The Vossel lab at the Mary S. Easton Center at UCLA investigates Alzheimer’s disease (AD) and related dementias with a focus on finding mechanisms and novel therapies that target the tau protein and epileptic activity in dementia pathology. Using our transgenic mouse models, we study cell-signaling functions of tau and other dementia-related molecules like the human amyloid protein precursor (hAPP), the hAPP-derived amyloid-beta peptide, and human alpha-synuclein.  Using techniques like proximity ligation assay, live imaging of cellular signaling, slice electrophysiology, and electroencephalography (EEG) in rodents, we are able to clarify the role of these molecules in pathological changes at the cell and molecular level and their contributions to neural network dysfunction, including epileptic activity.

We have shown that patients with Alzheimer’s disease have seizures and network hyperactivity at rates that are much higher than previous estimates, because they are usually non-motor or silent in nature. Seizures are important to recognize in patients with Alzheimer’s disease because they can lead to a more rapid cognitive decline (Lancet Neurology and Annals of Neurology). Our human clinical trials focus on silent epileptic activity in AD. We completed a phase 2a trial showing that low doses of an inexpensive and widely available antiseizure drug improves learning and memory and executive function in AD patients with epileptic activity (JAMA Neurology).