In my continual search for information concerning mitochondrial dysfunction and oxidative stress therapies, found the following:

Free Radic Biol Med. 2007 Feb 1;42(3):371-84. Epub 2006 Nov 10. Links
Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and alpha-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: Implications for Alzheimer's disease.Mohmmad Abdul H, Butterfield DA.

Oxidative stress has been shown to underlie neuropathological aspects of Alzheimer's disease (AD). 4-Hydroxy-2-nonenal (HNE) is a highly reactive product of lipid peroxidation of unsaturated lipids. HNE-induced oxidative toxicity is a well-described model of oxidative stress-induced neurodegeneration. GSH (glutathione) plays a key role in antioxidant defense, and HNE exposure causes an initial depletion of GSH that leads to gradual toxic accumulation of reactive oxygen species. In the current study, we investigated whether pretreatment of cortical neurons with acetyl-L-carnitine (ALCAR) and alpha-lipoic acid (LA) plays a protective role in cortical neuronal cells against HNE-mediated oxidative stress and neurotoxicity. Decreased cell survival of neurons treated with HNE correlated with increased protein oxidation (protein carbonyl, 3-nitrotyrosine) and lipid peroxidation (HNE) accumulation. Pretreatment of primary cortical neuronal cultures with ALCAR and LA significantly attenuated HNE-induced cytotoxicity, protein oxidation, lipid peroxidation, and apoptosis in a dose-dependent manner. Additionally, pretreatment of ALCAR and LA also led to elevated cellular GSH and heat shock protein (HSP) levels compared to untreated control cells. We have also determined that pretreatment of neurons with ALCAR and LA leads to the activation of phosphoinositol-3 kinase (PI3K), PKG, and ERK1/2 pathways, which play essential roles in neuronal cell survival. Thus, this study demonstrates a cross talk among the PI3K, PKG, and ERK1/2 pathways in cortical neuronal cultures that contributes to ALCAR and LA-mediated prosurvival signaling mechanisms. This evidence supports the pharmacological potential of cotreatment of ALCAR and LA in the management of neurodegenerative disorders associated with HNE-induced oxidative stress and neurotoxicity, including AD.

PMID: 17210450 [PubMed - in process]

Acetyl-L-Carnitine and ALA both are among the best things we can take. There is a wealth of info on Medline. One especially heartening one (that I can't lay my hands on right now of course) showed ALCAR to actually increase the cross sectional area of the nerve fibers and improve diabetic neuropathy by making the remaining nerves more efficient.

Here is a general clip from 12 years ago! Makes you wonder why it isn't a standard part of out treatment doesn't it!

1: Life Sci. 1994;54(17):1205-14.

Acetyl-L-carnitine affects aged brain receptorial system in rodents.

Castorina M, Ferraris L.

Institute for Research on Senescence, Sigma-Tau, Pomezia, Rome, Italy.

Acetyl-L-carnitine (ALCAR), the acetyl ester of carnitine, is regarded as a
compound of considerable interest because of its capacity to counteract several
physiological and pathological modifications typical of brain ageing processes.
In particular, it has been demonstrated that ALCAR can counteract the
age-dependent reduction of several receptors in the central nervous system of
rodents, such as the NMDA receptorial system, the Nerve Growth Factor (NGF)
receptors, those of glucocorticoids, neurotransmitters and others, thereby
enhancing the efficiency of synaptic transmission, which is considerably slowed
down by ageing. The present review thus postulates the importance of ALCAR
administration in preserving and/or facilitating the functionality of
carnitines, the concentrations of which are diminished in the brain of old
animals.

PMID: 8164502 [PubMed - indexed for MEDLINE]