Inhibition of a protein called LIMK1 may help prevent the loss of dendritic spines — the connections between neurons in the brain — triggered by the build-up of beta-amyloid in early stage Alzheimer’s disease, a study has found. "This is the first study to showcase that inhibiting LIMK1 could provide a protective effect for dendritic spines," Jeremy Herskowitz, PhD, said in a press release. Herskowitz is the study’s lead author and an assistant professor in the department of neurology, School of Medicine at University of Alabama at Birmingham (UBA). "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," Herskowitz said. The study, “Pharmacologic inhibition of LIMK1 provides dendritic spine resilience against β-amyloid,” was published in the journal Science Signaling. Loss of dendritic spines correlates more strongly with cognitive impairment in Alzheimer's than with the presence of amyloid plaques and tau tangles, two hallmarks of the disease. In fact, previous studies by the same team have shown that people carrying more and longer dendritic spines do not develop symptoms of dementia, even in the presence of beta-amyloid and tau tangles.