USF gets $1.5 M NIH grant to study cord bloods cells as potential Alzheimer's therapy

University of South Florida neuroscientists have been awarded a $1.5 million federal grant to evaluate a new treatment, human umbilical cord blood cells (HUCBC), in a mouse model for Alzheimer’s disease.

The five-year grant from the National Institute on Aging was awarded to Jun Tan, MD, PhD, Robert A. Silver Chair and Director of the Rashid Laboratory for Developmental Neurobiology at the Silver Child Development Center, USF Department of Psychiatry. The study co-investigators are Paul Sanberg, PhD, DSc, director of the Center of Excellence for Aging and Brain Repair, Department of Neurosurgery and Brain Repair, and David Morgan, PhD, professor in the Department of Molecular Pharmacology and Physiology and chief scientific officer of the Byrd Alzheimer Institute at USF Health.

Recent USF studies have shown that immunity can be transferred using human umbilical cord blood cells, which improves the pathology associated with Alzheimer’s disease in a mouse model. Other studies have demonstrated that a specific immune system suppression is correlated with significantly reduced abnormal levels of the beta amyloid protein linked to Alzheimer’s disease.

“This new NIH study will continue to build on our understanding of the HUCBC’s mechanism behind improvement in Alzheimer’s disease,” Dr. Tan said. “It will help provide a better understanding of brain immune cells called microglia, which promote brain inflammation in Alzheimer’s disease.”

Dr. Tan and his colleagues previously demonstrated that once a specific molecule, CD40, on the surface of these microglia cells becomes activated by its partner, CD40L (CD40 ligand), the scene is set for a cascade of events leading to brain inflammation that injures the brain’s neurons. They also showed that the trigger for this harmful immune response can be blocked by specific antibodies.

In this study, Dr. Tan and his team plan to test the hypothesis that HUCBC could reduce the interaction between the CD40L molecule and its CD40 target, which in turn would decrease Alzheimer’s pathology in the brain. The experiments will be performed on (transgenic) mice genetically modified to develop memory problems mimicking Alzheimer’s disease as they age.

Furthermore, the researchers plan to create a cocktail combining the precise molecules they believe are the key players behind HUCBC’s beneficial effects. “We will give the compound to these transgenic mice to assess the possibility of bypassing the need for HUCBC and making future therapies more cost effective,” Dr. Tan said.

“This approach shifts the focus from treating symptoms of Alzheimer’s disease to treatments that slow down the disease or prevent it altogether.” Dr. Tan said. “Our long-term goal is to move this combination treatment into phase I human trials for patients with mild to moderate Alzheimer’s disease.”

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