Protein behind Alzheimer`s spread identified
Washington: Researchers at Columbia University Medical Center (CUMC) have confirmed that a protein called caspase-2 is a key regulator of a signalling 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.
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