Scientists at the University of Alabama at Birmingham have identified an enzyme in the brain that may be an intriguing target for interventions against Alzheimer’s disease and other dementias.
The researchers suggest that the enzyme, a serine/threonine kinase known as LIMK1, may play an important role in the degradation of dendritic spines, the connections between neurons in the brain. In a paper published June 25 in Science Signaling, the team reports on the use of an experimental medication that appears to successfully inhibit LIMK1 and provide a level of protection for dendritic spines.
“This is the first study to showcase that inhibiting LIMK1 could provide a protective effect for dendritic spines,” said Jeremy Herskowitz, Ph.D., assistant professor in the Department of Neurology, School of Medicine at UAB. “In animal models, we’ve shown that increased activity of LIMK1 is linked to changes in the length and density of dendritic spines, which has implications for Alzheimer’s.”
Think of dendritic spines as bridges connecting one neuron to another. Previous research in Herskowitz’s laboratory showed that individuals with longer and more numerous spines did not develop symptoms of dementia, even if they had the well-known Alzheimer’s pathology of amyloid plaques and tau tangles.
Read more at University of Alabama at Birmingham
Image: Inhibiting an enzyme called LIMK1 seems to improve the length and density of dendritic spines, shown here in green. Healthy dendritic spines are thought to have a protective effect against Alzheimer's disease. (Credit: UAB)