Abstract
Parkinson’s disease (PD) is the second most common neurodegenerative disease in the world. The diagnosis of PD is based on movement dysfunctions. Many patients also suffer from comorbid depression in spite of adequate treatment with dopamine replacement, indicating that also other non-dopaminergic mechanisms are involved. Indeed, neuropeptides are critically implicated in the pathophysiology of major depressive disorder (MDD). To increase our understanding of the biochemical basis of depression in PD patients, we examined the levels of neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP) in cerebrospinal fluid (CSF) from PD patients, with or without comorbid depression, and compared them to the levels in patients with MDD. We also compared the levels of NPY and CGRP with 5-hydroxyindoleacetic acid (5-HIAA), the major serotonin metabolite. Both NPY and CGRP were higher in PD patients with comorbid depression compared to MDD patients. No similar difference was found in 5-HIAA levels. Accordingly, there were no correlations between NPY and 5-HIAA or CGRP and 5-HIAA levels. The finding of higher NPY and CGRP CSF levels in PD patients with MDD raises the possibility that different pathophysiological processes may underlie depression in PD and MDD.
Highlights
Parkinson’s disease (PD) is a debilitating inexorably progressing neurodegenerative disorder affecting about 1% of persons above the age of 65 [1]
In view of the above findings and since neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP) have apparently not been explored in PD, we examined their levels in cerebrospinal fluid (CSF) from PD patients, with or without comorbid depression, and compared them to the levels in patients with major depressive disorder (MDD)
There was no significant difference in severity of depression according to MADRS between PD patients with comorbid depression (16.6 ± 3.8) and MDD patients (21.6 ± 5.5)
Summary
Parkinson’s disease (PD) is a debilitating inexorably progressing neurodegenerative disorder affecting about 1% of persons above the age of 65 [1]. PD is characterized by a progressive loss of nigrostriatal dopaminergic neurons in the substantia nigra pars compacta resulting in bradykinesia, rigidity, and resting tremor [1]. In addition to the motor symptoms, PD patients suffer from non-motor symptoms, including depression, hyposmia, sleep disorders, autonomic dysfunctions, hallucinations, and cognitive impairments [2]. There is a poor understanding of the pathophysiology underlying depression in PD, resulting in a lack of consensus on the therapeutic antidepressant strategies [3]. There are no separate specific guidelines for treatment of major depressive disorder (MDD) in PD and patients have been treated
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