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rTMS REDUCES DELTA AND INCREASES THETA OSCILLATIONS IN ALZHEIMER’S DISEASE: A VISUAL-EVOKED AND EVENT-RELATED POTENTIALS STUDY
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  • Halil Aziz Velioglu,
  • Esra Zeynep Dudukcu,
  • Lütfü Hanoğlu,
  • Bahar Guntekin,
  • Tuba Aktürk,
  • Burak Yulug
Halil Aziz Velioglu
Northwell Health Feinstein Institutes for Medical Research
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Esra Zeynep Dudukcu
Istanbul Medeniyet University
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Lütfü Hanoğlu
Istanbul Medipol University
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Bahar Guntekin
Istanbul Medipol University
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Tuba Aktürk
Istanbul Medipol University
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Burak Yulug
Alanya Alaaddin Keykubat University

Corresponding Author:burak.yulug@alanya.edu.tr

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Abstract

Background: Repetitive transcranial magnetic stimulation (rTMS) has emerged as a promising alternative therapy for Alzheimer’s disease (AD) due to its ability to modulate neural networks and enhance cognitive function. This treatment offers the unique advantage of enabling real-time monitoring of immediate cognitive effects and dynamic brain changes through electroencephalography (EEG). Objective: This study focused on exploring the effects of left parietal rTMS stimulation on visual evoked potentials (VEP) and visual event-related potentials (VERP) in AD patients. Methods: Sixteen AD patients were recruited for this longitudinal study. EEG data were collected within a Faraday cage both pre and post-rTMS to evaluate its impact on potentials. Results: Significant alterations were found in both VEP and VERP oscillations. Specifically, delta power in VEP decreased while theta power in VERP increased post-rTMS, indicating a modulation of brain activities. Discussion: These findings confirm the positive modulatory impact of rTMS on brain activities in AD, evidenced by improved cognitive scores. They align with previous studies highlighting the potential of rTMS in managing hyperexcitability and oscillatory disturbances in the AD cortex. Conclusion: Cognitive improvements post-rTMS endorse its potential as a promising neuromodulatory treatment for cognitive enhancement in AD, thereby providing critical insights into the neurophysiological anomalies in AD and possible therapeutic avenues.