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      Age-related changes in grey and white matter structure throughout adulthood

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          Abstract

          Normal ageing is associated with gradual brain atrophy. Determining spatial and temporal patterns of change can help shed light on underlying mechanisms. Neuroimaging provides various measures of brain structure that can be used to assess such age-related change but studies to date have typically considered single imaging measures. Although there is consensus on the notion that brain structure deteriorates with age, evidence on the precise time course and spatial distribution of changes is mixed. We assessed grey matter (GM) and white matter (WM) structure in a group of 66 adults aged between 23 and 81. Multimodal imaging measures included voxel-based morphometry (VBM)-style analysis of GM and WM volume and diffusion tensor imaging (DTI) metrics of WM microstructure. We found widespread reductions in GM volume from middle age onwards but earlier reductions in GM were detected in frontal cortex. Widespread age-related deterioration in WM microstructure was detected from young adulthood onwards. WM decline was detected earlier and more sensitively using DTI-based measures of microstructure than using markers of WM volume derived from conventional T1-weighted imaging.

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          Most cited references54

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          Demyelination increases radial diffusivity in corpus callosum of mouse brain.

          Myelin damage, as seen in multiple sclerosis (MS) and other demyelinating diseases, impairs axonal conduction and can also be associated with axonal degeneration. Accurate assessments of these conditions may be highly beneficial in evaluating and selecting therapeutic strategies for patient management. Recently, an analytical approach examining diffusion tensor imaging (DTI) derived parameters has been proposed to assess the extent of axonal damage, demyelination, or both. The current study uses the well-characterized cuprizone model of experimental demyelination and remyelination of corpus callosum in mouse brain to evaluate the ability of DTI parameters to detect the progression of myelin degeneration and regeneration. Our results demonstrate that the extent of increased radial diffusivity reflects the severity of demyelination in corpus callosum of mouse brain affected by cuprizone treatment. Subsequently, radial diffusivity decreases with the progression of remyelination. Furthermore, radial diffusivity changes were specific to the time course of changes in myelin integrity as distinct from axonal injury, which was detected by betaAPP immunostaining and shown to be most extensive prior to demyelination. Radial diffusivity offers a specific assessment of demyelination and remyelination, as distinct from acute axonal damage.
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            Cerebral microvascular pathology in aging and Alzheimer's disease.

            The aging of the central nervous system and the development of incapacitating neurological diseases like Alzheimer's disease (AD) are generally associated with a wide range of histological and pathophysiological changes eventually leading to a compromised cognitive status. Although the diverse triggers of the neurodegenerative processes and their interactions are still the topic of extensive debate, the possible contribution of cerebrovascular deficiencies has been vigorously promoted in recent years. Various forms of cerebrovascular insufficiency such as reduced blood supply to the brain or disrupted microvascular integrity in cortical regions may occupy an initiating or intermediate position in the chain of events ending with cognitive failure. When, for example, vasoconstriction takes over a dominating role in the cerebral vessels, the perfusion rate of the brain can considerably decrease causing directly or through structural vascular damage a drop in cerebral glucose utilization. Consequently, cerebral metabolism can suffer a setback leading to neuronal damage and a concomitant suboptimal cognitive capacity. The present review focuses on the microvascular aspects of neurodegenerative processes in aging and AD with special attention to cerebral blood flow, neural metabolic changes and the abnormalities in microvascular ultrastructure. In this context, a few of the specific triggers leading to the prominent cerebrovascular pathology, as well as the potential neurological outcome of the compromised cerebral microvascular system are also going to be touched upon to a certain extent, without aiming at total comprehensiveness. Finally, a set of animal models are going to be presented that are frequently used to uncover the functional relationship between cerebrovascular factors and the damage to neural networks.
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              In vivo evidence for post-adolescent brain maturation in frontal and striatal regions.

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                Author and article information

                Journal
                Neuroimage
                Neuroimage
                Neuroimage
                Academic Press
                1053-8119
                1095-9572
                01 July 2010
                01 July 2010
                : 51
                : 3-2
                : 943-951
                Affiliations
                [a ]Centre for Functional MRI of the Brain, University of Oxford, Oxford, UK
                [b ]Neurology and Neurometabolic Unit, Department of Neurological and Behavioural Sciences, University of Siena, Italy
                [c ]Department of Neuroscience, University of Padua Medical School, Padua, Italy
                Author notes
                [* ]Corresponding author. FMRIB Centre, John Radcliffe Hospital, Headington, Oxford OX3 9DU, UK. Fax: + 44 1865 222717. heidi@ 123456fmrib.ox.ac.uk
                Article
                YNIMG7123
                10.1016/j.neuroimage.2010.03.004
                2896477
                20211265
                5b4b1679-b0de-4e0a-8667-c5602a424f32
                © 2010 Elsevier Inc.

                This document may be redistributed and reused, subject to certain conditions.

                History
                : 2 November 2009
                : 27 January 2010
                : 2 March 2010
                Categories
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                Neurosciences
                Neurosciences

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