Seizures in Alzheimer’s disease

Highlights • Clinical data from familial and sporadic AD patients reveal increased seizure risk. • Many APP-linked AD mouse models develop seizures and other EEG abnormalities. • APP and/or APP-derived peptides may link AD pathology to epileptiform activity. • Epileptiform activity in AD mouse model...

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Bibliographic Details
Published in:	Neuroscience Vol. 286; pp. 251 - 263
Main Author:	Born, H.A
Format:	Journal Article
Language:	English
Published:	United States Elsevier Ltd 12-02-2015
Subjects:	Alzheimer Disease - complications Alzheimer Disease - genetics Alzheimer’s disease Amyloid beta-Peptides - metabolism Amyloid beta-Protein Precursor - metabolism amyloid precursor protein amyloid β Animals antiepileptic therapy Brain - physiopathology Disease Models, Animal Electroencephalography Humans Mice mouse models Nerve Net - physiopathology Neurology Neurons - pathology Risk Factors seizures Seizures - drug therapy Seizures - etiology Seizures - genetics mouse models APP CTFβ pentylenetetrazol CTFα amyloid β VPA PSEN2 Electroencephalography PSEN1 EOFAD DS Aβ Cerebral amyloid angiopathy α C-terminal fragment soluble APPα soluble APPβ sharp wave discharges MMSE AICD PTZ antiepileptic therapy seizures SWD CAA AD Alzheimer’s disease lamotrigine EEG amyloid-β peptide presenilin 2 presenilin 1 Down syndrome valproic acid Amyloid precursor protein sAPPα fMRI early-onset familial AD MCI APP intracellular domain sAPPβ mild cognitive impairment LEV mini-mental state examination β C-terminal fragment functional magnetic resonance imaging LTG levetiracetam amyloid precursor protein
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Summary:	Highlights • Clinical data from familial and sporadic AD patients reveal increased seizure risk. • Many APP-linked AD mouse models develop seizures and other EEG abnormalities. • APP and/or APP-derived peptides may link AD pathology to epileptiform activity. • Epileptiform activity in AD mouse models can be rescued independent of Aβ reduction. • Anti-epileptic drugs such as LEV may rescue cognitive dysfunction in AD patients.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2014.11.051