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Elizabeth H. Corder, PhD; Vesna Jelic, MD; Hans Basun, MD, PhD; Lars Lannfelt, MD, PhD; Sven Valind, MD, PhD; Bengt Winblad, MD, PhD; Agneta Nordberg, MD, PhD

Arch Neurol. 1997;54(3):273-277.

Abstract
Background
Recent findings of a reduced cerebral metabolic rate of glucose (CMRGlu) in at-risk relatives of patients with Alzheimer disease (AD) who carry the apolipoprotein E (APOE) 4 allele suggest a causative role for the E4 isoform in cognitive changes that lead to AD. It is not known whether 4 allele—associated deficits exist in patients with clinical AD.

Objective
To determine whether distinct patterns of cerebral hypometabolism exist in patients who carry the 4 allele.

Patients and Methods
Information on the CMRGlu and APOE genotype was available for 46 patients at a memory disorders clinic: 31 patients were diagnosed as having probable AD, 3 demented patients did not meet criteria for AD, and 12 patients had mild memory complaints. Positron emission tomography with the use of ¹⁸F-fludeoxyglucose was used to calculate the CMRGlu in the frontal and temporoparietal regions of the cortex. Estimates were standardized to the sensorimotor area of the cortex. Linear regression models were constructed to relate the APOE genotype to the CMRGlu, adjusting for cognitive status (ie, the Mini-Mental State Examination score).

Results
Distinct patterns of the CMRGlu did not emerge for patients with different APOE genotypes. Bilateral deficits in the CMRGlu were found in the patients with AD. Left-right asymmetry was found in 8 of 12 patients with mild memory complaints: 7 of 8 had CMRGlu ratios less than 0.85 in the left side of the temporoparietal region of the cortex.

Conclusions
The APOE 4 allele does not appear to be associated with specific deficits in brain metabolism in patients with AD despite evidence that the 4 allele is associated with preclinical alterations. This finding is consistent with previous epidemiologic results that have demonstrated a higher risk for AD in carriers of the 4 allele, but no change in the rate of progression of AD.

Author Affiliations
From the Divisions of Geriatric Medicine (Drs Corder, Jelic, Basun, Lannfelt, Winblad, and Nordberg) and Nicotine Research (Dr Nordberg), Department of Clinical Neuroscience and Family Medicine, Karolinska Institute, Huddinge University Hospital, Huddinge, Sweden; the Center for Demographic Studies, Duke University, Durham, NC (Dr Corder); and the Uppsala University PET Centre, Uppsala, Sweden (Dr Valind).

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