Magnetic resonance imaging-measured atrophy and its relationship to cognitive functioning in vascular dementia and Alzheimer's disease patients. Academic Article uri icon

Overview

abstract

  • BACKGROUND: Recent pathological studies report vascular pathology in clinically diagnosed Alzheimer's disease (AD) and AD pathology in clinically diagnosed vascular dementia (VaD). We compared magnetic resonance imaging (MRI) measures of vascular brain injury (white matter hyperintensities [WMH] and infarcts) with neurodegenerative measures (medial-temporal atrophy [MTA] and cerebral atrophy [CA]) in clinically diagnosed subjects with either AD or VaD. We then examined relationships among these measures within and between the two groups and their relationship to mental status. METHODS: Semi-quantitative MRI measures were derived from blind ratings of MRI scans obtained from participants in a research clinical trial of VaD (N = 694) and a genetic epidemiological study of AD (N = 655). RESULTS: CA was similar in the two groups, but differences in the mean of MTA and WMH were pronounced. Infarcts were significantly associated with CA in VaD but not in AD; MTA and WMH were associated with CA in both. WMH was associated with MTA in both groups; however, MRI infarcts were associated with MTA in VaD but not with MTA in AD patients. MTA was strongly associated with Mini-Mental State Examination scores in both groups, whereas evidence of a modest association between WMH and Mini-Mental State Examination scores was seen in VaD patients. CONCLUSIONS: MRI data from two dementia cohorts with differing dementia etiologies find that the clinical consequences of dementia are most strongly associated with cerebral and medial-temporal atrophy, suggesting that tissue loss is the major substrate of the dementia syndrome.

publication date

  • July 1, 2011

Research

keywords

  • Alzheimer Disease
  • Cognition Disorders
  • Dementia, Vascular

Identity

PubMed Central ID

  • PMC3166967

Scopus Document Identifier

  • 80052311654

Digital Object Identifier (DOI)

  • 10.1016/j.jalz.2011.01.004

PubMed ID

  • 21723205

Additional Document Info

volume

  • 7

issue

  • 5