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William Bondareff, MD, PhD
Department of Psychiatry and Behavioral Sciences University of Southern California Health Science Campus 2025 Zonal Ave Los Angeles, CA 90033

Christopher Mountjoy, FRCPsych
(UK)

St Andrew's Hospital Northampton NN1 5DG United Kingdom

Martin Roth, MD, ScD, FRCP, FRCPsych
(UK)

Department of Psychiatry Clinical School University of Cambridge Cambridge CB2 2QQ United Kingdom

Martin N. Rossor, MD, MRCP
The National Hospitals for Nervous Diseases Queens Square London WC1N 3BG United Kingdom

Leslie L. Iversen, MA, PhD, FRS
Merck Sharp & Dohme Research Laboratories Neuroscience Research Centre Terlings Park Eastwick Road Harlow, Essex CM20 2QR United Kingdom

Gavin P. Reynolds, PhD
Department of Pathology Queen's Medical Centre University Hospital Nottingham NG7 2UH United Kingdom

Arch Gen Psychiatry. 1988;45(10):963.

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Mann and colleagues counted nLC neurons in 46 patients with AD (mean age, 77.73 ±9.42 years). They found two groups: one with a mean neuronal loss of 70% and the other with a mean neuronal loss of 28%. This compares well with our description of AD-1 (with a 20% loss of nLC neurons) and AD-2 (with an 80% loss). While these findings suggest the subdivision of AD into two subtypes, our case for subdivision rests on more evidence; in particular, on differences in neocortical norepinephrine concentration, choline acetyltransferase activity, plaques, and tangles.

Like Mann and associates, we found that although there were some dips in the distribution curve of nLC neuronal counts, clear modes could not be discerned. Discriminant function analyses, however, showed the existence of two groups, which were better differentiated by age at death than by loss of nLC neurons.

Although it is not known with certainty . . . [Full Text PDF of this Article]

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