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Table 4 Studies of mixed Alzheimer disease/vascular brain injury with Alzheimer disease defined by cerebrospinal fluid Aβ and phosphorylated tau

From: Clinical and imaging features of mixed Alzheimer and vascular pathologies

Study

N

AD =

VCI/VBI

VBI and AD correlations

ADNI [50]

N = 819

NINDS-ADRDA

VRFs

VRFs were not associated with AD biomarkers

229 NCI

 

WMH

Increased time-varying WMHs were associated with faster decline in executive function and lower FDG uptake in NCI

397 CI

193 AD

Amsterdam Dementia Cohort [49]

N = 914

NINDS-ADRDA

VCI by NINDS-AIREN criteria

The presence of both MBs and WMHs was associated with lower CSF levels of Aβ42, indicating a direct relationship between SVD and AD pathology (note: could SVD be CAA?)

337 NCI

547 AD

30 VCI

The presence of lacunes was associated with higher Aβ42 in vascular dementia (standardized beta = 0.17, P = 0.07) and lower tau in AD (standardized beta = -0.07, P = 0.05) but there were no effects for Aβ42 or phosphorylated tau181 in AD (note: could SVD with lacunes be arteriolosclerosis?)

  1. Aβ, amyloid-beta; AD, Alzheimer disease; ADNI, Alzheimer’s Disease Neuroimaging Initiative; CAA, cerebral amyloid angiopathy; CI, cognitively impaired; CSF, cerebrospinal fluid; FDG, [18 F]fluorodeoxyglucose; MB, microbleed; NCI, no cognitive impairment; NINDS-ADRDA, National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l’Enseignement en Neurosciences; NINDS-AIREN, National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l’Enseignement en Neurosciences; SVD, subcortical vascular dementia; VBI, vascular brain injury; VCI, vascular cognitive impairment; VRF, vascular risk factor; WMH, white matter hyperintensity.