Table 2.
Subcortical Ischemic Vascular Dementia (SIVD) Neuropathology study: imaging and clinical correlations
Autopsy study | N/pathological diagnosis | Mean age (years) | Diagnosis of AD | Diagnosis of VBI | Prevalence of mixed | Neuropsychology | Interaction between VBI and AD on risk of dementia |
---|---|---|---|---|---|---|---|
Subcortical Ischemic Vascular Dementia (SIVD) study [18] | N = 61 | 78 (at time of neuropsych) | CERAD | CVD-PS | Linear composite measures | AD patient scores were lower than EXEC by nearly a standard deviation on average. VBI patients were rather equally impaired on EXEC,MEM and NVMEM | |
AD = 23 | Braak and Braak ≥ IV | Infarct score ≥20 | |||||
VBI = 11 | GLOB | ||||||
Mixed = 9 | MEM | ||||||
NSP = 19 | EXEC | ||||||
SIVD study [19] | N = 79 | 82.8 ± 7.0 | NINDS-ADRDA criteria | ADDTC criteria | Clin Dx = 28% | Positive likelihood ratios: AD = 6.4 > VCI = 3.7 > mixed = 2.3 | |
AD = 34 | At time of death | ||||||
VBI = 15 | CERAD | CVD-PS | Path Dx = 11% | Cognitive status (CN, CIND, Dem) | AD pathology and hippocampal sclerosis have relatively greater effect on cognition than VBI | ||
Mix = 9 | Braak and Braak ≥ IV | Infarct score ≥20 | |||||
NSP = 21 | |||||||
SIVD study [20] | N = 93 | 84 | Lacunes associated with WMH | ||||
Normal = 12 | AD, atherosclerosis, and VBI contribute independently to cortical gray matter atrophy | ||||||
AD = 46 | AD and hippocampal sclerosis are associated with hippocampal atrophy | ||||||
VBI = 14 | |||||||
Mixed = 9 | |||||||
NSP = 12 | |||||||
SIVD study [21] | N = 163 | 84 | Cerebral atherosclerosis was positively associated with microinfarcts (OR, 2.3; 95% CI, 1.2-4.4) and cystic infarcts (OR, 2.0; 95% CI, 1.0-4.2) but not AD pathology | ||||
Normal = 23 | |||||||
AD = 81 | Cerebral amyloid angiopathy was inversely associated with lacunar infarcts (OR, 0.6; 95% CI, 0.41-1.1), but positively associated with Braak and Braak stage (OR, 1.5; 95% CI, 1.1-2.1) and Consortium to Establish a Registry for Alzheimer Disease plaque score (OR, 1.5; 95% CI, 1.1-2.2) | ||||||
VBI = 21 | |||||||
Mixed = 15 | |||||||
NSP = 23 | |||||||
SIVD study (Zheng et al., manuscript submitted for publication) | N = 116 | 84 | Pathological measures of AD, atherosclerosis, and VBI contribute independently to MRI cortical gray matter atrophy and cognitive impairment. Path analyses show that the adverse effects of atherosclerosis on cognition are largely mediated through subcortical infarcts to brain atrophy, while the effects of AD on cognition work equally through cortical atrophy as well as through a yet unmeasured direct pathway | ||||
Normal = 12 | |||||||
AD = 53 | |||||||
VBI = 18 | |||||||
Mixed = 9 | |||||||
NSP = 24 |
AD, Alzheimer disease; ADDTC, Alzheimer’s Disease Diagnostic and Treatment Centers; CERAD, Consortium to Establish a Registry for Alzheimer Disease; CI, confidence interval; CIND, Cognitive impairment not meeting criteria for dementia; Clin Dx, clinical diagnosis; CN, cognitively normal; CVD-PS, cerebrovascular disease-parenchymal score; Dem, dementia; EXEC, executive score; GLOB, global cognition score; MEM, memory score; NINDS-ADRDA, National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l’Enseignement en Neurosciences; NSP, non-significant pathology; NVMEM, non-verbal memory; OR, odds ratio; Path Dx, pathological diagnosis; VBI, vascular brain injury; WMH, white matter hyperintensity.