Hostname: page-component-586b7cd67f-2brh9 Total loading time: 0 Render date: 2024-11-23T22:52:08.169Z Has data issue: false hasContentIssue false
  • English
  • Français

In vivo imaging of neurodegeneration in dementia with Lewy bodies (DLB)

Published online by Cambridge University Press:  24 March 2016

Chiadi U. Onyike  and
Gwenn S. Smith
Chiadi U. Onyike*
Affiliation:
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Gwenn S. Smith
Affiliation:
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
*
Email: [email protected]
Get access Rights & Permissions [Opens in a new window]

Extract

For almost two decades, O'Brien and colleagues have investigated virtually every facet of dementia with Lewy bodies (DLB), phenomenology, treatment, and neurobiology, ranging from genetics to post-mortem and in vivo imaging studies. The latest study from this group, reported here, describes differences in regional grey matter volumes using magnetic resonance (MR) imaging and an automated segmentation analysis method in a well-characterized sample of patients with Alzheimer disease (AD), DLB, and a healthy control group (Watson et al., 2015). The study incorporated detailed psychometric assessments of cognitive and motor functions for correlation with the grey matter volumes, and age, gender and dementia severity were included as covariates in the statistical analysis. The key observations are relatively greater hippocampal volumes and lower subcortical volumes in DLB compared to AD, but it is to be noted that most of these differences in subcortical volume were demonstrated indirectly through comparisons of the disease groups with age-matched healthy control subjects. Thus, replication in studies that make direct comparisons between DLB and AD subjects, perhaps in a larger sample size, is necessary. Still, these results highlight the potential for MR imaging to provide indicators of the extent of the neurodegenerative process in DLB. Furthermore, the results underscore the importance of correcting molecular imaging data for the effects of cerebral atrophy (partial volume correction) that may further enhance the ability of these methods to reveal pathophysiological processes.

Type
Commentary paper of the month
Information
International Psychogeriatrics , Volume 28 , Issue 4 , April 2016 , pp. 527 - 528
Copyright
Copyright © International Psychogeriatric Association 2016 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Chien, D. T. et al. (2013). Early clinical PET imaging results with the novel PHF-tau radioligand [F-18]-T807. Journal of Alzheimer's Disease, 34, 457–468.Google Scholar
Jagust, W. J., Friedland, R. P. and Budinger, T. F. (1985). Positron emission tomography with [18F]fluorodeoxyglucose differentiates normal pressure hydrocephalus from Alzheimer-type dementia. Journal of Neurology, Neurosurgery and Psychiatry, 48, 1091–1096.CrossRefGoogle ScholarPubMed
Klunk, W. E. et al. (2004). Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B. Annals of Neurology, 55, 306–319.Google Scholar
Mak, E., Su, L., Williams, G. B. and O'Brien, J. T. (2014). Neuroimaging characteristics of dementia with Lewy bodies. Alzheimer's Research and Therapeutics, 6, 18.Google Scholar
McKeith, I. G. et al. (2005). Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology, 65, 1863–1872.Google Scholar
Neal, K. L. et al. (2013). Development and screening of contrast agents for in vivo imaging of Parkinson's disease. Molecular Imaging and Biology, 15, 585–595.Google Scholar
Reiman, E. M. et al. (2004). Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia. Proceedings of the National Academic Sciences of the United States of America, 101, 284–289.Google Scholar
Smith, G. S. et al. (1992). Topography of cross-sectional and longitudinal glucose metabolic deficits in Alzheimer's disease. Pathophysiologic implications. Archives of Neurology, 49, 1142–1150.Google Scholar
Watson, R., Colloby, S. J., Blamire, A. M. and O'Brien, J. T. (2015). Subcortical volume changes in dementia with Lewy bodies and Alzheimer's disease. A comparison with healthy aging. International Psychogeriatrics, 17, 1–8.Google Scholar