| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4343845 | Neuroscience Letters | 2014 | 5 Pages |
•Hypocretin concentrations in CSF do not differ between patients with Alzheimer's disease and major depression.•Hypocretin concentrations in CSF are related to Tau and phosphorylated Tau (pTau) in CSF.•Independent from diagnoses, hypocretin might be related to the regulation of Tau protein.
It has been suggested that sleep–wake regulation as well as hypocretins play a role in the pathophysiology of Alzheimer's disease. We analyzed Aβ40, Aβ42, Tau protein, phosphorylated Tau (pTau) protein as well as hypocretin-1 concentrations in the CSF of a detection sample of 10 patients with Alzheimer's disease (AD) as well as 10 age- and gender-matched patients with major depression as a comparison group of different pathology. In order to replicate the findings, we used a confirmation sample of 17 AD patients and 8 patients with major depression. We found hypocretin-1 concentrations in CSF not to differ between patients with depression and AD. However, hypocretin-1 was significantly related to Tau (r = 0.463, p < 0.001) and pTau (r = 0.630, p < 0.0001). These effects were more pronounced in depressed patients when compared to AD patients. We conclude that hypocretin-1 may play a role in the metabolism of Tau proteins across different diagnostic entities including AD. It has to be determined whether there is a causal relationship between hypocretin-1 and Tau as well as pTau.
