Mapping the progression of atrophy in early- and late-onset alzheimer's disease

Raffaella Migliaccio, Federica Agosta, Katherine L. Possin, Elisa Canu, Massimo Filippi, Gil D. Rabinovici, Howard J. Rosen, Bruce L. Miller, Maria Luisa Gorno-Tempini

Research output: Contribution to journalArticlepeer-review

Abstract

The term early-onset Alzheimer's disease (EOAD) identifies patients who meet criteria for AD, but show onset of symptoms before the age of 65. We map progression of gray matter atrophy in EOAD patients compared to late-onset AD (LOAD). T1-weighted MRI scans were obtained at diagnosis and one-year follow-up from 15 EOAD, 10 LOAD, and 38 agematched controls. Voxel-based and tensor-based morphometry were used, respectively, to assess the baseline and progression of atrophy. At baseline, EOAD patients already showed a widespread atrophy in temporal, parietal, occipital, and frontal cortices. After one year, EOAD had atrophy progression in medial temporal and medial parietal cortices. At baseline, LOAD patients showed atrophy in the medial temporal regions only, and, after one year, an extensive pattern of atrophy progression in the same neocortical cortices of EOAD. Although atrophy mainly involved different lateral neocortical or medial temporal hubs at baseline, it eventually progressed along the same brain default-network regions in both groups. The cortical region showing a significant progression in both groups was the medial precuneus/posterior cingulate.

Original languageEnglish
Pages (from-to)351-364
Number of pages14
JournalJournal of Alzheimer's Disease
Volume46
Issue number2
DOIs
Publication statusPublished - 2015

Keywords

  • Age of onset
  • Alzheimer's disease
  • atrophy progression
  • default mode network
  • tensor based morphometry
  • voxel based morphometry

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Geriatrics and Gerontology
  • Clinical Psychology

Fingerprint Dive into the research topics of 'Mapping the progression of atrophy in early- and late-onset alzheimer's disease'. Together they form a unique fingerprint.

Cite this