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Cerebrospinal fluid correlates of depression in Huntington's disease
1Department of Neurology, University of Rochester, School of Medicine, NY 14642.
Insights
Huntington's disease (HD) patients show elevated cerebrospinal fluid corticotropin-releasing factor (CRF). Depression severity in HD correlates with CRF, suggesting unique neurochemical pathways for HD-related depression.
Area of Science:
- Neuroscience
- Neurology
- Psychiatry
Background:
- Huntington's disease (HD) frequently co-occurs with depressive disorders.
- Previous studies linked major depression to elevated corticotropin-releasing factor (CRF) and reduced 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid (CSF).
Purpose of the Study:
- To investigate CSF CRF and 5-HIAA levels in early-stage, nonmedicated Huntington's disease patients.
- To explore the neurochemical underpinnings of depression in HD.
Main Methods:
- Examined CSF CRF and 5-HIAA concentrations in 56 early-stage HD patients and 21 healthy controls.
- Assessed depressive symptoms and correlated them with CSF analyte levels.
Main Results:
- Patients with HD exhibited elevated CSF CRF compared to controls.
- CSF 5-HIAA levels did not differ between HD patients and controls.
- No significant difference in CSF 5-HIAA or CRF was found between HD patients with and without depression.
- A positive correlation was observed between the severity of major depression and CSF CRF concentration in HD patients.
Conclusions:
- The neurochemical profile of depression in HD may differ from other major depressive disorders.
- Elevated CRF in HD depression suggests distinct pathophysiological mechanisms.
- Depressive symptoms in neurological disorders may represent heterogeneous conditions with varied neurochemical correlates.
Abstract:
Patients with Huntington's disease (HD) commonly have concomitant depressive disorders. Prompted by reports of elevated corticotropin releasing factor (CRF) and reduced 5-hydroxyindoleacetic acid (5-HIAA) concentrations in lumbar cerebrospinal fluid (CSF) of patients with major depression, these CSF constituents were examined in 56 nonmedicated patients who were in the early stages of HD. Elevated CRF concentrations were found in patients with HD in comparison with a control group of 21 subjects without neurologic illness. The CSF 5-HIAA concentrations in patients with HD did not differ from that in four normal volunteers. Patients with HD who had depressive disorders (major depression or dysthymia) did not differ from those without depression with respect to CSF 5-HIAA or CRF concentration. However, a positive correlation was observed between severity of major depression and CRF concentration. These findings suggest that the depression associated with HD may differ neurochemically from that seen in other major depressive disorders, and support the notion that clinically significant depressive symptoms reflect heterogeneous pathophysiologic conditions with different neurochemical correlates.