As we age, many elements of our lives and bodies begin to slow down a little bit. Unfortunately, some of that slow-down occurs in our brains, thereby slowing our abilities to think clearly, remember clearly, or problem solve the way we could in our younger years. In fact, age has been determined to be the major risk factor for the advancement of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis, and Huntington’s disease, in addition to general, age-associated cognitive impairment [1].

Scientists know that the cognitive decline that often accompanies aging is most often the result of oxidative stress in the brain, as well as mitochondrial failure to provide adequate cellular energy [2]. Oxidative stress occurs when reactive oxygen species, or “free radicals”, build up faster than antioxidants can work to quench them. It makes sense then, that ingesting potent antioxidants that can readily cross the blood brain barrier would aid in staving off or slowing some of the damage caused by oxidative stress. A growing body of evidence is showing that alpha lipoic acid (ALA) supplementation may just be an appropriate candidate for the job.

ALA (also referred to as lipoic acid, or LA) is a natural compound found in some foods we eat, similar in structure and function to a vitamin, and is considered to be promising nutritional support for cognitive health. This is because it is an ideal antioxidant. ALA is a super-antioxidant that does everything antioxidants do, and more. Some antioxidants, such as vitamin C, are hydrophilic and only soluble in water, and some, such as vitamin E, are lipophilic and only soluble in fat, but ALA is amphipathic, meaning it can work as an antioxidant in both fat and water, and it can cross the blood brain barrier allowing it to work everywhere in the body [2,3].

Aging is associated with mitochondria dysfunction. As the “powerhouse of the cell”, when mitochondria decay or cease to produce, there is not enough energy for the cell to continue to both function and self-repair, so cells die and their surrounding tissues start to degrade. This is aging. The current hypothesis is that mitochondrial dysfunction could possibly be reversed in aged animals (humans included) by ingesting mitochondrial nutrients. This is a very specialized category of nutrients that 1) target the mitochondria, 2) prevent generation of oxidants (a.k.a. free radicals), 3) scavenge oxidants or inhibit their reactivity, 4) repair oxidative damage, and 5) elevate the abundance or activity of cofactors for enzymes that will stimulate the mitochondria [1]. Thus, neurodegenerative diseases, such as AD and PD, and age-related cognitive dysfunction may be slowed or ameliorated by the action of mitochondrial nutrients delaying or repairing mitochondrial damage, thereby improving mitochondrial function, cellular function, and tissue function. ALA has been classified as a mitochondrial nutrient [1]. Theoretically, this system of cellular support and repair should be functional not only in brain tissue, but in many cell types and organ systems throughout the body.

Although a number of well-designed preclinical studies have published beneficial effects of ALA on memory function, and point to its potential as a neuroprotective agent, very few have examined its effects in humans [2]. However, multiple animal models of age-related memory loss and neurodegenerative disorders have shown that ALA improves memory in a variety of situations. For example, ALA has been demonstrated to partially reverse memory loss in aging rats and protect against acute glutamate neurotoxicity in the rat brain by modulating mitochondrial function [4]. Another rat study reported that ALA treatment appeared to reverse the impacts associated with a variety of experimental models of neurodegenerative disorders and exposure to neurotoxicants, as well as normal aging. They also noted that ALA treatment was observed to improve memory in different learning and memory paradigms, including aversive, spatial, and recognition memory [2].

The mechanisms by which ALA acts on the brain are many. There is, of course, its antioxidative action, cleaning up free radicals that may be causing cellular destruction, but it also helps to recycle other endogenous antioxidants. ALA also interacts with glutathione and vitamin C to repair and protect cell membranes, supporting the structure of cells [1]. Next, ALA increases glucose metabolism by enhancing glucose transport into cells and the activity of crucial enzymes for mitochondrial energy production (contributing to its classification as a mitochondrial nutrient). ALA chelates redox-active metals, which decreases the accumulation of lipid peroxidation products [4]. ALA has also been shown to improve the function of neurotransmitter systems, including dopamine, serotonin, and norepinephrine, sometimes even reversing age-related loss of both neurotransmitters and their receptors, which may underlie the apparent positive effects of ALA on cognition [2].

So what have you got to lose in trying ALA to ease the aging process and clear some of that brain fog? Nothing. And possibly some youth to gain! Evidence from clinical trials that have involved humans suggests that ALA supplementation is safe for all healthy individuals, although one clinical trial reported occasional minor stomach discomfort at very high doses [5]. ALA does increase glucose transport and so may lower blood sugar, which could be important for those with glucose-related health concerns. As always, check with your doctor before adding a new supplement to your health regimen.


  1. Hager, Klaus, et al. “Alpha-lipoic acid as a new treatment option for Alzheimer type dementia.” Archives of gerontology and geriatrics 32.3 (2001): 275-282.
  2. Molz, Patrícia and Nadja Schröder. “Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration” Frontiers in pharmacology vol. 8 849. 12 Dec. 2017, doi:10.3389/fphar.2017.00849
  3. Moini, Hadi, Lester Packer, and Nils-Erik L. Saris. “Antioxidant and prooxidant activities of α-lipoic acid and dihydrolipoic acid.” Toxicology and applied pharmacology 182.1 (2002): 84-90.
  4. A Farr, Susan, Tulin Price, William Banks, Nuran Ercal, and John Morely. “Effect of Alpha-Lipoic Acid on Memory, Oxidation, and Lifespan in SAMP8 Mice.” Journal of Alzheimer’s disease : JAD. 32. (2012): 447-55. ALA Side Effects.