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Neuroanatomical correlates of low body weight in Alzheimer's disease: a PET study.

Authors
  • Hu, XiaSheng
  • Okamura, Nobuyuki
  • Arai, Hiroyuki
  • Higuchi, Makoto
  • Maruyama, Masahiro
  • Itoh, Masatoshi
  • Yamaguchi, Keiichro
  • Sasaki, Hidetada
Type
Published Article
Journal
Progress in Neuro-Psychopharmacology and Biological Psychiatry
Publisher
Elsevier
Publication Date
Dec 01, 2002
Volume
26
Issue
7-8
Pages
1285–1289
Identifiers
PMID: 12502015
Source
Medline
License
Unknown

Abstract

Weight loss is a common problem in patients with Alzheimer's disease (AD) and this might be associated with an increased risk for mortality. Recent evidences have suggested that certain brain dysfunctions may result in impaired nutritional status in AD patients. However, the mechanism of body weight loss in AD remains enigmatic. To investigate a possible association between low body weight and regional brain dysfunction, the authors conducted the correlational analysis of body mass index (BMI) with regional brain glucose metabolism using positron emission tomography (PET) and [18F]fluorodeoxyglucose (FDG). Twenty-seven patients with probable AD were divided into two groups: the low BMI group and the normal BMI group. Regional brain glucose metabolic ratios were calculated using the cerebellar hemisphere as a reference region. Comparisons were made of regional brain metabolic ratios between the low BMI group and the normal BMI group. Correlations of the glucose metabolic ratio with BMI were also assessed in all patients with AD. In the comparison between the two groups, glucose metabolic ratio in the anterior cingulate cortex (ACC) was significantly lower in the low BMI group, whereas no significant differences were found in all the other brain regions. Furthermore, regional glucose metabolism in the ACC had a significant and positive correlation with BMI (r=.450, P=.018). After adjustment for age, gender and disease duration, regional glucose metabolism in the ACC was independently associated with BMI. Our findings suggest that the ACC may be preferentially involved in the regulation of nutritional status in AD patients, and provides a new insight into developing strategies for prevention and treatment of undernutritional demented patients.

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