johnwester130
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- Aug 6, 2015
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This article put a lot of people off taking DHEA.
Actually it is this type of DHEA that is elevated
7α-Hydroxy-DHEA - Wikipedia
en.wikipedia.org
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Another study reported elevated DHEA levels in the frontal cortex, hippocampus, and hypothalamus of AD patients when compared with controls, using high-performance liquid chromatography (HPLC) purification and GC-MS (Brown et al. 2003).
Brown et al. (2003) also reported that DHEA levels in cerebrospinal fluid (CSF) of AD patients were significantly higher than age-matched controls. These authors suggest that DHEA is formed in the AD brain by the oxidative stress metabolism of a precursor, and DHEA levels in the CSF in response to FeSO4 may serve as an indicator of AD
A second report also demonstrated higher DHEA levels in the CSF of patients with AD and vascular dementia (VD) using GC-MS preceded by HPLC (Kim et al. 2003). It is known that the human brain transforms DHEA into DHEAS, 7α-hydroxy-DHEA, 7β-hydroxy-DHEA, and 16α-hydroxy-DHEA (Figure 35.1). DHEA accumulation in the brain may result from a decreased production of such metabolites. Therefore, these authors have measured and compared the CSF levels of DHEA, DHEAS, 7α-hydroxy-DHEA, 7β-hydroxy-DHEA, and 16α-hydroxy-DHEA in patients with AD, controls, and patients with another common dementia such as VD. The neurosteroids found in the CSF of patients with AD and VD, compared with that in normal subjects, were DHEA precursors (pregnenolone and its sulfate), DHEA metabolites (7α-, 7β- and 16α-hydroxy-DHEA), DHEA, and DHEAS. CSF levels of DHEA metabolites were reported for the first time by Kim et al., who showed that CSF levels of DHEA were higher in AD and VD patients when compared with controls. However, CSF levels of DHEAS were higher in controls than in AD and VD patients. Taken together, these differences could help discriminate between controls and AD or VD patients. No significant difference was found between controls and AD and VD patients with regard to CSF levels of DHEA precursors and DHEA.
In contrast, the DHEA/(7α-hydroxy-DHEA + 7β-hydroxy- DHEA) ratio was significantly higher in AD and VD patients than in controls, and the 7β-hydroxy-DHEA/DHEA ratio was signifi- cantly higher in controls than in AD and VD patients. Specific differences between AD and VD patients were found by the 7α-hydroxy-DHEA/7β-hydroxy-DHEA ratio, which was significantly higher in AD patients and controls than in VD patients. However, the 7α-hydroxy-DHEA/DHEA ratio was found to be significantly higher in AD patients than in VD patients and controls. Taken together, these CSF steroid ratios help us discriminate between controls and AD or VD patients.
More recently, Naylor et al. (2008) attempted to establish the correlation between the neuro- steroid levels of CSF and those of the brain in patients with AD. DHEA and pregnenolone levels were measured by GC-MS preceded by HPLC in CSF and temporal cortex brain and compared with controls. These findings showed increased CSF DHEA levels in AD patients, which is consis- tent with the findings of Kim et al. (2003) and Brown et al. (2003). In addition, these results indicate that CSF DHEA levels are correlated with temporal cortex brain DHEA levels, which are elevated in AD patients, and may serve as an indicator for the pathophysiology of AD.