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Medical Sciences

Edith Cowan University

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Amyloid

Articles 1 - 6 of 6

Full-Text Articles in Medicine and Health Sciences

The Crosstalk Between Amyloid-Β, Retina, And Sleep For The Early Diagnosis Of Alzheimer's Disease: A Narrative Review, Isaiah Lorenzo De Guia, Shaun Eslick, Sharon L. Naismith, Swathi Kanduri, Tejal M. Shah, Ralph N. Martins Jun 2024

The Crosstalk Between Amyloid-Β, Retina, And Sleep For The Early Diagnosis Of Alzheimer's Disease: A Narrative Review, Isaiah Lorenzo De Guia, Shaun Eslick, Sharon L. Naismith, Swathi Kanduri, Tejal M. Shah, Ralph N. Martins

Research outputs 2022 to 2026

Alzheimer's disease (AD) is the most common type of dementia, which is characterised by progressive memory loss and accumulation of hallmark markers amyloid-β (Aβ) and neurofibrillary tangles in the diseased brain. The current gold standard diagnostic methods have limitations of being invasive, costly, and not easily accessible. Thus, there is a need for new avenues, such as imaging the retina for early AD diagnosis. Sleep disruption is symptomatically frequent across preclinical and AD subjects. As circadian activity, such as the sleep-wake cycle, is linked to the retina, analysis of their association may be useful additions for achieving predictive AD diagnosis. …


Suboptimal Self-Reported Sleep Efficiency And Duration Are Associated With Faster Accumulation Of Brain Amyloid Beta In Cognitively Unimpaired Older Adults, Louise N. Pivac, Belinda M. Brown, Kelsey R. Sewell, James D. Doecke, Victor L. Villemagne, Vincent Doré, Michael Weinborn, Hamid R. Sohrabi, Samantha L. Gardener, Romola S. Bucks, Simon M. Laws, Kevin Taddei, Paul Maruff, Colin L. Masters, Christopher Rowe, Ralph N. Martins, Stephanie R. Rainey-Smith Apr 2024

Suboptimal Self-Reported Sleep Efficiency And Duration Are Associated With Faster Accumulation Of Brain Amyloid Beta In Cognitively Unimpaired Older Adults, Louise N. Pivac, Belinda M. Brown, Kelsey R. Sewell, James D. Doecke, Victor L. Villemagne, Vincent Doré, Michael Weinborn, Hamid R. Sohrabi, Samantha L. Gardener, Romola S. Bucks, Simon M. Laws, Kevin Taddei, Paul Maruff, Colin L. Masters, Christopher Rowe, Ralph N. Martins, Stephanie R. Rainey-Smith

Research outputs 2022 to 2026

INTRODUCTION: This study investigated whether self-reported sleep quality is associated with brain amyloid beta (AB) accumulation. METHODS: Linear mixed effect model analyses were conducted for 189 cognitively unimpaired (CU) older adults (mean ± standard deviation 74.0 ± 6.2; 53.2% female), with baseline self-reported sleep data, and positron emission tomography-determined brain AB measured over a minimum of three time points (range 33.3–72.7 months). Analyses included random slopes and intercepts, interaction for apolipoprotein E (APOE) 4 allele status, and time, adjusting for sex and baseline age. RESULTS: Sleep duration < 6 hours, in APOE 4 carriers, and sleep efficiency < 65%, in the whole sample and APOE 4 non-carriers, is associated with faster accumulation of brain AB. DISCUSSION: These findings suggest a role for self-reported suboptimal sleep efficiency and duration in the accumulation of Alzheimer's disease (AD) neuropathology in CU individuals. Additionally, poor sleep efficiency represents a potential route via which individuals at lower genetic risk may progress to preclinical AD. Highlights: In cognitively unimpaired older adults self-report sleep is associated with brain amyloid beta (AB) accumulation. Across sleep characteristics, this relationship differs by apolipoprotein E (APOE) genotype. Sleep duration < 6 hours is associated with faster brain AB accumulation in APOE 4 carriers. Sleep efficiency < 65% is associated with faster brain AB accumulation in APOE 4 non-carriers. Personalized sleep interventions should be studied for potential to slow AB accumulation.


