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NEUROLOGY 2005;64:1704-1711
© 2005 American Academy of Neurology

Risk factors for progression of brain atrophy in aging

Six-year follow-up of normal subjects

C. Enzinger, MD, F. Fazekas, MD, P. M. Matthews, MD, DPhil, FRCP, S. Ropele, PhD, H. Schmidt, MD, S. Smith, DPhil and R. Schmidt, MD

From the Departments of Neurology (Drs. Enzinger, Fazekas, Ropele, and R. Schmidt) and Radiology, Section of Neuroradiology (Dr. Fazekas), MR Research Unit (Dr. Ropele), and the Institute of Medical Biochemistry and Molecular Genetics (Dr. H. Schmidt), Medical University of Graz, Austria; and the Centre for Functional MRI of the Brain (Drs. Matthews and Smith), John Radcliffe Hospital, University of Oxford, UK.

Address correspondence and reprint requests to Dr. Christian Enzinger, Department of Neurology, Medical University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria; e-mail: chris.enzinger{at}meduni-graz.at

Objectives: To determine the rate of brain atrophy in neurologically asymptomatic elderly and to investigate the impact of baseline variables including conventional cerebrovascular risk factors, APOE {epsilon}4, and white matter hyperintensity (WMH) on its progression.

Methods: We assessed the brain parenchymal fraction at baseline and subsequent annual brain volume changes over 6 years for 201 participants (F/M = 96/105; 59.8 ± 5.9 years) in the Austrian Stroke Prevention Study from 1.5-T MRI scans using SIENA (structural image evaluation using normalization of atrophy)/SIENAX (an adaptation of SIENA for cross-sectional measurement)(www.fmrib.ox.ac.uk/fsl). Hypertension, cardiac disease, diabetes mellitus, smoking, and regular alcohol intake were present in 64 (31.8%), 60 (29.9%), 5 (2.5%), 70 (39.3%), and 40 (20.7%) subjects, respectively. Plasma levels of fasting glucose (93.7 ± 18.6 mg/dL), glycated hemoglobin A (HbA1c; 5.6 ± 0.7%), total cholesterol (228.3 ± 40.3 mg/dL), and triglycerides (127.0 ± 75.2 mg/dL) were determined. WMH was rated as absent (n = 56), punctate (n = 120), early confluent (n = 14), and confluent (n = 11).

Results: The baseline brain parenchymal fraction of the entire cohort was 0.80 ± 0.02 with a mean annual brain volume change of –0.40 ± 0.29%. Univariate analysis demonstrated a higher rate of brain atrophy in older subjects (p = 0.0001), in those with higher HbA1c (p = 0.0001), higher body mass index (p = 0.02), high alcohol intake (p = 0.04), severe WMH (p = 0.03), and in APOE {epsilon}4 carriers (p = 0.07). Multivariate analysis suggested that baseline brain parenchymal fraction, HbA1c, and WMH score explain a major proportion of variance in the rates of brain atrophy in the cohort (corrected R2 = 0.27; p = 0.0001).

Conclusions: Neurologically asymptomatic elderly experience continuing brain volume loss, which appears to accelerate with age. Glycated hemoglobin A (HbA1c) was identified as a risk factor for a greater rate of brain atrophy. Clustering of factors associated with the so-called metabolic syndrome in subjects with high HbA1c suggests a link between this syndrome and late-life brain tissue loss.

Supported by grants P15158 (S.R.), P13180, and J2373-B02 (C.E.) from the FWF Austrian Science Fund (Vienna), and by the Austrian National Bank Jubilaeumsfonds (projects 3905, 4484, and 7776). P.M.M. acknowledges support from the MS Society of Great Britain and Northern Ireland and the MRC. S.S. is supported by an ERSRC Advanced Research Fellowship. The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report.

Presented in part at the 56th Annual Meeting of the American Academy of Neurology, San Francisco, CA, April 2004, and at the 14th Meeting of the European Neurological Society, Barcelona, Spain, June 2004.

Received August 13, 2004. Accepted in final form February 8, 2005.




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