RATIONALE: Globally, stroke and dementia are leading causes of disability and mortality. More than one third of stroke patients will develop dementia, but mechanisms are unclear. AIMS: The study aims to establish whether brain volume change is associated with poststroke dementia, and to elucidate potential causal mechanisms, including genetic markers, amyloid deposition and vascular risk factors. An understanding of whether - and in whom - stroke is neurodegenerative is critical for the strategic use of potential disease-modifying therapies. HYPOTHESES: That stroke patients will exhibit greater brain volume loss than comparable cohorts of stroke-free controls; and that those who develop dementia will exhibit greater brain volume loss than those who do not. DESIGN: Advanced brain imaging techniques are used to longitudinally measure brain volume and cortical thickness in 135 stroke patients. Concurrent neuropsychological testing will correlate clinical profile with these measures. PRIMARY OUTCOMES: Primary imaging end-point is brain volume change between three-months and three-years poststroke; primary clinical outcome is the presence of dementia at three-years. SECONDARY OUTCOMES: We will examine the correlations with the following variables: dementia subtype; physical activity levels; behavioral dysfunction as measured by patient and caregiver-reported scales; structural and functional brain connectivity disruption; apolipoprotein E; and specific neuropsychological test scores. DISCUSSION: Magnetic resonance imaging markers of structural brain aging and performance on neuropsychological tests are powerful predictors of dementia. We need to understand the trajectory of regional brain volume change and cognitive decline in patients after stroke. This will allow future risk stratification for prognostic counseling, service planning, and early therapeutic intervention.
RATIONALE: Globally, stroke and dementia are leading causes of disability and mortality. More than one third of strokepatients will develop dementia, but mechanisms are unclear. AIMS: The study aims to establish whether brain volume change is associated with poststroke dementia, and to elucidate potential causal mechanisms, including genetic markers, amyloid deposition and vascular risk factors. An understanding of whether - and in whom - stroke is neurodegenerative is critical for the strategic use of potential disease-modifying therapies. HYPOTHESES: That strokepatients will exhibit greater brain volume loss than comparable cohorts of stroke-free controls; and that those who develop dementia will exhibit greater brain volume loss than those who do not. DESIGN: Advanced brain imaging techniques are used to longitudinally measure brain volume and cortical thickness in 135 strokepatients. Concurrent neuropsychological testing will correlate clinical profile with these measures. PRIMARY OUTCOMES: Primary imaging end-point is brain volume change between three-months and three-years poststroke; primary clinical outcome is the presence of dementia at three-years. SECONDARY OUTCOMES: We will examine the correlations with the following variables: dementia subtype; physical activity levels; behavioral dysfunction as measured by patient and caregiver-reported scales; structural and functional brain connectivity disruption; apolipoprotein E; and specific neuropsychological test scores. DISCUSSION: Magnetic resonance imaging markers of structural brain aging and performance on neuropsychological tests are powerful predictors of dementia. We need to understand the trajectory of regional brain volume change and cognitive decline in patients after stroke. This will allow future risk stratification for prognostic counseling, service planning, and early therapeutic intervention.
Authors: Liam Johnson; Emilio Werden; Chris Shirbin; Laura Bird; Elizabeth Landau; Toby Cumming; Leonid Churilov; Julie A Bernhardt; Vincent Thijs; Amy Brodtmann Journal: Eur Stroke J Date: 2018-07-10
Authors: Perminder S Sachdev; Jessica W Lo; John D Crawford; Lisa Mellon; Anne Hickey; David Williams; Régis Bordet; Anne-Marie Mendyk; Patrick Gelé; Dominique Deplanque; Hee-Joon Bae; Jae-Sung Lim; Amy Brodtmann; Emilio Werden; Toby Cumming; Sebastian Köhler; Frans R J Verhey; Yan-Hong Dong; Hui Hui Tan; Christopher Chen; Xu Xin; Raj N Kalaria; Louise M Allan; Rufus O Akinyemi; Adesola Ogunniyi; Aleksandra Klimkowicz-Mrowiec; Martin Dichgans; Frank A Wollenweber; Vera Zietemann; Michael Hoffmann; David W Desmond; Thomas Linden; Christian Blomstrand; Björn Fagerberg; Ingmar Skoog; Olivier Godefroy; Mélanie Barbay; Martine Roussel; Byung-Chul Lee; Kyung-Ho Yu; Joanna Wardlaw; Stephen J Makin; Fergus N Doubal; Francesca M Chappell; Velandai K Srikanth; Amanda G Thrift; Geoffrey A Donnan; Nagaendran Kandiah; Russell J Chander; Xuling Lin; Charlotte Cordonnier; Solene Moulin; Costanza Rossi; Behnam Sabayan; David J Stott; J Wouter Jukema; Susanna Melkas; Hanna Jokinen; Timo Erkinjuntti; Vincent C T Mok; Adrian Wong; Bonnie Y K Lam; Didier Leys; Hilde Hénon; Stéphanie Bombois; Darren M Lipnicki; Nicole A Kochan Journal: Alzheimers Dement (Amst) Date: 2016-11-18
Authors: Sheila K Patel; Carolina Restrepo; Emilio Werden; Leonid Churilov; Elif I Ekinci; Piyush M Srivastava; Jay Ramchand; Bryan Wai; Brian Chambers; Christopher J O'Callaghan; David Darby; Vladimir Hachinski; Toby Cumming; Geoff Donnan; Louise M Burrell; Amy Brodtmann Journal: BMC Endocr Disord Date: 2017-04-07 Impact factor: 2.763