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NEUROLOGY 2005;65:323-325
© 2005 American Academy of Neurology
Brief Communications

Familial Alzheimer disease: Decreases in CSF Aß42 levels precede cognitive decline

M. Moonis, MD, J. M. Swearer, PhD, M. P. E. Dayaw, MD, P. St. George-Hyslop, MD, FRCP(C), E. Rogaeva, PhD, T. Kawarai, MD and D. A. Pollen, MD

From the Department of Neurology (Drs. Moonis, Swearer, Dayaw, and Pollen), University of Massachusetts Medical School, Worcester, MA; and Centre for Research in Neurodegenerative Diseases (Drs. St. George-Hyslop, Rogaeva, and Kawarai), Department of Medicine, University of Toronto and Toronto Western Hospital Research Institute, Movement Disorders Centre (Dr. St. George-Hyslop), Toronto Western Hospital Research Institute, Toronto Western Hospital and University of Toronto, and Division of Neurology (Drs. St. George-Hyslop and Rogaeva), Department of Medicine, University of Toronto, Ontario, Canada.

Address correspondence and reprint requests to Dr Pollen, Department of Neurology, University of Massachusetts Medical School, 55 Lake Ave. N., Worcester, MA 01655; e-mail: pollend{at}ummhc.org

CSF amyloid ß-peptide 42 (Aß42) levels in presymptomatic subjects with pathogenic mutations in the PS1 gene are significantly lower than in an age-matched control group. Consequently, in these subjects, there is a window of opportunity estimated as at least 4 to 12 years to evaluate the ability of any putative prophylactic therapy to decrease, arrest, or reverse abnormalities in Aß42 metabolism many years before clinical symptoms of Alzheimer disease are otherwise likely to occur.

Received February 12, 2005. Accepted in final form April 12, 2005.


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