par Nous, Amber;Seynaeve, Laura;Feys, Odile 
;Wens, Vincent ;De Tiège, Xavier;Van Mierlo, Pieter;Baroumand, Amir G;Nieboer, Koenraad;Allemeersch, Gert-Jan;Mangelschots, Shana;Michiels, Veronique;van der Zee, Julie;Van Broeckhoven, Christine;Ribbens, Annemie;Houbrechts, Ruben;De Witte, Sara;Wittens, Mandy Melissa Jane;Bjerke, Maria;Vanlersberghe, Caroline;Ceyssens, Sarah;Nagels, Guy;Smolders, Ilse;Engelborghs, Sebastiaan
Référence Alzheimer's research & therapy, 16, 1, page (19)
Publication Publié, 2024-01-01
;Wens, Vincent ;De Tiège, Xavier;Van Mierlo, Pieter;Baroumand, Amir G;Nieboer, Koenraad;Allemeersch, Gert-Jan;Mangelschots, Shana;Michiels, Veronique;van der Zee, Julie;Van Broeckhoven, Christine;Ribbens, Annemie;Houbrechts, Ruben;De Witte, Sara;Wittens, Mandy Melissa Jane;Bjerke, Maria;Vanlersberghe, Caroline;Ceyssens, Sarah;Nagels, Guy;Smolders, Ilse;Engelborghs, SebastiaanRéférence Alzheimer's research & therapy, 16, 1, page (19)
Publication Publié, 2024-01-01
Article révisé par les pairs
| Résumé : | Epileptic seizures are an established comorbidity of Alzheimer's disease (AD). Subclinical epileptiform activity (SEA) as detected by 24-h electroencephalography (EEG) or magneto-encephalography (MEG) has been reported in temporal regions of clinically diagnosed AD patients. Although epileptic activity in AD probably arises in the mesial temporal lobe, electrical activity within this region might not propagate to EEG scalp electrodes and could remain undetected by standard EEG. However, SEA might lead to faster cognitive decline in AD. |
