Epileptic seizures have long been recognised as a complication of the clinical syndrome of Alzheimer's disease, particularly in advanced disease, but have hitherto been viewed essentially as epiphenomena of the neurodegenerative process. Progress with animal models of Alzheimer's disease has suggested that this view may be incorrect, and that seizures may be a reflection of pathophysiological processes similar to or overlapping with those responsible for cognitive decline. This overlap between neuropsychological and neurophysiological changes suggests that seizures in Alzheimer's disease may be a valid therapeutic target, over and above symptomatic treatment. This article reviews data on the prevalence of seizures in Alzheimer's disease, seizure types, pathophysiology and treatment. Seizure prevalence increases with disease duration, but early-onset disease is associated with a greater risk of seizures, in part related to the frequency of presenilin-1 gene mutations in early-onset disease. Seizures are mostly of partial origin, with both complex partial and secondary generalised seizures. Seizure pathophysiology may relate to increased amyloid beta-peptide production, structural alterations in neurones related to cytoskeletal dysfunction, cerebrovascular changes, neurotransmitter dysfunction or combinations thereof. Through modification of these pathophysiological pathways, there may be possible roles for anti-epileptic drugs such as sodium valproate and lacosamide in the treatment of Alzheimer's disease. In summary, epileptic seizures are part of the AD phenotype, and merit further investigation.