Dissociations Among Structural-Perceptual, Lexical-Semantic, and Event-Fact Memory Systems in Alzheimer, Amnesic, and Normal Subjects

• Published in: Cortex Vol. 30; no. 1; pp. 75 - 103
• Main Authors: Gabrieli, John D.E., Keane, Margaret M., Stanger, Ben Z., Kjelgaard, Margaret M., Corkin, Suzanne, Growdon, John H.
• Format: Journal Article
• Language: English
• Published: Italy Elsevier Ltd 01.03.1994
• Subjects: Adult; Aged; Alzheimer Disease - diagnosis; Alzheimer Disease - physiopathology; Alzheimer Disease - psychology; Amnesia - diagnosis; Amnesia - physiopathology; Amnesia - psychology; Attention - physiology; Brain Damage, Chronic - diagnosis; Brain Damage, Chronic - physiopathology; Brain Damage, Chronic - psychology; Brain Mapping; Cerebral Cortex - physiopathology; Female; Humans; Limbic System - physiopathology; Male; Mental Recall - physiology; Middle Aged; Neuropsychological Tests; Paired-Associate Learning - physiology; Pattern Recognition, Visual - physiology; Reference Values; Retention (Psychology) - physiology; Verbal Learning - physiology
• ISSN: 0010-9452; 1973-8102
• DOI: 10.1016/S0010-9452(13)80325-5

Patients with Alzheimer's disease (AD), patients with global amnesia (AMN), and nornal control (NC) subjects received tests of recall and recognition, word-completion priming, ind incomplete-picture priming. The AD and AMN patients had impaired recall and recoglition. The AD patients, but not the AMN patients, had impaired word-completion priming. In contrast, the AD patients had intact incomplete-picture priming, a form of priming shown to be perceptual in normal subjects. These results provide neuropsychological evidence for a dissociation between two components of repetition priming, perceptual priming as measured with identification tasks and nonperceptual priming as measured with generation tasks. Preserverd perceptual priming in AD may be mediated by the occipital regions that are relatively spared in AD; compromised nonperceptual priming may be mediated by temporal regions that show dense neuropathological changes early in AD.