Cognitive impairment in Parkinson's disease (PD) and atypical parkinsonian syndromes is gaining increased clinical significance. The neurochemical and neuropathological basis in the various parkinsonian forms and even in an individual patient are not fully elucidated yet and could be heterogeneous. Loss of dopaminergic, cholinergic and noradrenergic innervation has been suggested to be the underlying neurochemical deficits for cognitive impairment and dementia in PD, but the onset of cognitive impairment and the progression to dementia may not share the same underlying neurochemical basis. Similarly, pathological evidence is also heterogeneous, ranging from subcortical pathology, limbic or cortical Lewy body type degeneration, and Alzheimer's type pathology that can be found even in the same patient with PD dementia (PDD). Typically, the prototype of early cognitive deficit in PD is a dysexecutive syndrome, but other cognitive domains are more involved when dementia develops, mainly including visuospatial, language and memory dysfunction. Functional radionuclide neuroimaging, by means of single-photon emission computed tomography and positron emission tomography, are contributing to characterize the topographic cortical pattern of cognitive impairment, as well as to define the underlying neurochemical deficit. Lastly, the advent of amyloid PET may help clarifying the meaning of amyloid load in diffuse Lewy body disease and PDD. Knowing the neurochemical and pathophysiological substrate of cognitive deficit in patients with PD or other degenerative Parkinsonisms may help the clinician in understanding the clinical condition of an individual patient in order to plan pharmacological and non-pharmacological intervention. The introduction of acetylcholinesterase inhibitors for therapy of PDD is an example of information integration between clinical-neuropsychological and pathophysiological-neurochemical aspects obtained also with the key contribution of functional neuroimaging.