Parkinson’s, dementia: Is this the key to preventive therapy?
Parkinson’s disease and dementia with Lewy bodies are both characterized by impaired brain function tied to neural death. A landmark new study has identified how a main culprit behind neuron damage — the alpha-synuclein protein — harms the neurons.
A new ‘groundbreaking study’ may help us to understand what drives neural damage in Parkinson’s disease and dementia.
Parkinson’s disease is a neurodegenerative condition characterized by impaired motor function and sense of physical balance.
Its symptoms stem from brain cell damage and death, also a feature of the neurodegenerative disease dementia with Lewy bodies (DLB).
DLB features both the impaired motor function of Parkinson’s, and the memory loss and other types of cognitive decline characteristic of Alzheimer’s disease.
People with Parkinson’s disease may also develop a form of dementia called “Parkinson’s disease dementia.”
In all of these diseases, the misfolding — faulty structuring — of a protein called “alpha-synuclein” leads to the formation of deposits that interfere with the healthy functioning of brain cells.
Typically, these form in neurons found in the hippocampus, the brain region that plays a key role in learning processes, and memory formation and recall.
Although it is known that misfolded alpha-synuclein protein aggregates eventually lead to brain cell death, and thus to the heavy impairment of various cognitive functions, so far, researchers have not understood the underlying mechanisms that lead to this outcome.
In a new study, senior researcher Laura Volpicelli-Daley — who works in the University of Alabama at Birmingham School of Medicine — and colleagues have decided to search for that missing insight.
Their paper — which is now published in the journal Acta Neuropathologica Communications — explains what changes take place at cellular level in the brain, after the formation of alpha-synuclein aggregates, and before neural death.
Volpicelli-Daley and her colleagues are hopeful that their findings may eventually lead to improved treatments that may prevent, or even help to reverse, neural damage likely to lead to dementia.
“In Parkinson’s disease, you can give levodopa to improve motor function; but there is nothing to stop the non-motor symptoms,” Volpicelli-Daley explains.
Mapping out abnormal neural changes
In a previous study, Volpicelli-Daley and her team at that time developed an experimental model of artificial alpha-sinuclein deposits in vitro, which allowed them to simulate the development of these aggregates in brain cells.
For the purpose of the new research, the scientists applied this technique to obtain alpha-sinuclein aggregates, which they then introduced to the brain cells of mice.
Then, they studied the changes that occurred in hippocampal neurons at the 7-day mark — a point at which brain cell death will not yet have been triggered.