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dc.contributor.authorBokde, Arun L W
dc.contributor.authorEwers, Michael
dc.contributor.authorHampel, Harald
dc.date.accessioned2012-02-01T10:48:45Z
dc.date.available2012-02-01T10:48:45Z
dc.date.issued2012-02-01T10:48:45Z
dc.identifier.citationProg Neurobiol. 2009 Oct;89(2):125-33. Epub 2009 Jun 26.en_GB
dc.identifier.issn1873-5118 (Electronic)en_GB
dc.identifier.issn0301-0082 (Linking)en_GB
dc.identifier.pmid19560509en_GB
dc.identifier.doi10.1016/j.pneurobio.2009.06.004en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207871
dc.description.abstractFindings derived from neuroimaging of the structural and functional organization of the human brain have led to the widely supported hypothesis that neuronal networks of temporally coordinated brain activity across different regional brain structures underpin cognitive function. Failure of integration within a network leads to cognitive dysfunction. The current discussion on Alzheimer's disease (AD) argues that it presents in part a disconnection syndrome. Studies using functional magnetic resonance imaging, positron emission tomography and electroencephalography demonstrate that synchronicity of brain activity is altered in AD and correlates with cognitive deficits. Moreover, recent advances in diffusion tensor imaging have made it possible to track axonal projections across the brain, revealing substantial regional impairment in fiber-tract integrity in AD. Accumulating evidence points towards a network breakdown reflecting disconnection at both the structural and functional system level. The exact relationship among these multiple mechanistic variables and their contribution to cognitive alterations and ultimately decline is yet unknown. Focused research efforts aimed at the integration of both function and structure hold great promise not only in improving our understanding of cognition but also of its characteristic progressive metamorphosis in complex chronic neurodegenerative disorders such as AD.
dc.language.isoengen_GB
dc.subject.meshAlzheimer Disease/complications/*pathology/radionuclide imagingen_GB
dc.subject.mesh*Brain Mappingen_GB
dc.subject.meshCognition Disorders/etiologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshImage Processing, Computer-Assisteden_GB
dc.subject.meshMagnetic Resonance Imaging/methodsen_GB
dc.subject.meshNerve Net/*pathology/*physiopathology/radionuclide imagingen_GB
dc.subject.meshNeural Pathways/pathology/physiopathology/radionuclide imagingen_GB
dc.subject.meshOxygen/blooden_GB
dc.subject.meshPositron-Emission Tomography/methodsen_GB
dc.titleAssessing neuronal networks: understanding Alzheimer's disease.en_GB
dc.contributor.departmentDiscipline of Psychiatry, School of Medicine and Trinity College Institute of, Neuroscience (TCIN), Laboratory of Neuroimaging & Biomarker Research, Trinity, College Dublin, The Adelaide and Meath Hospital incorporating the National, Children's Hospital (AMiNCH), Dublin 24, Ireland.en_GB
dc.identifier.journalProgress in neurobiologyen_GB
dc.description.provinceLeinster
html.description.abstractFindings derived from neuroimaging of the structural and functional organization of the human brain have led to the widely supported hypothesis that neuronal networks of temporally coordinated brain activity across different regional brain structures underpin cognitive function. Failure of integration within a network leads to cognitive dysfunction. The current discussion on Alzheimer's disease (AD) argues that it presents in part a disconnection syndrome. Studies using functional magnetic resonance imaging, positron emission tomography and electroencephalography demonstrate that synchronicity of brain activity is altered in AD and correlates with cognitive deficits. Moreover, recent advances in diffusion tensor imaging have made it possible to track axonal projections across the brain, revealing substantial regional impairment in fiber-tract integrity in AD. Accumulating evidence points towards a network breakdown reflecting disconnection at both the structural and functional system level. The exact relationship among these multiple mechanistic variables and their contribution to cognitive alterations and ultimately decline is yet unknown. Focused research efforts aimed at the integration of both function and structure hold great promise not only in improving our understanding of cognition but also of its characteristic progressive metamorphosis in complex chronic neurodegenerative disorders such as AD.


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