Left frontal hub connectivity delays cognitive impairment in autosomal-dominant and sporadic Alzheimer's disease
| Autor: | Josef Priller, Daniel Janowitz, Johannes Levin, Miguel Ángel Araque Caballero, Henning Boecker, Christiana Franke, Anne M. Fagan, Frank Jessen, Martin Dichgans, Jens Wiltfang, Michael T. Heneka, Christian Haass, Michael W. Weiner, Alison Goate, Peter Falkai, Daniel Bittner, Felix Menne, Marc Suárez-Calvet, Anja Schneider, Barbara Kofler, Oliver Peters, Eike Jakob Spruth, Marco Duering, Michael Wagner, Stefan J. Teipel, Colin L. Masters, Oliver Speck, Robert Perneczky, Peter J. Nestor, Tammie L.S. Benzinger, Coraline D. Metzger, Frederic Brosseron, Jae-Hong Lee, Manuel Fuentes, Christine Westerteicher, Jasmeer P. Chhatwal, Cihan Catak, Katrina L. Paumier, Claudia Bartels, Martin N. Rossor, Adrian Danek, Stephen Salloway, Mathias Jucker, Ingo Kilimann, Klaus Fliessbach, Peter R. Schofield, Alfredo Ramirez, Nicolai Franzmeier, Annika Spottke, Emrah Düzel, Steffen Wolfsgruber, Katharina Buerger, Christoph Laske, John C. Morris, Randall J. Bateman, Michael Ewers |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
Male
Aging Alzheimer's Disease Brain mapping Imaging 0302 clinical medicine Medicine Aetiology 10. No inequality Cognitive reserve FUNCTIONAL CONNECTIVITY 11 Medical And Health Sciences Frontal Lobe CORTICAL HUBS genetics [Amyloid beta-Protein Precursor] BRAIN RESERVE Biomedical Imaging LOW-FREQUENCY Alzheimer's disease Clinical Trials and Supportive Activities Basic Behavioral and Social Science 03 medical and health sciences PSEN1 protein human WORKING-MEMORY Clinical Research Alzheimer Disease Humans Cognitive Dysfunction OLDER-ADULTS Science & Technology Working memory physiology [Functional Laterality] medicine.disease 030104 developmental biology Mutation Dementia Neurosciences & Neurology Neurology (clinical) Neuroscience diagnostic imaging [Alzheimer Disease] 030217 neurology & neurosurgery 0301 basic medicine diagnostic imaging [Cognitive Dysfunction] genetics [Alzheimer Disease] Neurodegenerative Medical and Health Sciences Functional Laterality etiology [Cognitive Dysfunction] memory Amyloid beta-Protein Precursor 2.1 Biological and endogenous factors Cognitive decline Brain Mapping complications [Alzheimer Disease] genetics [Presenilin-1] Middle Aged cognitive reserve Magnetic Resonance Imaging Frontal lobe IMAGING BIOMARKERS Neurological Female physiology [Nerve Net] Life Sciences & Biomedicine Alzheimer’s disease Adult Clinical Neurology genetics [Mutation] genetics [Presenilin-2] dementia biomarkers 17 Psychology And Cognitive Sciences Imaging Three-Dimensional diagnostic imaging [Frontal Lobe] Behavioral and Social Science HIPPOCAMPAL FUNCTION Presenilin-2 Acquired Cognitive Impairment Presenilin-1 Journal Article Effects of sleep deprivation on cognitive performance ddc:610 Neurology & Neurosurgery Resting state fMRI business.industry diagnostic imaging [Nerve Net] PSEN2 protein human Psychology and Cognitive Sciences Neurosciences Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) Original Articles Brain Disorders PHYSICAL-ACTIVITY MEMORY VARIANCE Three-Dimensional resting state connectivity Nerve Net business |
