The Behavioral Neurology Section diagnoses and treats patients with memory, cognitive and behavioral issues. These disorders include benign memory loss due to aging, mild cognitive Impairment, Alzheimer’s disease, dementia with Lewy bodies, vascular cognitive impairment, and frontotemporal degeneration (FTD) including Pick’s disease, progressive supranuclear palsy, cortical basal ganglionic degeneration, primary progressive aphasia, and normal pressure hydrocephalus. Primary age-related tauopathy, TDP43 encephalopathy, Limbic Associated TDP Encephalopathy, and normal pressure hydrocephalus are among other neurodegenerative disorders.
The Behavioral Neurology clinic evaluates about 1000 new patients each year and provides ongoing care for over 3,000 patients annually. We see patients in the James W. Aston Ambulatory Care Center at UT Southwestern and the Parkland Outpatient Clinic. The Behavioral Neurology Section collaborates with other clinical centers at UT Southwestern to provide diagnostic and therapeutic services, including comprehensive neuropsychological assessment, MRI, MRA, and positron emission tomographic (PET) studies, and lumbar puncture (spinal tap). Therapeutic inventions are planned and coordinated as part of the diagnostic and treatment plan, where appropriate.
We collaborate closely with Neurosurgery and Neuropathology in cases in which brain or nerve biopsies are required. We coordinate medical care with the departments of Internal Medicine, Neuropsychology, Psychiatry, and Pediatrics when these specialties are required for a comprehensive evaluation.
The Behavioral Neurology section faculty is active in teaching medical students, residents, fellows, and a diverse array of faculty, scientists and visiting physician-scientists. The Behavioral Neurology and Neuropsychiatry Fellowship is accredited by the United Council of Neurological Subspecialties, offering advanced training in clinical care and research focusing on neurodegenerative diseases. We are invited to present our research at the Texas Neurological Society, the American Academy of Neurology, the Texas Alzheimer’s Research and Care Consortium, the American Society of Neuropsychology, and the American Society of Neuropathology.
- Marc Diamond, M.D. (Section Head)
- Hsueh Sheng Chiang, M.D., Ph.D.
- Munro Cullum, Ph.D.
- Joachim Herz, M.D.
- Linda Hynan, Ph.D.
- Brendan Kelley, M.D.
- Alka Khera, M.D.
- Laura Lacritz, Ph.D.
- Christian Lobue, Ph.D.
- Douglas Menendez, M.D.
- Trung Nguyen, M.D., Ph.D.
- Roger N. Rosenberg, M.D.
- Charles White, III, M.D.
Our faculty is engaged in a comprehensive program to develop knowledge about the biology of behavioral diseases and conduct clinical and basic research to develop new therapies. Our research is funded by the National Institutes of Health (NIH) and various foundations and charities. Our research results are regularly published in outstanding peer review journals, including JAMA Neurology, Neurology, and Neurobiology of Disease, among others.
The Behavioral Neurology section conducts numerous clinical research trials. Please contact us if you are interested in participating in a clinical research project.
The NIH funded Late Onset Alzheimer’s Disease study for families with multiple members affected by Alzheimer’s disease focuses on identifying genetic factors that increase or decrease the risk of developing Alzheimer’s.
Our faculty contributed to the A4 Study and AHEAD A3-45 studies investigating anti-amyloid monoclonal antibodies as a preventive strategy for Alzheimer’s disease. Magnetoencephalography (MEG) is being evaluated to analyze complex wave forms present in dementing disorders, and high-intensity focused ultrasound is being evaluated as a therapeutic intervention to open the blood-brain barrier to deliver anti-tau monoclonal antibodies. Numerous other studies are being conducted to advance our understanding of Alzheimer’s disease and other neurodegenerative diseases.
Research Overview Videos
Center for Alzheimer’s and Neurodegenerative Diseases
The Center for Alzheimer’s and Neurodegenerative Diseases (CAND) consists of a multidisciplinary group of investigators who translate basic biological knowledge about neurodegenerative diseases into new diagnostics and therapies. These include individuals focused on the structural biology of disease-causing proteins, cell and molecular biology, and gene therapy. Additionally, affiliated CAND faculty include experts in focused ultrasound, neuropathology, systems biology, machine learning, and biophysics.
