Impairment of nonverbal recognition in Alzheimer disease: a PET O-15 study.
OBJECTIVE
To characterize deficits in nonverbal recognition memory and functional brain changes associated with these deficits in Alzheimer disease (AD).


METHODS
Using O-15 PET, we studied 11 patients with AD and 17 cognitively intact elders during the combined encoding and retrieval periods of a nonverbal recognition task. Both task conditions involved recognition of line drawings of abstract shapes. In both conditions, subjects were first presented a list of shapes as study items, and then a list as test items, containing items from the study list and foils. In the titrated demand condition, the shape study list size (SLS) was adjusted prior to imaging so that each subject performed at approximately 75% recognition accuracy; difficulty during PET scanning in this condition was approximately matched across subjects. A control task was used in which SLS = 1 shape.


RESULTS
During performance of the titrated demand condition, SLS averaged 4.55 (+/-1.86) shapes for patients with AD and 7.53 (+/-4.81) for healthy elderly subjects (p = 0.031). However, both groups of subjects were closely matched on performance in the titrated demand condition during PET scanning with 72.17% (+/-7.98%) correct for patients with AD and 72.25% (+/-7.03%) for elders (p = 0.979). PET results demonstrated that patients with AD showed greater mean differences between the titrated demand condition and control in areas including the left fusiform and inferior frontal regions (Brodmann areas 19 and 45).


CONCLUSIONS
Relative fusiform and inferior frontal differences may reflect the Alzheimer disease (AD) patients' compensatory engagement of alternate brain regions. The strategy used by patients with AD is likely to be a general mechanism of compensation, rather than task-specific.
Anderson
K E
KE
Cognitive Neuroscience Division, Taub Institute for Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY, USA.
Brickman
A M
AM
Flynn
J
J
Scarmeas
N
N
Van Heertum
R
R
Sackeim
H
H
Marder
K S
KS
Bell
K
K
Moeller
J R
JR
Stern
Y
Y
D000222:Adaptation, Physiological; D000368:Aged; D000544:Alzheimer Disease / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology*; D001931:Brain Mapping; D002560:Cerebrovascular Circulation; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use; D000077265:Donepezil; D005260:Female; D005625:Frontal Lobe / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006624:Hippocampus / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D007189:Indans / Q000627:therapeutic use; D008279:Magnetic Resonance Imaging; D008297:Male; D008569:Memory Disorders / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology / Q000523:psychology*; D008875:Middle Aged; D009483:Neuropsychological Tests; D018697:Nootropic Agents / Q000627:therapeutic use; D010104:Oxygen Radioisotopes; D010364:Pattern Recognition, Visual / Q000502:physiology; D048448:Phenylcarbamates / Q000627:therapeutic use; D010880:Piperidines / Q000627:therapeutic use; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals; D000068836:Rivastigmine; D013702:Temporal Lobe / Q000000981:diagnostic imaging / Q000503:physiopathology*
D002800:Cholinesterase Inhibitors; D007189:Indans; D018697:Nootropic Agents; D010104:Oxygen Radioisotopes; D048448:Phenylcarbamates; D010880:Piperidines; D019275:Radiopharmaceuticals; D000077265:Donepezil; D000068836:Rivastigmine