Low brain ascorbic acid increases susceptibility to seizures in mouse models of decreased brain ascorbic acid transport and Alzheimer's disease

• Published in: Epilepsy research Vol. 110; pp. 20 - 25
• Main Authors: Warner, Timothy A, Kang, Jing-Qiong, Kennard, John A, Harrison, Fiona E
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01-02-2015
• Subjects: Alzheimer Disease - physiopathology; Alzheimer's disease; Amyloid beta-Protein Precursor - genetics; Amyloid beta-Protein Precursor - metabolism; Animals; Ascorbic Acid - metabolism; Ascorbic Acid Deficiency - physiopathology; Brain - physiopathology; Disease Models, Animal; Electrodes, Implanted; Electroencephalography; Female; Humans; Kainic Acid; Male; Malondialdehyde - metabolism; Mice, Knockout; Mice, Transgenic; Mouse model; Neurology; Oxidative Stress - physiology; Pentylenetetrazol; Pentylenetetrazole; Presenilin-1 - genetics; Presenilin-1 - metabolism; Seizures - physiopathology; Sodium-Coupled Vitamin C Transporters - deficiency; Sodium-Coupled Vitamin C Transporters - genetics; Vitamin C; APP; electroencephalography; ascorbic acid; pentylenetetrazol; AD; kainic acid; sodium dependent vitamin C transporter; EEG; SVCT2; presenilin 1; MDA; PSEN1; ASC; amyloid precursor protein; electromyography; KA; PTZ; Vitamin C; Mouse model; malondialdehyde; Alzheimer's disease; EMG; Pentylenetetrazol; Electroencephalography; Kainic acid
• ISSN: 0920-1211; 1872-6844
• DOI: 10.1016/j.eplepsyres.2014.11.017

Highlights • Ascorbic acid deficiency shortened latency to onset of kainic acid-induced seizures. • APP/PSEN1 mutations shortened latency to onset of kainic acid-induced seizures. • SVCT2+/−APP/PSEN1 mice have abnormal EEG response to pentylenetetrazol.