The key element that regulates the development of symptoms similar to dementia in Parkinson’s disease has been found. It is a protein called alpha-Synuclein, which only leads to cognitive decline if it aggregates in certain areas of the brain.
The study that led to the breakthrough was conducted by the Italian Research Council's Institute of Biochemistry and Cell Biology (Ibbc-Cnr), the Telethon Institute of Genetics and Medicine at Pozzuoli, the San Raffaele IRCCS in Rome and Rome's Universita' Cattolica del Sacro Cuore.
It was published in the Nature Parkinson's Disease (NPJ) journal and is a fundamental step to be able to understand the mechanisms of Parkinson’s disease dementia and thus be able to intervene rapidly with targeted therapies.
Parkinson’s disease is often linked to the development of hallucinations and memory defects, which in some cases can lead to the onset of dementia.The cause is the accumulation of alpha-Synuclein. It is normal for this molecule to be present in the brain but it can lead to the death of neurons when it accumulates. Not all early memory deficits, however, turn into dementia.
"Research on mice showed that, when alpha-Synuclein aggregates in the hippocampus it causes memory defects that remain stable and do not get worse," said study coordinator Elvira De Leonibus of Ibbc-Cnr and Tigem. "When alpha-Synuclein aggregates in the mesencephalon, on the other hand, it leads to symptoms similar to human dementia".
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