| Zdroj: | Franzmeier, N, Düzel, E, Jessen, F, Buerger, K, Levin, J, Duering, M, Dichgans, M, Haass, C, Suárez-Calvet, M, Fagan, A M, Paumier, K, Benzinger, T, Masters, C L, Morris, J C, Perneczky, R, Janowitz, D, Catak, C, Wolfsgruber, S, Wagner, M, Teipel, S, Kilimann, I, Ramirez, A, Rossor, M, Jucker, M, Chhatwal, J, Spottke, A, Boecker, H, Brosseron, F, Falkai, P, Fliessbach, K, Heneka, M T, Laske, C, Nestor, P, Peters, O, Fuentes, M, Menne, F, Priller, J, Spruth, E J, Franke, C, Schneider, A, Kofler, B, Westerteicher, C, Speck, O, Wiltfang, J, Bartels, C, Araque Caballero, M Á, Metzger, C, Bittner, D, Weiner, M, Lee, J-H, Salloway, S, Danek, A, Goate, A, Schofield, P R, Bateman, R J & Ewers, M 2018, ' Left frontal hub connectivity delays cognitive impairment in autosomal-dominant and sporadic Alzheimer's disease ', Brain . https://doi.org/10.1093/brain/awy008 Brain 141(4), 1186-1200 (2018). doi:10.1093/brain/awy008 Brain Brain : a journal of neurology, vol 141, iss 4 |
| DOI: | 10.1093/brain/awy008 |
| Popis: | The neural basis of reserve capacity in Alzheimer’s disease is yet to be fully determined. Franzmeier et al. show that greater left frontal hub connectivity within the fronto-parietal control network is associated with greater resilience of cognitive performance during the early stages of autosomal dominant and sporadic Alzheimer’s disease. Patients with Alzheimer’s disease vary in their ability to sustain cognitive abilities in the presence of brain pathology. A major open question is which brain mechanisms may support higher reserve capacity, i.e. relatively high cognitive performance at a given level of Alzheimer’s pathology. Higher functional MRI-assessed functional connectivity of a hub in the left frontal cortex is a core candidate brain mechanism underlying reserve as it is associated with education (i.e. a protective factor often associated with higher reserve) and attenuated cognitive impairment in prodromal Alzheimer’s disease. However, no study has yet assessed whether such hub connectivity of the left frontal cortex supports reserve throughout the evolution of pathological brain changes in Alzheimer’s disease, including the presymptomatic stage when cognitive decline is subtle. To address this research gap, we obtained cross-sectional resting state functional MRI in 74 participants with autosomal dominant Alzheimer’s disease, 55 controls from the Dominantly Inherited Alzheimer’s Network and 75 amyloid-positive elderly participants, as well as 41 amyloid-negative cognitively normal elderly subjects from the German Center of Neurodegenerative Diseases multicentre study on biomarkers in sporadic Alzheimer’s disease. For each participant, global left frontal cortex connectivity was computed as the average resting state functional connectivity between the left frontal cortex (seed) and each voxel in the grey matter. As a marker of disease stage, we applied estimated years from symptom onset in autosomal dominantly inherited Alzheimer’s disease and cerebrospinal fluid tau levels in sporadic Alzheimer’s disease cases. In both autosomal dominant and sporadic Alzheimer’s disease patients, higher levels of left frontal cortex connectivity were correlated with greater education. For autosomal dominant Alzheimer’s disease, a significant left frontal cortex connectivity × estimated years of onset interaction was found, indicating slower decline of memory and global cognition at higher levels of connectivity. Similarly, in sporadic amyloid-positive elderly subjects, the effect of tau on cognition was attenuated at higher levels of left frontal cortex connectivity. Polynomial regression analysis showed that the trajectory of cognitive decline was shifted towards a later stage of Alzheimer’s disease in patients with higher levels of left frontal cortex connectivity. Together, our findings suggest that higher resilience against the development of cognitive impairment throughout the early stages of Alzheimer’s disease is at least partially attributable to higher left frontal cortex-hub connectivity. |
| Databáze: | OpenAIRE |
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