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Multidimensional apathy in non-depressed Parkinson’s disease patients with and without cognitive impairment: clinical subtypes and neural correlates

Description

Apathy is a recurrent symptom in a variety of neurological and psychiatric disorders, including schizophrenia, depression, dementia, and Parkinson’s disease. In some cases, however, it may also present as an isolated syndrome. According to the definition of the European Psychiatric Association, apathy is understood as a reduction of goal-directed activity compared to the patient’s previous level of functioning. To assess apathy, Marin (1990) developed the Apathy Evaluation Scale (AES), which can be applied across different conditions and has also been validated in a German version. Current research distinguishes three subtypes of apathy within the so-called ABC model:

Cognitive apathy, characterized by difficulties in planning actions,
Behavioral apathy, marked by the absence of self-initiated thoughts and actions, and
Emotional apathy, defined as a disturbed link between emotions and behavior.
So far, the ABC model has received only marginal attention in research and has mainly been studied in the context of dementia.
In about 40% of Parkinson’s disease cases, apathy manifests and is associated with several factors, including advanced age, depression, cognitive deficits, greater disability, and significantly higher UPDRS scores. Neuroimaging studies have shown correlations between apathy and hypometabolism in prefrontal and parietal regions as well as the anterior cingulate gyrus. Mild Cognitive Impairment (MCI) is particularly relevant in Parkinson’s disease, as it is linked to striatofrontal dysregulation – a circuit essential for motivation and executive functions. This suggests that apathy, especially its cognitive subtype, may be more pronounced in Parkinson’s patients with MCI.

The planned study aims to investigate differences in apathy expression between Parkinson’s patients with and without MCI and healthy controls. Furthermore, it will assess which subtypes are most affected and examine neural correlates of these manifestations.

Contact

Mrs. Alicia Hagedorn
Telefone: 06421/58 - 65299
Telefax: 06421/58 - 67055
david.pedrosa@staff.*

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