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Neurology 2000;54:100
© 2000 American Academy of Neurology
Articles

AMY plaques in familial AD

Comparison with sporadic Alzheimer’s disease

C. F. Lippa, MD, M. L. Schmidt, PhD, L. E. Nee, MSW, T. Bird, MD, D. Nochlin, MD, C. Hulette, PhD, H. Mori, PhD, V. M.- Y. Lee and J. Q. Trojanowski, MD, PhD

From the Department of Neurology (Dr. Lippa), MCP-Hahnemann University, Philadelphia, PA; Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (Drs. Schmidt, Lee, and Trojanowski), University of Pennsylvania School of Medicine, Philadelphia, PA; Family Studies Unit (L. E. Nee), National Institute of Neurological Disorders and Stroke, Clinical Center, Bethesda, MD; Department of Neurology (Dr. Bird), VA Medical Center and University of Washington School of Medicine, Seattle, WA; Department of Pathology (Dr. Nochlin), University of Washington, Seattle, WA; Department of Pathology (Dr. Hulette), Duke University Medical Center, Durham, NC; and the Department of Neuroscience (Dr. Mori), Osaka City University Medical School, Aebnoku, Japan.

Address correspondence and reprint requests to Dr. Carol F. Lippa, Department of Neurology, MCP-Hahnemann University, 3300 Henry Avenue, Philadelphia, PA 19102; e-mail: lippa{at}auhs.edu

OBJECTIVE: To assess AMY expression in familial AD (FAD).

BACKGROUND: The discovery of nonß-amyloid (Aß), plaque-like deposits composed of a 100-kd protein (AMY) in sporadic AD (SAD) brains prompted us to determine whether these plaques (AMY plaques) also occur in AD due to mutations of the presenilin-1 (PS-1), presenilin-2 (PS-2), or the amyloid precursor protein (APP) genes.

METHODS: We used immunohistochemistry and confocal laser scanning microscopy to probe the brains of 22 patients with FAD (13 with PS-1, 5 with PS-2, and 4 with APP mutations) and 14 patients with SAD.

RESULTS: AMY plaques were present in all SAD and FAD brains, including an FAD/PS-1 brain from an individual with preclinical disease. The morphology of AMY plaques in SAD and FAD brains was indistinguishable, but they differed from Aß deposits because AMY plaques lacked an immunoreactive core. AMY plaques sometimes colocalized with Aßx-42 deposits, but they did not colocalize with Aßx-40 plaque cores in either SAD or FAD brains. The percent of cortical area occupied by AMY was greater in FAD than in SAD brains (mean percent area = 9.8% and 5.9%, t = 2.487, p = 0.018). In particular, APP and PS-1 cases had more AMY deposition than PS-2 or SAD cases (12.9%, 10.5%, 6.2% in APP, PS-1, and PS-2 AD).

CONCLUSIONS: AMY plaques are consistently present in familial AD due to presenilin-1 (PS-1), PS-2, and amyloid precursor protein mutations, and they can begin to accumulate before the emergence of dementia.

Key words: AD—AMY—Amyloid precursor protein—Confocal laser scanning microscopy—Familial AD—Presenilin






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