A5047385288- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- Prion Diseases and Protein Misfolding
- Cholinesterase and Neurodegenerative Diseases
- Trace Elements in Health
- Functional Brain Connectivity Studies
- Computational Drug Discovery Methods
- Medical Imaging Techniques and Applications
- Parkinson's Disease Mechanisms and Treatments
- Health, Environment, Cognitive Aging
- Advanced Neuroimaging Techniques and Applications
- Neurological Disease Mechanisms and Treatments
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Neurological diseases and metabolism
- Bioinformatics and Genomic Networks
- Nuclear Receptors and Signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- Advanced MRI Techniques and Applications
- Folate and B Vitamins Research
- Frailty in Older Adults
- Nutritional Studies and Diet
- S100 Proteins and Annexins
- Neuroscience and Neuropharmacology Research
- Health Systems, Economic Evaluations, Quality of Life
- Amyotrophic Lateral Sclerosis Research
Florey Institute of Neuroscience and Mental Health
2016-2025
The University of Melbourne
2016-2025
Australian e-Health Research Centre
2010-2024
CSIRO Health and Biosecurity
2016-2024
Edith Cowan University
2011-2024
Austin Health
2008-2024
The Ohio State University
2024
Curtin University
2024
Breast Cancer Network Australia
2024
Tokyo Women's Medical University
2019-2023
We have purified and characterized the cerebral amyloid protein that forms plaque core in Alzheimer disease aged individuals with Down syndrome. The consists of multimeric aggregates a polypeptide about 40 residues (4 kDa). amino acid composition, molecular mass, NH2-terminal sequence this are almost identical to those described for deposited congophilic angiopathy syndrome, but proteins ragged NH2 termini. shared 4-kDa subunit indicates common origin amyloids angiopathy. There superficial...
The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the develops over many years. Autosomal dominant has a predictable age at onset provides an opportunity to determine sequence changes that culminate symptomatic disease.
Genetic evidence strongly supports the view that Aβ amyloid production is central to cause of Alzheimer's disease. The kinetics, compartmentation, and form its temporal relation neurodegenerative process remain uncertain. levels soluble insoluble were determined by using western blot techniques, findings assessed in indices severity mean level increased threefold disease correlates highly with markers severity. In contrast, (also a measure total load) found only discriminate from controls,...
Aβ1-40, a major component of Alzheimer's disease cerebral amyloid, is present in the cerebrospinal fluid and remains relatively soluble at high concentrations (less than or equal to 3.7 mM). Thus, physiological factors which induce Aβ amyloid formation could provide clues pathogenesis disease. It has been shown that human specifically saturably binds zinc. Here, zinc above 300 nM rapidly destabilized Aβ1-40 solutions, inducing tinctorial formation. However, rat less avidly immune these...
<b>Objective: </b> To compare brain β-amyloid (Aβ) burden measured with [<sup>11</sup>C]Pittsburgh Compound B (PIB) PET in normal aging, Alzheimer disease (AD), and other dementias. <b>Methods: Thirty-three subjects dementia (17 AD, 10 Lewy bodies [DLB], 6 frontotemporal [FTD]), 9 mild cognitive impairment (MCI), 27 age-matched healthy control (HCs) were studied. Aβ was quantified using PIB distribution volume ratio. <b>Results: Cortical binding markedly elevated every AD subject regardless...
Background: Alzheimer disease (AD) may be caused by the toxic accumulation of -amyloid (A).Objective: To test this theory, we developed a clinical intervention using clioquinol, metal-proteinattenuating compound (MPAC) that inhibits zinc and copper ions from binding to A, thereby promoting A dissolution diminishing its properties.Methods: A pilot phase 2 trial in patients with moderately severe disease.Results: Thirty-six subjects were randomized.The effect treatment was significant more...
The Australian Imaging, Biomarkers and Lifestyle (AIBL) flagship study of aging aimed to recruit 1000 individuals aged over 60 assist with prospective research into Alzheimer's disease (AD). This paper describes the recruitment cohort gives information about methodology, baseline demography, diagnoses, medical comorbidities, medication use, cognitive function participants.Volunteers underwent a screening interview, had comprehensive testing, gave 80 ml blood, completed health lifestyle...
β-amyloid (Aβ) deposition is pathognomic for Alzheimer's disease (AD), but may occur in normal elderly people without apparent cognitive effect. Episodic memory impairment an early and prominent sign of AD, its relationship with Aβ burden non-demented persons AD patients unclear. We examined this using 11C-PIB-PET as a quantitative marker vivo healthy ageing (HA), mild (MCI) AD. Thirty-one 33 MCI 32 HA participants completed neuropsychological assessment brain scan. Multiple linear...
Abstract Objective Assess Aβ deposition longitudinally and explore its relationship with cognition disease progression. Methods Clinical follow‐up was obtained 20 ± 3 months after [ 11 C]Pittsburgh compound B (PiB)‐positron emission tomography in 206 subjects: 35 dementia of the Alzheimer type (DAT), 65 mild cognitive impairment (MCI), 106 age‐matched healthy controls (HCs). A second PiB scan at 185 subjects a third years 57. Results At baseline, 97% DAT, 69% MCI, 31% HC showed high...
Oxidative stress markers as well high concentrations of copper are found in the vicinity Aβ amyloid deposits Alzheimer's disease. The neurotoxicity cell culture has been linked to H<sub>2</sub>O<sub>2</sub>generation by an unknown mechanism. We now report that Cu(II) markedly potentiates exhibited culture. potentiation toxicity is greatest for Aβ1–42 > Aβ1–40 ≫ mouse/rat Aβ1–40, corresponding their relative capacities reduce Cu(I), form H<sub>2</sub>O<sub>2</sub> cell-free assays and exhibit...
In the brains of aged humans and cases Alzheimer disease, deposits amyloid in senile plaques are located proximity to nerve processes. The principal component this extracellular is beta/A4, a peptide derived from larger precursor protein (APP), which actively expressed brain systemic organs. Mechanisms that result proteolysis APP form previously termed beta-amyloid protein, subsequent deposition unknown. If beta/A4 neuronally synthesized deposited at locations remote sites synthesis, then...