title: Homocysteine and electroencephalographic rhythms in Alzheimer disease: a multicentric study.
abstract: High plasma concentration of homocysteine is an independent risk factor for Alzheimer's disease (AD), due to microvascular impairment and consequent neural loss [Seshadri S, Beiser A, Selhub J, Jacques PF, Rosenberg IH, D'Agostino RB, Wilson PW, Wolf PA (2002) Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N Engl J Med 346(7):476-483]. Is high plasma homocysteine level related to slow electroencephalographic (EEG) rhythms in awake resting AD subjects, as a reflection of known relationships between cortical neural loss and these rhythms? To test this hypothesis, we enrolled 34 mild AD patients and 34 subjects with mild cognitive impairment (MCI). Enrolled people were then subdivided into four sub-groups of 17 persons: MCI and AD subjects with low homocysteine level (MCI- and AD-, homocysteine level <11 micromol/l); MCI and AD subjects with high homocysteine level (MCI+ and AD+, homocysteine level >or=11 micromol/l). Resting eyes-closed EEG data were recorded. EEG rhythms of interest were delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), and beta 2 (20-30 Hz). EEG cortical sources were estimated by low-resolution brain electromagnetic tomography (LORETA). Results showed that delta (frontal and temporal), theta (central, frontal, parietal, occipital, and temporal), alpha 1 (parietal, occipital, and temporal), and alpha 2 (parietal and occipital) sources were stronger in magnitude in AD+ than AD- group. Instead, no difference was found between MCI- and MCI+ groups. In conclusion, high plasma homocysteine level is related to unselective increment of cortical delta, theta, and alpha rhythms in mild AD, thus unveiling possible relationships among that level, microvascular concomitants of advanced neurodegenerative processes, and synchronization mechanisms generating EEG rhythms.
authors.affiliation: Dipartimento di Fisiologia Umana e Farmacologia, Università degli Studi di Roma La Sapienza, Rome, Italy. claudio.babiloni@uniroma1.it <claudio.babiloni@uniroma1.it>
authors.forename: C
authors.initials: C
authors.lastname: Babiloni
authors.forename: P
authors.initials: P
authors.lastname: Bosco
authors.forename: R
authors.initials: R
authors.lastname: Ghidoni
authors.forename: C
authors.initials: C
authors.lastname: Del Percio
authors.forename: R
authors.initials: R
authors.lastname: Squitti
authors.forename: G
authors.initials: G
authors.lastname: Binetti
authors.forename: L
authors.initials: L
authors.lastname: Benussi
authors.forename: R
authors.initials: R
authors.lastname: Ferri
authors.forename: G
authors.initials: G
authors.lastname: Frisoni
authors.forename: B
authors.initials: B
authors.lastname: Lanuzza
authors.forename: E
authors.initials: E
authors.lastname: Cassetta
authors.forename: G
authors.initials: G
authors.lastname: Anello
authors.forename: M
authors.initials: M
authors.lastname: Gurzì
authors.forename: S
authors.initials: S
authors.lastname: Bartesaghi
authors.forename: R
authors.initials: R
authors.lastname: Lizio
authors.forename: M
authors.initials: M
authors.lastname: Tombini
authors.forename: P M
authors.initials: PM
authors.lastname: Rossini
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D001921:Brain / Q000033:anatomy & histology / Q000503:physiopathology*; D003072:Cognition Disorders / Q000503:physiopathology; D004569:Electroencephalography; D005260:Female; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008297:Male
chemical_list: D015415:Biomarkers; D006710:Homocysteine