Acetyl-L-carnitine reduces Alzheimer's-like changes associated with elevated homocysteine

An article published online on October 6, 2011 in the journal Rejuvenation Research describes a role for supplementation with acetyl-L-carnitine (ALC) in reducing the effects of high levels of homocysteine that are associated with some of the features of Alzheimer's disease.

In their introduction to the article, Peng Zhou and colleagues at Huazhong University of Science and Technology in China remark that Alzheimer's disease-like changes including cognitive dysfunction, disrupted blood-brain barrier integrity, increased amyloid-beta levels and tau hyperphosphorylation have been observed in mice in which elevated homocysteine levels were induced. Studies have shown that acetyl-L-carnitine reduces some of the cognitive impairment and functional degeneration found in humans with Alzheimer's disease. While in vitro experiments have suggested that acetyl-L-carnitine can reduce amyloid beta neurotoxicity, it had not previously been known whether the amino acid would have a beneficial effect in an animal model.

For the current experiment, 40 rats received water maze training prior to injection with homocysteine or saline for 14 days. Half of the animals in each group were given drinking water supplemented with acetyl-L-carnitine for the two week treatment period. Water maze tests were conducted before and after treatment to assess cognitive function.

Among homocysteine-treated rats that received acetyl-L-carnitine, memory deficits, tau hyperphosphorylation and amyloid beta accumulation were reduced in comparison with animals that did not receive the amino acid. The team additionally found that supplementing with ALC suppressed amyloid beta precursor protein phosphorylation, which is a possible mechanism for the reduction of amyloid beta observed in the study.

"We found that supplement of ALC by drinking water for two weeks could effectively reverse the homocysteine-induced tau protein hyperphosphorylation, amyloid beta accumulation, and memory deficits in rats," the authors conclude. "Our data suggest that ALC may serve as a promising candidate for Alzheimer's disease therapy."

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