The human brain is a complex organ that may undergo changes during the aging process. Age-related declines in cognitive function and neurological health may be related to multiple biological pathways. These may include neuroinflammation, oxidative stress, and mitochondrial dysfunction. Mitochondria are the powerhouse of the cell. Some nutraceuticals, such as acetyl L-carnitine (ALC), have been shown to play a supportive role in mitochondrial and cognitive function, brain health, and healthy aging. 

L-carnitine is found in most tissues in the human body. Although it can be obtained from dietary sources, it is considered a conditionally essential nutrient with conditions in which the intracellular levels are low, such as in the elderly population, premature infants, and in the presence of certain genetic conditions, mitochondrial dysfunction, and diabetes. Short- and medium-chain fatty acids can enter mitochondria by diffusion, but long-chain fatty acids require the carnitine shuttle to facilitate fatty acid transportation. The carnitine shuttle is critical for the prevention of the buildup of potentially harmful long-chain substrates and acyl-coenzyme A. Carnitine may also play a role in the transference of toxic compounds out of the mitochondria.

ALC is the acetyl derivative of L-carnitine. ALC has been shown to have greater absorption in the small intestine than L-carnitine. It may also pass through the blood-brain barrier blood-brain barrier at greater efficiency. Research has shown ALC supports the body’s response to oxidative stress and inflammation. ALC participates in neurological function, glycogen synthesis, glucose metabolism modulation, increasing plasma adenosine triphosphate concentration. ALC may also play a neuroprotective role. In particular, ALC facilitates cholinergic neurotransmission directly and by providing an acetyl group for acetylcholine synthesis. 

Studies on neurodegenerative diseases, such as Alzheimer’s disease (AD), note disturbances in the metabolism and biosynthesis of carnitine in individuals with AD. Low plasma and tissue concentrations of ALC have been observed in many AD studies. The proposed mechanism for the presence of low ALC levels in neurodegeneration involves loss of the carnitine shuttle, resulting in reduced mitochondrial function. Additionally, ALC may stimulate the synthesis of nerve growth factor receptors in the hippocampus and basal forebrain and prevent the loss of muscarinic receptors. 

ALC has also been shown to significantly increase dopamine levels in parts of the brain, including the hippocampus, striatum, and cortex. Animal studies show that supplementation with ALC prevents tau protein hyperphosphorylation induced by homocysteine and inhibits beta-amyloid phosphorylation. Finally, a meta-analysis showed that supplementation with ALC significantly reduced depressive symptoms as compared to a placebo.

Molecules, such as ALC, may support brain health and neurological function. ALC may also support mitochondrial function and healthy aging. 

By Colleen Ambrose, ND, MAT