Update on neuroimaging in non-Alzheimer's disease dementia: a focus on the Lewy body disease spectrum.

PURPOSE OF REVIEW: An accurate differential diagnosis between Alzheimer's disease (AD) and non-AD dementia is of paramount importance to study disease mechanisms, define prognosis, and select patients for disease-specific treatments. The purpose of the present review is to describe the most recent neuroimaging studies in Lewy body disease spectrum (LBDS), focusing on differences with AD. RECENT FINDINGS: Different neuroimaging methods are used to investigate patterns of alterations, which can be helpful to distinguish LBDS from AD. Positron emission tomography radiotracers and advanced MRI structural and functional methods discriminate these two conditions with increasing accuracy. Prodromal disease stages can be identified, allowing an increasingly earlier diagnosis. SUMMARY: Neuroimaging biomarkers can aid in obtaining the best diagnostic accuracy in LBDS. Despite the main role of neuroimaging in clinical setting is to exclude secondary causes of dementia, structural and metabolic imaging techniques give an essential help to study in-vivo pathophysiological mechanisms of diseases. The importance of neuroimaging in LBDS is given by the increasing number of imaging biomarker developed and studied in the last years.

A multiparametric MRI study of structural brain damage in dementia with lewy bodies: A comparison with Alzheimer's disease.

INTRODUCTION: Differential diagnosis between dementia with Lewy bodies (DLB) and Alzheimer's disease (AD) is crucial for an adequate patients' management but might be challenging. We investigated with advanced MRI techniques gray (GM) and white matter (WM) damage in DLB patients compared to those with AD. METHODS: 24 DLB patients, 26 age- and disease severity-matched AD patients, and 20 age and sex-matched controls performed clinical and neuropsychological assessment, and brain structural and diffusion-tensor MRI. We measured GM atrophy using voxel-based morphometry, WM hyperintensities (WMH) using a local thresholding segmentation technique, and normal-appearing WM (NAWM) damage using tract-based spatial statistic. RESULTS: DLB and AD patients exhibited mild-to-moderate-stage dementia. Compared to controls, GM damage was diffuse in AD, while limited to bilateral thalamus and temporal regions in DLB. Compared to DLB, AD patients exhibited GM atrophy in bilateral fronto-temporal and occipital regions. DLB and AD patients showed higher WMH load than controls, with no differences among each other. WMH in DLB were diffuse with relative prevalence in posterior parietal-occipital regions. Compared to controls, both DLB and AD patients showed reduced microstructural integrity of the main supratentorial and infratentorial NAWM tracts. AD patients exhibited greater posterior NAWM damage than DLB. CONCLUSIONS: DLB showed prominent WM degeneration compared to the limited GM atrophy, while in AD both tissue compartments were severely involved. In DLB, NAWM microstructural degeneration was independent of WMH, thus revealing two possible underlying processes. Different pathophysiological mechanisms are likely to drive GM and WM damage distribution in DLB and AD.