Spectral analysis of EEG in Alzheimer's disease: Relation to apolipoprotein E polymorphism

Apolipoprotein E (ApoE) epsilon 4 allele is a risk factor for late-onset Alzheimer's disease (AD) and proposed to have a direct impact on cholinergic function in AD. Slowing of the EEG is characteristic in AD and the cholinergic system has an important role in modulating EEG. Fifty-eight AD patients at the early stage of the disease and 34 age- and sex-matched controls were studied using the quantitative EEG recorded from T6-O2 derivation. AD patients were divided into two subgroups: a) according to the ApoE allele (2 epsilon, 1 epsilon 4, and 0 epsilon 4) and b) according to familial aggregation. AD subgroups did not differ in clinical severity or duration of dementia. The AD patients with the epsilon 4 allele had higher relative theta amplitude and lower relative beta amplitude than controls and patients without the epsilon 4 allele. The peak frequencies were lower in all AD subgroups compared to controls. In conclusion, we found a tendency towards more pronounced EEG slowing in AD patients carrying the epsilon 4 allele. The minor differences in EEG may suggest differences in the degree of the cholinergic deficit in these subgroups.

[1]  M. Hamilton.  A RATING SCALE FOR DEPRESSION , 1960, Journal of neurology, neurosurgery, and psychiatry.

[2]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[3]  J. Sirviö,et al.  Relationship between the cortical choline acetyltransferase content and EEG delta-power , 1990, Neuroscience Research.

[4]  H. Soininen,et al.  Longitudinal EEG spectral analysis in early stage of Alzheimer's disease. , 1989, Electroencephalography and clinical neurophysiology.

[5]  D. T. Vernier,et al.  Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI. , 1990, Journal of lipid research.

[6]  T. Teramoto,et al.  Determination by PCR-RFLP of apo E genotype in a Japanese population. , 1993, The Journal of laboratory and clinical medicine.

[7]  M. Pericak-Vance,et al.  Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[8]  V. Hachinski,et al.  Electroencephalography as an aid in the exclusion of Alzheimer's disease. , 1994, Archives of neurology.

[9]  R. Wurtman.  Choline metabolism as a basis for the selective vulnerability of cholinergic neurons , 1992, Trends in Neurosciences.

[10]  B. Reisberg.  The Brief Cognitive Rating Scale (BCRS) : findings in primary degenerativ dementia (PDD) , 1983 .

[11]  Margaret A. Pericak-Vance,et al.  Hypothesis: Microtubule Instability and Paired Helical Filament Formation in the Alzheimer Disease Brain Are Related to Apolipoprotein E Genotype , 1994, Experimental Neurology.

[12]  Thomas Wisniewski,et al.  Apolipoprotein E: A pathological chaperone protein in patients with cerebral and systemic amyloid , 1992, Neuroscience Letters.

[13]  F H Duffy,et al.  Brain electrical activity in patients with presenile and senile dementia of the Alzheimer type , 1984, Annals of neurology.

[14]  H. Soininen,et al.  Apolipoprotein E polymorphism and Alzheimer's disease in Eastern Finland , 1995, Neuroscience Letters.

[15]  H. Soininen,et al.  Quantitative analysis of occipital EEG in different stages of Alzheimer's disease. , 1985, Electroencephalography and clinical neurophysiology.

[16]  D. Schaid,et al.  Apolipoprotein E: risk factor for Alzheimer disease. , 1994, American journal of human genetics.

[17]  E. Otomo,et al.  Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease , 1991, Brain Research.

[18]  Arto Mannermaa,et al.  A severe loss of choline acetyltransferase in the frontal cortex of Alzheimer patients carrying apolipoprotein ε4 allele , 1995, Neuroscience Letters.

[19]  T. Gasser,et al.  Transformations towards the normal distribution of broad band spectral parameters of the EEG. , 1982, Electroencephalography and clinical neurophysiology.

[20]  S. Folstein,et al.  "Mini-mental state". A practical method for grading the cognitive state of patients for the clinician. , 1975, Journal of psychiatric research.

[21]  A. D. Roses,et al.  Association of apolipoprotein E allele €4 with late-onset familial and sporadic Alzheimer’s disease , 2006 .

[22]  R. Katzman.,et al.  Pathological verification of ischemic score in differentiation of dementias , 1980, Annals of neurology.

[23]  M. Pericak-Vance,et al.  Linkage studies in familial Alzheimer disease: evidence for chromosome 19 linkage. , 1991, American journal of human genetics.

[24]  H. Soininen,et al.  Slowing of electroencephalogram and choline acetyltransferase activity in post mortem frontal cortex in definite Alzheimer's disease , 1992, Neuroscience.

[25]  B. Tycko,et al.  The apolipoprotein ε4 allele in patients with Alzheimer's disease , 1993, Annals of neurology.

[26]  S. Gauthier,et al.  Apolipoprotein E polymorphism and Alzheimer's disease , 1993, The Lancet.

[27]  J. Poirier.  Apolipoprotein E in animal models of CNS injury and in alzheimer's disease , 1994, Trends in Neurosciences.

[28]  A Pääkkönen,et al.  Serial EEG in Alzheimer's disease: 3 year follow-up and clinical outcome. , 1991, Electroencephalography and clinical neurophysiology.

[29]  B. Hyman,et al.  Apolipoprotein E in sporadic Alzheimer's disease: Allelic variation and receptor interactions , 1993, Neuron.

[30]  G. Buzsáki,et al.  The cholinergic system and EEG slow waves. , 1991, Electroencephalography and clinical neurophysiology.