dstandaertProfessor and Neurology Chair

Primary Department Affiliation
: Neurology
Primary Research Area: Neurodegeneration and Neurodegenerative Disorders
Neurotransmitter and Neurotrophin Receptors and Cell Signaling
Systems Neuroscience and Vision

Email: dstandaert@uab.edu
Phone: 205.996.6329
Fax: 205.996.6580

Recent Publications

Dr. David Standaert
joined our department on July 1, 2006, from the Department of Neurology at Massachusetts General Hospital/Harvard Medical School as the John and Juanelle Strain Professor of Neurology and Director of the newly established Center for Neurodegeneration and Experimental Therapeutics and the Division of Movement Disorders. Dr. Standaert is an internationally renowned physician scientist whose work focuses on understanding the causes of Parkinson's Disease and other Movement Disorders with the goal of developing new treatments. He is also an outstanding Movement Disorder Neurologist and he will have a subspecialty practice in UAB's Kirklin Clinic.

Dr. Standaert brings a very distinguished academic background…Honors graduate of Harvard College, graduate of the Washington University School of Medicine Medical Scientist Training Program with an MD/PhD in Pharmacology, graduate of the University of Pennsylvania Neurology Residency Program, and graduate of a research and clinical Fellowship in Movement Disorders at Massachusetts General Hospital/Harvard Medical School before joining the faculty there.

As Director of the American Parkinson Disease Association Advanced Center for Parkinson Research at Massachusetts General Hospital (MGH), his laboratory was working on understanding both the root causes of Parkinson's disease as well as origin of disabling symptoms appearing after long-term treatment of the disease. He also saw patients in the Parkinson Disease and Movement Disorders Clinic at MGH. Similarly, Dr. Standaert will be continuing with his research and seeing patients with movement disorders at UAB.

Dr. Standaert's laboratory is working on understanding both the root causes of Parkinson disease (PD) as well as the origin of the disabling symptoms that appear after long term treatment of the disease. The lab has a strong translational orientation – our goal is to accelerate the delivery of new therapies for Parkinson disease to the patients who desperately need them

A primary focus of the laboratory is understanding the role of the protein alpha-synuclein in PD pathophysiology, and searching for novel approaches for protecting the brain from the effects of excess alpha-synuclein. We use a variety of cellular and rodent models, and are exploring the effects of several chaperone molecules, including those derived from open-ended screens in simple non-mammalian systems.

A related interest is the role of neuroinflammation in PD. In human PD, there is a marked brain inflammatory response. Recent work in the Standaert lab using mouse models has led to the idea that this inflammation may be triggered directly by the presence of excess alpha-synuclein. The response involves both microglia as well as the adaptive immune system, and both components may be targets of therapies to prevent or retard the disease.

We are also exploring the effect of levodopa on brain function in PD. Levodopa remains the most effective existing treatment, but long-term therapy leads to many unwanted side effects (“wearing off” and “dyskinesia”). The Standaert lab has shown that many of the effects result from abnormal synaptic plasticity in the basal ganglia, and mislocalization of glutamate receptor systems. Recently, we found that the mechanisms responsible for the maintenance of this aberrant plasticity is likely the result of levodopa-induced epigenetic modifications.