Nedelska Z, Schwarz CG, Boeve BF, Lowe VJ, Reid RI, Przybelski SA, Lesnick TG, Gunter JL, Senjem ML, Ferman TJ, Smith GE, Geda YE, Knopman DS, Petersen RC, Jack CR Jr, Kantarci K. Neurobiology of Aging. 2015 Jun;36(6):2010–7. doi: 10.1016/j.neurobiolaging.2015.03.007. Epub 2015 Mar 14. IF: 5.013
MUDr. Zuzana Nedelská, Department of Neurology
Many patients with dementia with Lewy bodies (DLB) have overlapping Alzheimer's disease (AD)-related pathology, which may contribute to white matter (WM) diffusivity alterations on diffusion tensor imaging (DTI). Consecutive patients with DLB (n = 30), age- and sex-matched AD patients (n = 30), and cognitively normal controls (n = 60) were recruited. All subjects underwent DTI, 18F 2-fluoro-deoxy-d-glucose, and (11)C Pittsburgh compound B positron emission tomography scans. DLB patients had reduced fractional anisotropy (FA) in the parietooccipital WM but not elsewhere compared with cognitively normal controls, and elevated FA in parahippocampal WM compared with AD patients, which persisted after controlling for β-amyloid load in DLB. The pattern of WM FA alterations on DTI was consistent with the more diffuse posterior parietal and occipital glucose hypometabolism of 2-fluoro-deoxy-d-glucose positron emission tomography in the cortex. DLB is characterized by a loss of parietooccipital WM integrity, independent of concomitant AD-related β-amyloid load. Cortical glucose hypometabolism accompanies WM FA alterations with a concordant pattern of gray and WM involvement in the parietooccipital lobes in DLB.
For this topic, see also following article:
Pattern of brain atrophy rates in autopsy-confirmed dementia with Lewy bodies.
Nedelska Z, Ferman TJ, Boeve BF, Przybelski SA, Lesnick TG, Murray ME, Gunter JL, Senjem ML, Vemuri P, Smith GE, Geda YE, Graff-Radford J, Knopman DS, Petersen RC, Parisi JE, Dickson DW, Jack CR Jr, Kantarci K. Neurobiology of Aging. 2015 Jan;36(1):452–61. doi: 10.1016/j.neurobiolaging.2014.07.005. Epub 2014 Jul 15. IF: 5.013
Dementia with Lewy bodies (DLB) is characterized by preserved whole brain and medial temporal lobe volumes compared with Alzheimer's disease dementia (AD) on magnetic resonance imaging. However, frequently coexistent AD-type pathology may influence the pattern of regional brain atrophy rates in DLB patients. We investigated the pattern and magnitude of the atrophy rates from 2 serial MRIs in autopsy-confirmed DLB patients (n = 20) and mixed DLB/AD patients (n = 22), compared with AD (n = 30) and elderly nondemented control subjects (n = 15), followed ante mortem. DLB patients without significant AD-type pathology were characterized by lower global and regional rates of atrophy, similar to control subjects. The mixed DLB/AD patients displayed greater atrophy rates in the whole brain, temporoparietal cortices, hippocampus and amygdala, and ventricle expansion, similar to AD patients. In the DLB and DLB/AD patients, the atrophy rates correlated with Braak neurofibrillary tangle stage, cognitive decline, and progression of motor symptoms. Global and regional atrophy rates are associated with AD-type pathology in DLB, and these rates can be used as biomarkers of AD progression in patients with LB pathology.