The Diamond Lab, as part of the CAND, studies the biology of protein amyloids (especially tau) in the initiation and progression of neurodegenerative diseases. Tau can adopt multiple shapes, and in disease it forms assemblies, or aggregates, that cause neurodegeneration. The lab is focused on the molecular and structural determinants of the tau protein’s conformational shifts from a healthy to a disease-causing form. The lab additionally studies mechanisms by which pathological tau aggregates might escape one cell, move to another, and serve as templates for their own amplification of abnormal structures. This process appears to underlie disease progression. The lab has determined that different types of neurodegenerative diseases caused by tau are based in the three-dimensional structure of underlying tau assemblies. This knowledge is being used to develop more effective diagnostic and therapeutic strategies.
Herz Lab/Center for Translational Neurodegeneration Research
The Herz Lab within the Center for Translational Neurodegeneration Research is investigating neurodegenerative diseases that are affected by Apolipoprotein E (APOE) genotype, APOE receptors and the misregulation of endolysosomal homeostasis in Alzheimer’s disease, frontotemporal lobar degeneration and multiple sclerosis. The primary tools used in these studies are complex mouse genetic models, electrophysiology of the synapse and the cell biology of vesicular trafficking, with a focus on the early endosomal compartment and the lysosome.
The Kelley Lab’s clinical research focuses on developing biological markers for Alzheimer’s and related dementias, testing treatment strategies to prevent or slow the progression of neurodegenerative diseases, and testing interventions that aim to reduce the global burden of dementia. We collaborate with the Alzheimer’s Clinical Trial Consortium in several trials testing treatments to prevent Alzheimer’s disease from developing in people who already have amyloid deposited in their brain. We are working with the Zhang Lab to examine the role of blood vessel reactivity in Alzheimer’s disease and with the Vongpatanasin lab to test whether intensive blood pressure management can reduce the risk of dementia in large populations. In collaboration with the Monson lab , we are studying the role of the immune system in Alzheimer’s disease. This aims to better understand the role the immune system plays in preventing neurodegeneration and may also lead to improved ability to accurately diagnose Alzheimer’s disease. Our work with the Juengst lab focuses on interventions to reduce the burnout and distress often experienced by care partners of people with dementia. In collaboration with the Davenport lab and the Yu lab in Radiology, we are investigating magnetoencephalography and advanced MRI techniques to identify biomarkers to diagnose and track Alzheimer’s disease. Our work with the Shah lab is studying the role of high intensity-focused ultrasound as a possible treatment for Alzheimer’s disease. We also collaborate with researchers at UT Dallas who are studying how the brain encodes memories, and ways to modulate brain function.
The prime objective of the Rosenberg lab's research is to develop a DNA Aβ42 trimer vaccine to delay or prevent Alzheimer’s disease. The vaccine is designed to produce anti-Aβ42 antibody, which we have shown reduces the levels of the toxic proteins amyloid ( Aβ42 peptide) and tau by 50 percent in the brains of 3xTg-AD model mice. Life span is significantly increased in vaccinated mice, and nest building, an innate behavior, is improved compared to control mice. The vaccine reduces significantly the levels of expression of inflammatory genes and increases the expression of early immediate genes beneficial for synaptic stability and neurotransmitter release. The vaccine also produces effective levels of anti-Aβ42 antibody in three species: mouse, New Zealand white rabbit and rhesus monkey. The immune response in all three species is non-inflammatory, and all animals remained healthy with no evidence of autoimmune encephalitis. It is our intent to test it in patients with early Alzheimer’s disease.
Our research has been published in outstanding peer reviewed journals, including Journal of Neuroimmunology, Alzheimer’s Research and Therapy, Journal of Alzheimer’s Disease Research, Vaccine, JAMA Neurology, JAMA, and Neurobiology of Disease, among others.