Affiliations: [a] New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA | [b] Medical University of Gdansk, Gdansk, Poland | [c] Ottawa Civic Hospital, Ottawa, Ontario, Canada | [d] New York University School of Medicine, Aging and Dementia Research Center, New York, NY, USA | [e] New York University Medical Center, Aging and Dementia Research Center, New York, NY, USA
Correspondence:
[*]
Correspondence to: Jerzy Wegiel, PhD, Department of Pathological Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA. Tel.: +1 718 4945231; Fax: +1 718 4945480; E-mail: J_Wegiel@email.msn.com
Abstract: A morphometric study of amyloid-ß-positive plaques in the neocortex of eight non-demented people from 68 to 82 years of age and 17 subjects with late-stage Alzheimer disease (GDS stage 7/FAST stages 7a–f) from 73 to 93 years of age shows a shift from prevalence of fibrillar plaques to prevalence of nonfibrillar plaques. In the aged, non-demented subjects, about 4/mm2 plaques are detectable in the neocortex, and the majority are fibrillar plaques. Specifically, 64% found to be classical fibrillar and Thioflavin-S-positive bright primitive plaques. A lower percentage of pale primitive plaques (35%) relatively small proportion of plaques that are poor in thioflavin S-positive fibrils. The numerical density of plaques in the severe stage of AD increases to about 41/mm2. Severely demented subjects appear to maintain an active process of fibrillar plaque formation. This is reflected in the presence of 3% bright primitive plaques. Severely demented subjects also manifest plaque degradation, reflected in the presence of 22% and 48% percentages of classical fibrillar plaques in non-demented subjects and in the end stage of disease suggest that once activated, the process of fibrillar plaque formation persists at a somewhat stable rate during the whole course of brain amyloidosis.
