Stathmin-2 as a New Biomarker and Disease Modifier in Alzheimer's Disease

I will test whether abnormal Stathmin-2 can be detected in a subpopulation of Alzheimer’s disease patients (those with TDP-43 pathology), and if it contributes to neuronal malfunction and death.

First, I will test if I can detect abnormal Stathmin-2 in tissue from patients suffering from Alzheimer’s disease. For this I will both analyze brain tissue as well as neurons derived from skin cells of donors. Then, I will further study these neurons to test whether transport of essential components for neuronal survival is compromised by abnormal Stathmin-2. Problems in neuronal transport can contribute to the neuronal death observed in Alzheimer’s disease, and so these studies might uncover Stathminn-2 as both a novel biomarker as well as a disease modifying pathway.

My project is the first to test the role of Stathmin-2 in Alzheimer’s disease. This protein has been shown to be abnormal in other similar diseases, like frontotemporal dementia, and I will bridge the expertise of both fields. In addition, my collaborators have access to brain and neurons obtained from the same patients. As such, I can link the knowledge obtained from postmortem brain tissue, with the results from live neurons with the same genetic background. Finally, this work will combine the expertise of clinicians, computational biologists and researchers. Alzheimer’s disease is a devastating disorder and highly heterogenous. My research will help better subcategorize patients suffering from Alzheimer’s disease. This will be important to both better understand the disease mechanisms as well as to achieve more precise diagnosis. Importantly, given the promise of Stathmin-2 in other disorders, there are currently companies developing novel technologies to better detect abnormal Stathmin-2 in patients, as well as to develop therapeutical strategies to correct abnormal Stathmin-2.

My project is the first to test the role of Stathmin-2 in Alzheimer’s disease. This protein has been shown to be abnormal in other similar diseases, like frontotemporal dementia, and I will bridge the expertise of both fields. In addition, my collaborators have access to brain and neurons obtained from the same patients. As such, I can link the knowledge obtained from postmortem brain tissue, with the results from live neurons with the same genetic background. Finally, this work will combine the expertise of clinicians, computational biologists and researchers.

Alzheimer’s disease is a devastating disorder and highly heterogenous. My research will help better subcategorize patients suffering from Alzheimer’s disease. This will be important to both better understand the disease mechanisms as well as to achieve more precise diagnosis. Importantly, given the promise of Stathmin-2 in other disorders, there are currently companies developing novel technologies to better detect abnormal Stathmin-2 in patients, as well as to develop therapeutical strategies to correct abnormal Stathmin-2.