JDFAF has just funded a breakthrough research project integrating the expertise and resources of researchers at three University of California campuses.

The John Douglas French Alzheimer's Foundation has just funded a breakthrough research project integrating the expertise and resources of researchers at three University of California campuses. 

Researchers at UCSF (led by Bruce Miller, MD), UCLA (led by Giovanni Coppola, MD and Daniel Geschwind, MD, PhD), and UCSB (led by Kenneth Kosik, MD) will employ three different forms of the very latest genomic technologies to probe variation across the entire genome to identify patterns of gene expression that define the varied types and stages of neurodegeneration, and to evaluate repertoires of immune cells at the single-cell level to allow better tracking of disease progression and inter-individual variation in disease.

The entire project will be under the direction of the Foundation's Chief Medical Officer, Bruce L. Miller, MD, who was recently elected to the National Academy of Medicine.

These groundbreaking studies leverage and integrate the unique expertise of the research teams at the three universities, and are driven by new advances in technology that have brought new tools to the study of genomics, while dramatically driving down the costs for these studies.  

Simultaneously, the massive and creative efforts at UCSF to collect large numbers of healthy elders and patients in the preclinical, early and more advanced stages of differing dementias, and the detection of new isolated populations in the Basque-country in Spain, and Columbia, South America will make these studies unique, powerful and transformative.  

Variation across the genome provides the biological foundation from which brain health is maintained and disease occurs during aging. By understanding the genetic contributions to specific forms of early-onset forms of frontotemporal lobar degeneration (FTLD) and Alzheimer’s disease (AD) we can gain a better understanding of the biological changes that promote risk for these diseases across the lifespan. Conversely, by characterizing individuals who benefit from healthy cognitive aging we can gain insight into factors that may protect the aging brain and promote better function. 

Studying patients from both groups will enable better identification of individuals at risk for neurodegeneration and will provide new biological targets for treating disease. Although genes that cause familial forms of FTLD and AD have been identified, most of the genetic contribution to these disorders remains unknown. In addition to genes encoding proteins directly involved in disease pathology, evidence is mounting to support the role of immune dysregulation and inflammation as important contributors to both neurodegeneration and healthy cognitive aging.