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Homocysteine and electroencephalographic rhythms in Alzheimer disease: a multicentric study
C Babiloni1, P Bosco, R Ghidoni
1Dipartimento di Fisiologia Umana e Farmacologia, Università degli Studi di Roma La Sapienza, Rome, Italy. claudio.babiloni@uniroma1.it <claudio.babiloni@uniroma1.it>
Insights
High homocysteine levels correlate with increased slow brain wave activity in Alzheimer's disease (AD) patients, suggesting a link between homocysteine, brain health, and EEG patterns.
Area of Science:
- Neuroscience
- Biochemistry
- Medical Imaging
Background:
- High plasma homocysteine is an independent risk factor for Alzheimer's disease (AD).
- Homocysteine's role in AD is linked to microvascular impairment and neural loss.
- Slow electroencephalographic (EEG) rhythms may reflect cortical neural loss in AD.
Purpose of the Study:
- To investigate the relationship between high plasma homocysteine levels and slow EEG rhythms in awake resting AD subjects.
- To determine if elevated homocysteine is associated with specific EEG alterations in mild AD and mild cognitive impairment (MCI).
Main Methods:
- Recruited 34 mild AD patients and 34 MCI subjects.
- Subdivided participants into low (<11 micromol/l) and high (>=11 micromol/l) homocysteine groups.
- Recorded resting eyes-closed EEG, analyzed delta, theta, alpha, and beta rhythms.
- Estimated EEG cortical sources using low-resolution brain electromagnetic tomography (LORETA).
Main Results:
- AD subjects with high homocysteine (AD+) showed stronger delta, theta, alpha 1, and alpha 2 cortical sources compared to AD subjects with low homocysteine (AD-).
- Delta and theta increases were observed across frontal, temporal, central, and parietal regions.
- Alpha rhythm increases were noted in parietal and occipital regions.
- No significant differences in EEG rhythms were found between MCI subjects with low and high homocysteine levels.
Conclusions:
- High plasma homocysteine is associated with an unselective increase in cortical delta, theta, and alpha rhythms in mild AD.
- Findings suggest a connection between homocysteine levels, microvascular changes in neurodegeneration, and EEG rhythm generation.
- Elevated homocysteine may impact neural synchronization mechanisms reflected in EEG patterns in AD.
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.
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