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Medicine and Health Sciences Commons

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Nervous System Diseases

Edith Cowan University

Series

Alzheimer's disease

Articles 1 - 4 of 4

Full-Text Articles in Medicine and Health Sciences

Plasma High-Density Lipoprotein Cargo Is Altered In Alzheimer's Disease And Is Associated With Regional Brain Volume, Steve Pedrini, James D. Doecke, Eugene Hone, Penghao Wang, Rohith Thota, Ashley I. Bush, Christopher C. Rowe, Vincent Dore, Victor L. Villemagne, David Ames, Stephanie Rainey-Smith, Giuseppe Verdile, Hamid R. Sohrabi, Manfred R. Raida, Kevin Taddei, Sam Gandy, Colin L. Masters, Pratishtha Chatterjee, Ralph N. Martins, Aibl Research Group Oct 2022

Plasma High-Density Lipoprotein Cargo Is Altered In Alzheimer's Disease And Is Associated With Regional Brain Volume, Steve Pedrini, James D. Doecke, Eugene Hone, Penghao Wang, Rohith Thota, Ashley I. Bush, Christopher C. Rowe, Vincent Dore, Victor L. Villemagne, David Ames, Stephanie Rainey-Smith, Giuseppe Verdile, Hamid R. Sohrabi, Manfred R. Raida, Kevin Taddei, Sam Gandy, Colin L. Masters, Pratishtha Chatterjee, Ralph N. Martins, Aibl Research Group

Research outputs 2022 to 2026

Cholesterol levels have been repeatedly linked to Alzheimer's Disease (AD), suggesting that high levels could be detrimental, but this effect is likely attributed to Low-Density Lipoprotein (LDL) cholesterol. On the other hand, High-Density Lipoproteins (HDL) cholesterol levels have been associated with reduced brain amyloidosis and improved cognitive function. However, recent findings have suggested that HDL-functionality, which depends upon the HDL-cargo proteins associated with HDL, rather than HDL levels, appears to be the key factor, suggesting a quality over quantity status. In this report, we have assessed the HDL-cargo (Cholesterol, ApoA-I, ApoA-II, ApoC-I, ApoC-III, ApoD, ApoE, ApoH, ApoJ, CRP, and SAA) …


Plasma Glial Fibrillary Acidic Protein Is Elevated In Cognitively Normal Older Adults At Risk Of Alzheimer’S Disease, Pratishtha Chatterjee, Steve Pedrini, Erik Stoops, Kathryn Goozee, Victor L. Villemagne, Prita R. Asih, Inge M. W. Verberk, Preeti Dave, Kevin Taddei, Hamid R. Sohrabi, Henrik Zetterberg, Kaj Blennow, Charlotte E. Teunissen, Hugo M. Vanderstichele, Ralph N. Martins Jan 2021

Plasma Glial Fibrillary Acidic Protein Is Elevated In Cognitively Normal Older Adults At Risk Of Alzheimer’S Disease, Pratishtha Chatterjee, Steve Pedrini, Erik Stoops, Kathryn Goozee, Victor L. Villemagne, Prita R. Asih, Inge M. W. Verberk, Preeti Dave, Kevin Taddei, Hamid R. Sohrabi, Henrik Zetterberg, Kaj Blennow, Charlotte E. Teunissen, Hugo M. Vanderstichele, Ralph N. Martins

Research outputs 2014 to 2021

© 2021, The Author(s). Glial fibrillary acidic protein (GFAP), an astrocytic cytoskeletal protein, can be measured in blood samples, and has been associated with Alzheimer’s disease (AD). However, plasma GFAP has not been investigated in cognitively normal older adults at risk of AD, based on brain amyloid-β (Aβ) load. Cross-sectional analyses were carried out for plasma GFAP and plasma Aβ1–42/Aβ1–40 ratio, a blood-based marker associated with brain Aβ load, in participants (65–90 years) categorised into low (Aβ−, n = 63) and high (Aβ+, n = 33) brain Aβ load groups via Aβ positron emission tomography. Plasma GFAP, Aβ1–42, and Aβ1–40 …


Asymmetric Thinning Of The Cerebral Cortex Across The Adult Lifespan Is Accelerated In Alzheimer’S Disease, James M. Roe, Didac Vidal-Piñeiro, Øystein Sørensen, Andreas M. Brandmaier, Sandra Düzel, Hector A. Gonzalez, Rogier A. Kievit, Ethan Knights, Simone Kühn, Ulman Lindenberger, Athanasia M. Mowinckel, Lars Nyberg, Denise C. Park, Sara Pudas, Melissa M. Rundle, Kristine B. Walhovd, Anders M. Fjell, René Westerhausen, Colin L. Masters, Ashley I. Bush, Christopher Fowler, David Darby, Kelly Pertile, Carolina Restrepo, Blaine Roberts, Jo Robertson, Rebecca Rumble Jan 2021

Asymmetric Thinning Of The Cerebral Cortex Across The Adult Lifespan Is Accelerated In Alzheimer’S Disease, James M. Roe, Didac Vidal-Piñeiro, Øystein Sørensen, Andreas M. Brandmaier, Sandra Düzel, Hector A. Gonzalez, Rogier A. Kievit, Ethan Knights, Simone Kühn, Ulman Lindenberger, Athanasia M. Mowinckel, Lars Nyberg, Denise C. Park, Sara Pudas, Melissa M. Rundle, Kristine B. Walhovd, Anders M. Fjell, René Westerhausen, Colin L. Masters, Ashley I. Bush, Christopher Fowler, David Darby, Kelly Pertile, Carolina Restrepo, Blaine Roberts, Jo Robertson, Rebecca Rumble

Research outputs 2014 to 2021

© 2021, The Author(s). Aging and Alzheimer’s disease (AD) are associated with progressive brain disorganization. Although structural asymmetry is an organizing feature of the cerebral cortex it is unknown whether continuous age- and AD-related cortical degradation alters cortical asymmetry. Here, in multiple longitudinal adult lifespan cohorts we show that higher-order cortical regions exhibiting pronounced asymmetry at age ~20 also show progressive asymmetry-loss across the adult lifespan. Hence, accelerated thinning of the (previously) thicker homotopic hemisphere is a feature of aging. This organizational principle showed high consistency across cohorts in the Lifebrain consortium, and both the topological patterns and temporal dynamics …


The Effects Of Latrepirdine On Amyloid-Β Aggregation And Toxicity, Tenielle Porter, Prashant Bharadwaj, David Groth, Adrian Paxman, Simon Laws, Ralph Martins, Guiseppe Verdile Jan 2016

The Effects Of Latrepirdine On Amyloid-Β Aggregation And Toxicity, Tenielle Porter, Prashant Bharadwaj, David Groth, Adrian Paxman, Simon Laws, Ralph Martins, Guiseppe Verdile

Research outputs 2014 to 2021

Latrepirdine (DimebonTM) has been demonstrated to be a neuroprotective and cognition improving agent in neurodegenerative diseases that feature protein aggregation and deposition, such as Alzheimer's disease (AD). The accumulation of amyloid-β (Aβ) protein aggregates is a key event in the neurodegenerative process in AD. This study explores if latrepirdine modulation of protein aggregation contributes to its neuroprotective mechanism of action. Assessment of neuronal cell death showed that there was a significant reduction in lactate dehydrogenase release at an equimolar ratio of Aβ:latrepirdine and with lower concentrations of latrepirdine. The ability of latrepirdine to alter the formation of Aβ42 aggregates was …