Lipoic acid as treatment for Alzheimer's

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that destroys patient memory and cognition, communication ability with the social environment and the ability to carry out daily activities. Despite extensive research into the pathogenesis of AD, a neuroprotective treatment - particularly for the early stages of disease - remains unavailable for clinical use. In this review, we advance the suggestion that lipoic acid may fulfil this therapeutic need. A naturally occurring cofactor for the mitochondrial enzymes pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, lipoic acid has been shown to have a variety of properties which can interfere with the pathogenesis or progression of AD. For example, lipoic acid increases acetylcholine production by activation of choline acetyltransferase and increases glucose uptake, thus supplying more acetyl-CoA for the production of acetylcholine. lipoic acid chelates redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and also scavenges reactive oxygen species, thereby increasing the levels of reduced glutathione. In addition, lipoic acid down-regulates the expression of redox-sensitive pro-inflammatory proteins including TNF and inducible nitric oxide synthase. Furthermore, lipoic acid can scavenge lipid peroxidation products such as hydroxynonenal and acrolein. In human plasma, lipoic acid exists in an equilibrium of free and plasma protein bound form. Up to 150 muM, it is bound completely, most likely binding to high affinity fatty acid sites on human serum albumin, suggesting that one large dose rather than continuous low doses (as provided by "slow release" lipoic acid) will be beneficial for delivery of lipoic acid to the brain. Evidence for a clinical benefit for lipoic acid in dementia is yet limited. There are only two published studies, in which 600 mg lipoic acid was given daily to 43 patients with AD (receiving a standard treatment with choline-esterase inhibitors) in an open-label study over an observation period of up to 48 months. Whereas the improvement in patients with moderate dementia was not significant, the disease progressed extremely slowly (change in ADAScog: 1.2 points=year, MMSE: -0.6 points=year) in patients with mild dementia (ADAScog<15). style="font-weight: bold;" size="1">...Adv Drug Deliv Rev. 2008 Oct-Nov;60(13-14):1463-70

Coffee may decrease the risk of Alzheimer’s

Coffee may decrease the risk of Alzheimer’s: Study ... of dementia and Alzheimer's disease by 65 per cent, says a new study from Scandinavia. ... of dementia and Alzheimer's disease by 65 per cent, says a new study from Scandinavia. ... in the new issue of Alzheimer’s Disease . "We aimed to study the association between coffee and tea on the central nervous system was still unknown, and as the pathologic processes leading to Alzheimer's disease. ...http://www.nutraingredients.com

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