Quantitative MRI to understand Alzheimer's disease pathophysiology

Marco Bozzali, Laura Serra, Mara Cercignani

Research output: Contribution to journalReview articlepeer-review

Abstract

Purpose of review The role of white matter damage in the progression of Alzheimer's disease and the associated cognitive symptoms is becoming increasingly clearer. This is partly because of the advent of diffusion tensor imaging, which, in combination with other quantitative MRI techniques, offers unique insights into the patholophysiology of Alzheimer's disease in vivo. The purpose of this review is to integrate the most recent imaging findings, with respect to understanding Alzheimer's disease pathophysiology, and identifying potential biomarkers with diagnostic and prognostic value. Recent findings Consistent with patterns of gray matter atrophy, white matter damage in Alzheimer's disease is localized within white matter tracts connecting the temporal lobe with the rest of the brain, including the cingulum, the uncinate fasciculus and the fornix. These abnormalities are often correlated with adjacent gray matter tissue loss, and with cognitive performance. The relationship between these findings and loss of functional connectivity supports the hypothesis of disconnection as a mechanism for the spread of Alzheimer's disease. Summary White matter abnormalities occur early in Alzheimer's disease, and might actively contribute to the progression of the disease. Functional and structural gray matter abnormalities parallel the white matter changes, and successful biomarkers are likely to be multiparametric.

Original languageEnglish
Pages (from-to)437-444
Number of pages8
JournalCurrent Opinion in Neurology
Volume29
Issue number4
DOIs
Publication statusPublished - Aug 1 2016

Keywords

  • Alzheimer's disease
  • diffusion
  • functional MRI
  • magnetization transfer
  • mild cognitive impairment
  • MRI

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Fingerprint Dive into the research topics of 'Quantitative MRI to understand Alzheimer's disease pathophysiology'. Together they form a unique fingerprint.

Cite this