Limbic hypometabolism in Alzheimer's disease and mild cognitive impairment

Ann Neurol. 2003 Sep;54(3):343-51. doi: 10.1002/ana.10669.


The neural basis of the amnesia characterizing early Alzheimer's disease (AD) remains uncertain. Postmortem pathological studies have suggested early involvement of the mesial temporal lobe, whereas in vivo metabolic studies have shown hypometabolism of the posterior cingulate cortex. Using a technique that combined the anatomic precision of magnetic resonance imaging with positron emission tomography, we found severe reductions of metabolism throughout a network of limbic structures (the hippocampal complex, medial thalamus, mamillary bodies, and posterior cingulate) in patients with mild AD. We then studied a cohort with mild cognitive impairment in whom amnesia was the only cognitive abnormality and found comparable hypometabolism through the same network. The AD and mild cognitive impairment groups were differentiated, however, by changes outside this network, the former showing significant hypometabolism in amygdala and temporoparietal and frontal association cortex, whereas the latter did not. The amnesia of very early AD reflects severe but localized limbic dysfunction.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / complications
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / physiopathology
  • Amnesia / etiology
  • Brain Mapping*
  • Cognition Disorders / complications
  • Cognition Disorders / metabolism*
  • Cognition Disorders / physiopathology
  • Female
  • Fluorodeoxyglucose F18
  • Glucose / metabolism
  • Humans
  • Image Processing, Computer-Assisted
  • Limbic System / metabolism*
  • Magnetic Resonance Imaging
  • Male
  • Middle Aged
  • Neuropsychological Tests
  • Tomography, Emission-Computed


  • Fluorodeoxyglucose F18
  • Glucose