Autophagy Modulation As A Treatment Of Amyloid Diseases, Zoe Mputhia, Eugene Hone, Timir Tripathi, Tim Sargeant, Ralph Martins, Prashant Bharadwaj Sep 2019

Autophagy Modulation As A Treatment Of Amyloid Diseases, Zoe Mputhia, Eugene Hone, Timir Tripathi, Tim Sargeant, Ralph Martins, Prashant Bharadwaj

Research outputs 2014 to 2021

Amyloids are fibrous proteins aggregated into toxic forms that are implicated in several chronic disorders. More than 30 diseases show deposition of fibrous amyloid proteins associated with cell loss and degeneration in the affected tissues. Evidence demonstrates that amyloid diseases result from protein aggregation or impaired amyloid clearance, but the connection between amyloid accumulation and tissue degeneration is not clear. Common examples of amyloid diseases are Alzheimer's disease (AD), Parkinson's disease (PD) and tauopathies, which are the most common forms of neurodegenerative diseases, as well as polyglutamine disorders and certain peripheral metabolic diseases. In these diseases, increased accumulation of toxic …


Examining The Potential Clinical Value Of Curcumin In The Prevention And Diagnosis Of Alzheimer's Disease, K. G. Goozee, T. M. Shah, Hamid R. Sohrabi, Stephanie Rainey-Smith, B. Brown, Guiseppe Verdile, Ralph Martins Jan 2016

Examining The Potential Clinical Value Of Curcumin In The Prevention And Diagnosis Of Alzheimer's Disease, K. G. Goozee, T. M. Shah, Hamid R. Sohrabi, Stephanie Rainey-Smith, B. Brown, Guiseppe Verdile, Ralph Martins

Research outputs 2014 to 2021

Curcumin derived from turmeric is well documented for its anti-carcinogenic, antioxidant and anti-inflammatory properties. Recent studies show that curcumin also possesses neuroprotective and cognitive-enhancing properties that may help delay or prevent neurodegenerative diseases, including Alzheimer’s disease (AD). Currently, clinical diagnosis of AD is onerous, and it is primarily based on the exclusion of other causes of dementia. In addition, phase III clinical trials of potential treatments have mostly failed, leaving disease-modifying interventions elusive. AD can be characterised neuropathologically by the deposition of extracellular β amyloid (Aβ) plaques and intracellular accumulation of tau-containing neurofibrillary tangles. Disruptions in Aβ metabolism/clearance contribute to …


Biomarkers Of Alzheimer's Disease Risk In Peripheral Tissues; Focus On Buccal Cells, Maxime François, Wayne Leifert, Ralph Martins, Philip Thomas, Michael Fenech Jan 2014

Biomarkers Of Alzheimer's Disease Risk In Peripheral Tissues; Focus On Buccal Cells, Maxime François, Wayne Leifert, Ralph Martins, Philip Thomas, Michael Fenech

Research outputs 2014 to 2021

Alzheimer's disease (AD) is a progressive degenerative disorder of the brain and is the most common form of dementia. To-date no simple, inexpensive and minimally invasive procedure is available to confirm with certainty the early diagnosis of AD prior to the manifestations of symptoms characteristic of the disease. Therefore, if population screening of individuals is to be performed, more suitable, easily accessible tissues would need to be used for a diagnostic test that would identify those who exhibit cellular pathology indicative of mild cognitive impairment (MCI) and AD risk so that they can be prioritized for primary prevention. This need …


Retinal Vascular Biomarkers For Early Detection And Monitoring Of Alzheimer's Disease, Shawn Frost, Yogi Kanagasingam, Hamid Sohrabi, J Vignarajan, P Bourgeat, Olivier Salvado, Victor Villemagne, Christopher Rowe, S Lance Macaulay, Cassandra Szoeke, Kathryn A. Ellis, David Ames, Colin L. Masters, Stephanie Rainey-Smith, Ralph N. Martins Jan 2013

Retinal Vascular Biomarkers For Early Detection And Monitoring Of Alzheimer's Disease, Shawn Frost, Yogi Kanagasingam, Hamid Sohrabi, J Vignarajan, P Bourgeat, Olivier Salvado, Victor Villemagne, Christopher Rowe, S Lance Macaulay, Cassandra Szoeke, Kathryn A. Ellis, David Ames, Colin L. Masters, Stephanie Rainey-Smith, Ralph N. Martins

Research outputs 2013

The earliest detectable change in Alzheimer's disease (AD) is the buildup of amyloid plaque in the brain. Early detection of AD, prior to irreversible neurological damage, is important for the efficacy of current interventions as well as for the development of new treatments. Although PiB-PET imaging and CSF amyloid are the gold standards for early AD diagnosis, there are practical limitations for population screening. AD-related pathology occurs primarily in the brain, but some of the hallmarks of the disease have also been shown to occur in other tissues, including the retina, which is more accessible for imaging. Retinal vascular changes …