The key that regulates the development of dementia-like symptoms has been found in the Parkinson: it’s a a protein called α-synucleinwhich only leads to cognitive decline if it accumulates in certain areas of the brain.
The study was conducted by theInstitute of Biochemistry and Cell Biology of the National Research Councilin collaboration with theTelethon Institute of Genetics and Medicine of Pozzuolil’Irccs San Raffaele of Rome and theCatholic University of the Sacred Heart of Rome. Research, published in the journal Nature Parkinson’s disease NPJ, is essential to understand the mechanisms of dementia in Parkinson’s and to be able to intervene promptly with targeted therapies.
Parkinson’s disease is known for movement disorders caused by the death of neurons in the midbrain, an area of the brain involved in vision, regulation of muscle movements and reward mechanisms.
Often, however, this pathology is also associated with the appearance of hallucinations or memory defects, which in some cases can lead to the onset of dementia: the cause is the accumulation of α-synuclein, a molecule normally present in the brain, but which when it accumulates it can lead to the death of neurons. However, not all early memory deficits progress to dementia.
“Using mice in which it is possible to selectively increase (i.e. in specific areas of the brain) the expression of the protein believed to cause the symptoms, we observed that when α-synuclein accumulates in the hippocampus it causes defects in memory which however remain stable and do not get worse”, explains Elvira De Leonibus of Ibbc-Cnr and Tigem, who coordinated the research. “Conversely, when α-synuclein accumulates in the midbrain, it leads to symptoms similar to human dementia.”