Cortical thickness and hippocampal shape in pure vascular mild cognitive impairment and dementia of subcortical type

Abstract

Background and purpose The progression pattern of brain structural changes in patients with isolated cerebrovascular disease (CVD) remains unclear. To investigate the role of isolated CVD in cognitive impairment patients, patterns of cortical thinning and hippocampal atrophy in pure subcortical vascular mild cognitive impairment (svMCI) and pure subcortical vascular dementia (SVaD) patients were characterized. Methods Forty-five patients with svMCI and 46 patients with SVaD who were negative on Pittsburgh compound B (PiB) positron emission tomography imaging and 75 individuals with normal cognition (NC) were recruited. Results Compared with NC, patients with PiB(−) svMCI exhibited frontal, language and retrieval type memory dysfunctions, which in patients with PiB(−) SVaD were further impaired and accompanied by visuospatial and recognition memory dysfunctions. Compared with NC, patients with PiB(−) svMCI exhibited cortical thinning in the frontal, perisylvian, basal temporal and posterior cingulate regions. This atrophy was more prominent and extended further toward the lateral parietal and medial temporal regions in patients with PiB(−) SVaD. Compared with NC subjects, patients with PiB(−) svMCI exhibited hippocampal shape deformities in the lateral body, whilst patients with PiB(−) SVaD exhibited additional deformities within the lateral head and inferior body. Conclusions Our findings suggest that patients with CVD in the absence of Alzheimer’s disease pathology can be demented, showing cognitive impairment in multiple domains, which is consistent with the topography of cortical thinning and hippocampal shape deformity.

Molecular Neuroimaging in Vascular Cognitive Impairment

“…Subjects with pure subcortical vascular MCI had lower mean cortical thickness and hippocampal volume than HCs, and both these measures were significantly decreased in patients with pure subcortical vascular dementia when compared with those with pure subcortical vascular MCI. 37 Despite the fact that the classification into amyloid-negative category may not totally rule out amyloid-related effects on cerebral cortex, this study suggests a dose-dependent relationship between pure forms of moderate-to-severe SVD and cortical atrophy in patients without AD. The same group of investigators has also presented topographical changes in cortical thickness in PiB(−) and PiB(+) amnestic MCI patients compared with HC.…”

“…A study of hippocampal and cortical thickness of patients with amyloid-negative PET scans derived from this cohort has given further insights into cortical atrophy that might be attributable to arteriolosclerotic SVD rather than Alzheimer's pathology. 37 The authors have diagnosed pure subcortical vascular mild cognitive impairment (MCI) and pure subcortical vascular dementia based on PiB(-) PET scan, defined as a PiB retention ratio <1.5. Subjects with pure subcortical vascular MCI had lower mean cortical thickness and hippocampal volume than HCs, and both these measures were significantly decreased in patients with pure subcortical vascular dementia when compared with those with pure subcortical vascular MCI.…”

Responses of the Human Brain to Mild Dehydration and Rehydration Explored In Vivo by1H-MR Imaging and Spectroscopy

“…Reversible cortical thinning by short-term dehydration is not uniformly distributed over the cerebral surface (Fig 4) (ie, the brain does not seem to simply shrink by global scaling during dehydration). Instead, detected changes of cortical thickness reveal some but no exclusive overlap with the following: 1) known areas of pronounced cortical thickness 30 ; and 2) atrophy patterns found in Alzheimer disease, 31 cerebrovascular dementia, 32 and eating disorders, 33 for example. Also, more generally, brain volume changes due to osmotic stress are in/near the magnitude of changes attributed to annual volume decrease by aging (0.2%), 34,35 Alzheimer disease (2%), Lewy body dementia (1.4%), or vascular dementia (1.9%).…”

Blood glucose levels and cortical thinning in cognitively normal, middle-aged adults

“…It may be that higher glucose levels lead to grey matter atrophy via cerebral glucose hypometabolism, which leads to neuronal injury, which has been shown to be independent of Aβ accumulation [48]. Although research has shown that cortical thinning occurs in the prodromal stages of several types of dementia (i.e., dementia with Lewy bodies, AD, and vascular dementia) [4,13,14, 35], few studies have investigated cortical thickness in a cognitively normal, healthy sample [17,34,42]. …”