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Department of Pathology (Drs. Dickson, Ruan, Davies, Kress, and Yen), and the Rose F. Kennedy Center for Research in Mental Retardation and Human Development, Albert Einstein College of Medicine; Department of Neurology (Dr. Crystal), Albert Einstein College of Medicine, Bronx, NY; and Department of Neurology (Dr. Mark), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ.
Immunocytochemistry with antibodies to ubiquitin is currently the most sensitive method for detecting cortical Lewy bodies, which are a sine qua non for the diagnosis of diffuse Lewy body disease (DLBD), an increasingly recognized form of primary degenerative dementia. In the systematic application of ubiquitin immunocytochemistry to sections of hippocampus from control subjects and patients with a wide spectrum of neurodegenerative diseases, we noted the frequent occurrence of ubiquitin-immunoreactive neurites in the CA2–3 region in DLBD. The nature of these neurites was investigated with immunocytochemistry in DLBD, Alzheimer's disease (AD), normal elderly subjects, and Parkinson's disease (PD). Although the number of neurites varied from case to case, they were virtually always detected in DLBD but not in normal, AD, or PD brains. Double immunolabeling studies with anti-ubiquitin demonstrated a small fraction of double-stained neurites with antibodies to neurofilament or Alz-50, but no double staining with an antibody to Alzheimer neurofibrillary tangles. These results are different from those for neurites in AD, which are rarely seen in CA2–3 and which are immunoreactive with all these antibodies. Neuritic degeneration in the CA2–3 region of the hippocampus appears to be a specific histopathologic feature of DLBD.
Address correspondence and reprint requests to Dr. Dennis W. Dickson, Department of Pathology, K-438, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461.
Supported by NIA AG06803 and AG03949.
Received December 21, 1990. Accepted for publication in final form February 14, 1991.
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