According to a study published Online First by Archives of Neurology, one of the JAMA/Archives journals, researchers from the University of California, San Diego, have found no association between an antioxidant combination of vitamin E, vitamin C and α-lipoic acid (E/C/ALA) and changes in some cerebrospinal fluid biomarkers related to Alzheimer’s disease.
In the brain, oxidative impairment is linked to aging and is common in individuals with Alzheimer’s disease (AD). Even though some studies have indicated that a diet rich in antioxidants may lower the risk of developing AD, results from antioxidant studies in AD have been mixed.
Douglas R. Galasko, M.D., of the University of California, San Diego, and his team enrolled 78 patients from the Alzheimer’s Disease Cooperative Study (ADCS) Antioxidant Biomarker study in order to analyze alterations in cerebrospinal fluid (CSP) biomarkers associated to AD and oxidative stress, function and cognition.
The researchers assigned participants to one of three groups:
- 800 IU/per day of vitamin E (α-tocopherol) in addition to 500 mg/per day of vitamin C and 900 mg/per day of α-lipoic acid (E/C/ALA)
- 400 mg of coenzyme Q (CoQ) three times per day
During the 16-week trial, 66 participants provided serial CSF specimens suitable for biochemical examination.
The researchers explained:
“The combination of E/C/ALA did not affect CSF biomarkers related to Aβ, tau or P-tau (which are related to AD).”
The researchers found that although participants in the E/C/ALA group saw a decrease of CSF F2-isoprostane levels, indicating a reduction of oxidative stress in the brain, the treatment raised caution regarding faster cognitive decline as evaluated by the Mini-Mental State Examination (MMSE).
The researchers said:
“It is unclear whether the relatively small reduction in CSF F2-isoprostane level seen in this study may lead to clinical benefits in AD. The more rapid MMSE score decline raises a caution and indicates that cognitive performance would need to be assessed if a longer-term clinical trial of this antioxidant combination is considered.”
In addition, the researchers highlight that although the results suggest that CoQ was safe and well tolerated in the participants, the absence of a biomarker signal in CSF indicates that CoQ, at the tested dose, does not enhance indices of neurodegenration or oxidative stress.
The researchers conclude:
“These results do not support further clinical trial development of CoQ in AD.”
Written by Grace Rattue