Cortical event-related potentials in preclinical familial Alzheimer disease

被引:84
作者
Golob, E. J. [1 ,2 ]
Ringman, J. M. [3 ,4 ]
Irimajiri, R. [2 ]
Bright, S. [1 ]
Schaffer, B. [4 ]
Medina, L. D. [3 ,4 ]
Starr, A. [2 ]
机构
[1] Tulane Univ, Dept Psychol, New Orleans, LA 70118 USA
[2] Univ Calif Irvine, Dept Neurol, Irvine, CA 92717 USA
[3] Univ Calif Los Angeles, Mary S Easton Ctr Alzheimers Dis Res, Los Angeles, CA USA
[4] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA
基金
美国国家科学基金会;
关键词
MILD COGNITIVE IMPAIRMENT; EVOKED-POTENTIALS; P300; SUBCOMPONENTS; PRESENILIN-1; GENE; TARGET DETECTION; MIDDLE-LATENCY; COMPONENTS; MUTATIONS; DEMENTIA; VARIABILITY;
D O I
10.1212/WNL.0b013e3181c1de77
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Objective: To define changes in cortical function in persons inheriting familial Alzheimer disease (FAD) mutations before the onset of cognitive decline. Methods: Twenty-six subjects with a family history of FAD were divided into 2 subgroups according to genotype (FAD mutation carriers, n = 15; FAD noncarriers, n = 11). Subjects were given standardized tests of cognitive function and the Clinical Dementia Rating scale (CDR). Sensory (P50, N100, P200) and cognitive (N200, P300) event-related potentials were recorded during an auditory discrimination task. Amplitudes and latencies of cortical potentials were compared among FAD mutation carriers and noncarriers. Results: FAD mutation carriers and noncarriers did not significantly differ in age or on measures of cognitive function, but FAD carriers had a greater incidence of 0.5 CDR scores (1/10 noncarriers, 5/15 carriers). Relative to noncarriers, FAD mutation carriers had significantly longer latencies of the N100, P200, N200, and P300 components, and smaller slow wave amplitudes. Subanalyses of subjects having CDR scores of 0.0 also showed latency increases in FAD mutation carriers. Conclusions: Auditory sensory and cognitive cortical potentials in persons with familial Alzheimer disease (FAD) mutations are abnormal approximately 10 years before dementia will be manifest. Longer event-related potential latencies suggest slowing of cortical information processing in FAD mutation carriers. Neurology (R) 2009; 73: 1649-1655
引用
收藏
页码:1649 / 1655
页数:7
相关论文
共 36 条
[1]
[Anonymous], 2005, Electric fields of the brain: The neurophysics of eeg
[2]
The Topographical and Neuroanatomical Distribution of Neurofibrillary Tangles and Neuritic Plaques in the Cerebral Cortex of Patients with Alzheimer's Disease [J].
Arnold, Steven E. ;
Hyman, Bradley T. ;
Flory, Jill ;
Damasio, Antonio R. ;
Van Hoesen, Gary W. .
CEREBRAL CORTEX, 1991, 1 (01) :103-116
[3]
Diagnostic value of event-related evoked Potentials N200 and P300 subcomponents in early diagnosis of Alzheimer's disease and mild cognitive impairment [J].
Bennys, Karim ;
Portet, Florence ;
Touchon, Jacques ;
Rondouin, Gerard .
JOURNAL OF CLINICAL NEUROPHYSIOLOGY, 2007, 24 (05) :405-412
[4]
A review of the evidence for P2 being an independent component process: age, sleep and modality [J].
Crowley, KE ;
Colrain, IM .
CLINICAL NEUROPHYSIOLOGY, 2004, 115 (04) :732-744
[5]
Closed head injury-related information processing deficits: An event-related potential analysis [J].
Duncan, CC ;
Kosmidis, MH ;
Mirsky, AF .
INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY, 2005, 58 (2-3) :133-157
[6]
MINI-MENTAL STATE - PRACTICAL METHOD FOR GRADING COGNITIVE STATE OF PATIENTS FOR CLINICIAN [J].
FOLSTEIN, MF ;
FOLSTEIN, SE ;
MCHUGH, PR .
JOURNAL OF PSYCHIATRIC RESEARCH, 1975, 12 (03) :189-198
[7]
Clinicopathological features of familial Alzheimer's disease associated with the M139V mutation in the presenilin 1 gene - Pedigree but not mutation specific age at onset provides evidence for a further genetic factor [J].
Fox, NC ;
Kennedy, AM ;
Harvey, RJ ;
Lantos, PL ;
Roques, PK ;
Collinge, J ;
Hardy, J ;
Hutton, M ;
Stevens, JM ;
Warrington, EK ;
Rossor, MN .
BRAIN, 1997, 120 :491-501
[8]
Value of event-related P300 subcomponents in the clinical diagnosis of mild cognitive impairment and Alzheimer's Disease [J].
Frodl, T ;
Hampel, H ;
Juckel, G ;
Bürger, K ;
Padberg, F ;
Engel, RR ;
Möller, HJ ;
Hegerl, U .
PSYCHOPHYSIOLOGY, 2002, 39 (02) :175-181
[9]
SEGREGATION OF A MISSENSE MUTATION IN THE AMYLOID PRECURSOR PROTEIN GENE WITH FAMILIAL ALZHEIMERS-DISEASE [J].
GOATE, A ;
CHARTIERHARLIN, MC ;
MULLAN, M ;
BROWN, J ;
CRAWFORD, F ;
FIDANI, L ;
GIUFFRA, L ;
HAYNES, A ;
IRVING, N ;
JAMES, L ;
MANT, R ;
NEWTON, P ;
ROOKE, K ;
ROQUES, P ;
TALBOT, C ;
PERICAKVANCE, M ;
ROSES, A ;
WILLIAMSON, R ;
ROSSOR, M ;
OWEN, M ;
HARDY, J .
NATURE, 1991, 349 (6311) :704-706
[10]
Auditory cortical activity in amnestic mild cognitive impairment: relationship to subtype and conversion to dementia [J].
Golob, Edward J. ;
Irimajiri, Rie ;
Starr, Arnold .
BRAIN, 2007, 130 :740-752