Alzheimer disease (AD) is a common cause of dementia in the elderly population. The pathophysiology of AD is marked by oxidative stress and energy depletion in the neurons. Antioxidants such as alpha lipoic acid (ALA) have positive effects on glucose metabolism, and may therefore be of benefit in patients with AD. Now a group of researchers from the Department of Medical Rehabilitation and Geriatrics, Henriettenstiftung, Hannover, Germany, have presented data that suggests that using ALA may have a ‘neuroprotective’ action in AD (Journal of Neural Transmission. Supplementum, 2007).

The group analyzed 43 patients of AD over a period of 48 months. The patients received ALA (600 mg/day) in addition to regular acetylcholinesterase drugs. The cognitive functions were assessed using neuropsychological tests. They noted that the disease progression was markedly slower in patients with mild dementia at baseline (AD assessment scale, cognitive subscale or ADAScog <15). The increase in scores on ADAScog was 1.2 points per year in this group and that on the mini mental scale was -0.6 points/year. In patients with moderate dementia, the progression was approximately double.

The research team had previously analyzed 9 patients with AD and related dementias, who were receiving acetylcholinesterase inhibitors. These patients were given 600 mg of ALA daily over an observation period of an average of 12 months. During this period, the team noted a stabilization of cognitive functions in the study group, which was demonstrated using neuropsychological test scores.

Among dietary constituents and supplements, the role of omega 3 fatty acids has also been investigated in AD by Freund-Levi et al (Archives of Neurology, 2006). They noted that administration of omega-3 fatty acids, for a duration of 12 months, in patients with mild to moderate AD did not delay the rate of cognitive decline (as evaluated using the MMSE or ADAScog). However, a positive effect was seen in a small group of patients with very mild AD (MMSE >27 points).

In the presently reported study, Hager et al have shown that in patients given ALA over a longer period, ALA delays/slows the progression of dementia in AD, and the progression of dementia is lower than that reported for untreated patients or patients on choline-esterase inhibitors. Possibly, patients with early/mild dementia may benefit from supplements of ALA in terms of delaying disability and dependence that results from dementia. However, this was an open label, non-randomized trial with a small number of patients, and a larger, randomized and placebo controlled trial may help elucidate the possible role of ALA in prevention of AD.

References

1. Hager K, Kenklies M, McAfoose J, Engel J, Münch G. Alpha-lipoic acid as a new treatment option for Alzheimer’s disease–a 48 months follow-up analysis. J Neural Transm Suppl. 2007;(72):189-93.

2. Hager K, Marahrens A, Kenklies M, Riederer P, Münch G. Alpha-lipoic acid as a new treatment option for Azheimer type dementia. Arch Gerontol Geriatr. 2001 Jun;32(3):275-282.

3. Freund-Levi Y, Eriksdotter-Jönhagen M et al. Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial. Arch Neurol. 2006 Oct;63(10):1402-8.