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Executive dysfunction in hyperhomocystinemia responds to homocysteine-lowering treatment -- Boxer et al. 64 (8): 1431 -- Neurology

Executive dysfunction in hyperhomocystinemia responds to homocysteine-lowering treatment -- Boxer et al. 64 (8): 1431 -- Neurology

Executive dysfunction in hyperhomocystinemia responds to homocysteine-lowering treatment
A. L. Boxer, MD, PhD, J. H. Kramer, PsyD, K. Johnston, MD, J. Goldman, MS, MPhil, R. Finley, BPh and B. L. Miller, MD

From the Memory and Aging Center, Department of Neurology (Drs. Boxer, Kramer, and Miller, J. Goldman and R. Finley), UCSF, and Genetics Department (Dr. Johnston), Permanente Medical Group, San Francisco, CA.

Address correspondence and reprint requests to Dr Boxer, Memory and Aging Center, Department of Neurology, UCSF, Box 1207, San Francisco, CA 94143-1207; e-mail: adam.boxer@memory.ucsf.edu

An elevated serum homocysteine level is a risk factor for the development of cognitive impairment. Reported is a late-onset case of hyperhomocystinemia due to a vitamin B12 metabolic deficit (cobalamin C) with cognitive impairment, primarily in frontal/executive function. After homocysteine-lowering therapy, the patient’s functional and neuropsychological status improved in conjunction with a decrease in leukoariosis on his MRI scan. These findings suggest that homocysteine-related cognitive impairment may be partially reversible.
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