Parkinson’s disease causes both movement and cognitive deficits, and for a long time both were thought to be caused by the accumulation of a protein called alpha-synuclein in the brain. But a new Nature Communications study has found that the cognitive deficits arise through a different—and unexpected—mechanism.
The new findings suggest that mutations in a gene called GBA—which are a risk factor for developing Parkinson’s disease—drive cognitive decline by disrupting how neurons communicate with each other in the brain. Patients living with Parkinson’s disease can experience cognitive symptoms such as difficulty with concentrating and forgetfulness. Over time, many go on to develop dementia, in which they experience profound memory loss among other symptoms.
“Dementia is often the scariest thing for many patients with Parkinson’s disease, more so than motor symptoms,” says Sreeganga Chandra, PhD, professor of neurology and of neuroscience at Yale School of Medicine (YSM) and the study’s principal investigator. “We are trying to understand the basis of cognitive dysfunction and whether we can find targets to ameliorate it.”
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