Washington, June 26 (ANI): Researchers at Columbia University Medical Center (CUMC) have confirmed that a protein called caspase-2 is a key regulator of a signaling pathway that leads to cognitive decline in Alzheimer's disease.
The findings, made from a mouse model of Alzheimer's, suggest that inhibiting this protein could prevent the neuronal damage and subsequent cognitive decline associated with the disease.
One of the earliest events in Alzheimer's is disruption of the brain's synapses, which can lead to neuronal death.
Although what drives this process has not been clear, studies have indicated that caspace-2 might be involved, according to senior author Michael Shelanski, MD, PhD, the Delafield Professor of Pathology and Cell Biology, chair of the Department of Pathology and Cell Biology, and co-director of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC.
Several years ago, in tissue culture studies of mouse neurons, Dr. Shelanski found that caspace-2 plays a critical role in the death of neurons in the presence of amyloid beta, the protein that accumulates in the neurons of people with Alzheimer's.
Other researchers have shown that caspase-2 also contributes to the maintenance of normal synaptic functions.
Dr. Shelanski and his team hypothesized that aberrant activation of caspase-2 may cause synaptic changes in Alzheimer's disease.
The study is published in the online journal Nature Communications. (ANI)