothelia pericytes have been carried out using immortalised cell lines or non-human-derived cells. Whether these representative primary human is unclear systematic comparisons inflammatory responses brain-derived has yet to be performed.To study effects neuroinflammation at BBB, brain were isolated from...
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG expansion in the gene-encoding Huntingtin (HTT). Transcriptome dysregulation major feature of HD pathogenesis, as revealed large body work on gene expression profiling tissues from human patients and mouse models. These studies were primarily focused transcriptional changes affecting steady-state overall levels using microarray based approaches. A missing component, however, has been study...
Widespread brain-copper deficiency in patients with Alzheimer's dementia (red) compared to controls (blue).