Cynthia M Carlsson

Associate Professor


Dr. Carlsson’s research focuses on the effects of vascular risk factors and their treatments on cognition and biomarkers for Alzheimer’s disease in persons at risk for dementia. Vascular risk factors in midlife, such as high cholesterol and elevated blood pressure, have been associated with an increased risk of developing Alzheimer’s disease decades later. It is unknown, however, whether treating vascular risk factors will reduce the risk of dementia. Through partnering with colleagues in geriatrics, neuropsychology, cardiovascular medicine, neuroradiology, medical physics, and clinical chemistry, as well as asymptomatic adult children of persons with Alzheimer’s disease, Dr. Carlsson is conducting clinical trials investigating:

  • The impact of vascular risk factors on risk of cognitive decline in middle-aged adult children of persons with Alzheimer’s disease
  • How vascular risk factors are related to biomarkers for Alzheimer’s disease found in the blood, cerebrospinal fluid (CSF), and on MRI scans measuring brain blood flow
  • The relationship between endothelial function, a measure of blood vessel function, and brain blood flow and activation patterns on MRI
  • The effects of cholesterol-lowering medications known as “statins”: on CSF biomarkers for Alzheimer’s disease, brain blood flow and activation patterns, and cognition in asymptomatic middle-aged adult children of persons with Alzheimer’s disease

Dr. Carlsson’s work is supported by a Paul B. Beeson Career Development Award, a grant jointly sponsored by the National Institute on Aging (NIA), the American Federation for Aging Research (AFAR), the John A. Hartford Foundation, Atlantic Philanthropies, and the Starr Foundation. In addition, she has received support from the State of Wisconsin and the University of Wisconsin General Clinical Research Center.
Through their work, Dr. Carlsson and her colleagues hope to identify preclinical markers of Alzheimer’s disease risk as well as effective treatment strategies to delay the onset of dementia in persons at risk for the disease.