Cerebral amyloid deposition and diffuse plaques in``normal''aging: Evidence for presymptomatic and very mild Alzheimer's disease

JC Morris, M Storandt, DW McKeel Jr, EH Rubin… - Neurology, 1996 - AAN Enterprises
JC Morris, M Storandt, DW McKeel Jr, EH Rubin, JL Price, EA Grant, L Berg
Neurology, 1996AAN Enterprises
Methods. Subjects. All were enrolled as healthy elderly control subjects in a longitudinal
study of DAT for which the recruitment, entry characteristics, and assessment methods have
been described previously.[26] Control subjects were living in the community and had no
evidence for dementia or for neurologic, psychiatric, or medical disorders with the potential
to cause dementia, as determined by exclusionary criteria used in our clinical diagnosis of
DAT.[27] Diagnostic accuracy for AD with these clinical criteria is 96%(AD confirmed …
Methods.
Subjects.
All were enrolled as healthy elderly control subjects in a longitudinal study of DAT for which the recruitment, entry characteristics, and assessment methods have been described previously.[26] Control subjects were living in the community and had no evidence for dementia or for neurologic, psychiatric, or medical disorders with the potential to cause dementia, as determined by exclusionary criteria used in our clinical diagnosis of DAT.[27] Diagnostic accuracy for AD with these clinical criteria is 96%(AD confirmed histologically in 102/106 consecutive autopsies in DAT subjects).[28] After enrollment, subjects were assessed at regular intervals (generally annually) unless prevented by death, refusal, or relocation far from St. Louis. Since the initial subject entered in 1979, 261 control subjects were recruited through June 30, 1994. Only nine (3.5%) subjects were lost to follow-up (two relocated, seven refused further participation).
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