For many years Parkinson’s disease (PD) was regarded primarily as a motor disorder and attempts to discover treatments focused on therapies for rigidity, bradykinesia, and tremor. The brain pathology studies concentrated on the nigrostriatal pathways and dopamine. It was the success of the dopamine replacement therapies which opened the way to discuss the non-motor manifestations of the disease, particularly mental health manifestations and dementia.

Cognitive impairment is very frequent in PD and actually may eventually affect all patients if they live long enough [1], causing additional suffering to patients and caregivers. It is not clear what the anatomical basis of cognitive impairment is, but it is thought to reflect α-synuclein deposition in the cortex and particularly in the limbic system, although most PD patients also bear β-amyloid and TDP-43 deposits once they become demented.