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When our brain ages, our body follows. The brain controls all our life systems. Its 10 billion neurons and supporting glial cells define our identity and generate our thoughts and feelings. When our brain cells malfunction or die, our memories fade, our thinking ability disappears, our muscles atrophy, our bones become brittle, our arteries harden, our immune system weakens, our coordination declines, and our life begins to slip away.

In seeking to derail aging, there's nothing more important than our brain. Therapies that slow brain aging pay multiple dividends; they help to maintain our identity, while preserving the vital functions that enable us to enjoy our lives in good health and vigor. There is considerable evidence that a wide variety of compounds have beneficial effects on brain aging, including vitamin E, selenium, beta-carotene, hydergine, piracetam, centrophenoxine, phosphatidylcholine, and phosphatidylserine. Based upon current evidence however, the two most potent anti-aging therapies for the brain are DEPRENYL and ACETYL-L-CARNITINE.


Researchers have shown that age-dependent brain cell changes can be slowed or prevented by treatment with Acetyl-l-carnitine (ALC). In one study at the University of Tor Vergata in Rome (Arch Gerontol Geriatr, 10:173-185:1 990), scientists used ALC to prevent the age-dependent loss of neurons in certain areas of the rat brain, especially the hippocampus, one of the primary memory centers in the brain.

The benefits of ALC's ability to protect neurons in the memory center of rats can be seen in a study in which treatment for eight months with ALC prevented the age-related loss of the ability of rats to find their way through a radial maze (Prog Neuro Psychopharmacol & Biol Psychiat, 1 4 :359-369 :1 990).


There is solid evidence that many of the neurodegenerative changes associated with brain aging may be caused, in part, by a decline in the activity of a class of neurochemicals called Nerve Growth Factor (NGF) that provide support for the healthy functioning of brain cells, especially in the hippocampus and frontal cortex of the brain. (Molecular Brain Research, 3:55-60:1987). Further evidence that the decline in NGF is a cause of the degeneration of brain cells comes from studies in which intracere broventricular infusion of NGF was able to reverse both structural and behavioral deficits in aged rats. (Nature, 329:6568:1 987).


A recent study at the University of Rome in Italy provides striking new evidence to explain the anti-aging benefits of Acetyl-l-carnitine in improving cognitive and behavioral function in aging humans (Experimental Gerontology, 29:55-66:1994). In this study, ALC was dissolved in the drinking water of rats (at a dosage level of 150mg/kg per day) for six months, starting at the advanced age of 21 months. In another part of the study, ALC was injected intraperitoneally (100mg\kg) twice a day for eight consecutive days.

The scientists found that both short term and long-term administration of ALC increased NGF levels by 39% in the central nervous system (CNS) of aging rats. Moreover,long-term treatment with ALC completely prevented the loss of choline acetyltransferase (CHAT) activity in the brain of these rats. CHAT is the enzyme that helps to transform the nutrient choline into the neurotransmitter acetylcholine, which plays an essential role in learning and memory.

The scientists concluded that: "These results indicate that short term treatment with ALC is able to induce NGF production and its subsequent utilization in the CNS of aged rats, whereas treatment with ALC which starts at a time when senescence-related CNS impairments are taking place will protect neurons by maintaining NGF activity. This would imply for ALC either curative properties when given to aged subjects, or preventive properties when administered to aging ones".


These findings help to explain how ALC can slow down the deterioration of Alzheimer's patients. In one such study at the Institute Mario Negri in Milan, Italy, 130 patients with Alzheimer's Disease were given 2 grams a day of ALC for a year and were compared to patients receiving placebo (Neurology, 41:17261732 1991). The results showed a markedly slower rate of deterioration in patients receiving acetyl-l-carnitine in 13 of the 14 functions measured!

They also suggest that ALC might be even more beneficial in slowing or preventing cognitive and behavioral deficits in normally-aging persons without overt signs of disease. The evidence suggests that, at a minimum, long-term treatment with Acetyl-l-carnitine could stop us from getting age related neurodegenerative diseases such as Alzheimer's Disease and, at best, could slow normal aging in humans dramatically.

  1. Arch Gerontol Geriatr, 10:173-185:1990
  2. Prog Neuro-Psychopharacol & Biol Psychiat, 14:359-369:1990
  3. Molecular Brain Research, 3:55-66:1987
  4. Nature, 329:65-68:1987
  5. Experimental Gerontology, 29:55-66:1994
  6. Neurology, 41:1726-1732:1991


New research offers strong evidence that L-Carnitine and Acetyl-l-Carnitine can greatly effect the repair of DNA damage in peripheral blood Iymphocytes (white blood cells), suggesting that both compounds can help to prevent the age-related decline of the immune system and, perhaps, other systems as well. DNA repair is at the very heart of all our life functions and any therapy that can aid this process is of great value.

The DNA in the nucleus of our cells contains the blueprint for the healthy functioning of the entire organism. If the double-stranded DNA molecule-which includes the chromosomes that harbor the genes that control our every function-fails to maintain its structural integrity, the results can be catastrophic cell death, soon resulting in the death of the organism.

Our DNA is constantly subject to attack from radiation and chemicals in our food, water, and air. These attacks cause frequent structural and sequential damage to one or both DNA strands, which would lead rapidly to massive cell death if it wasn't for nuclear enzymes that constantly repair DNA damage. One of the most studied method of DNA repair is the "cut-and-patch" method in which the damaged components of DNA (nucleotides) are excised by "cutting" enzymes followed by the synthesis of healthy replacem ent nucleotides in the appropriate order.

DNA repair is an absolutely critical function - it maintains the healthy function of our cells and may play a critical role in the rate of normal aging and the determination of maximum lifespan in different species. It's also been suggested that diminished DNA repair capacity may play an important role in our progressively higher risk of Alzheimer's disease, Parkinson's disease, and other neurodegenerative diseases with increasing age.

There are several well-documented DNA repair disorders, including Xeroderma Pigmentosum (XP), Cockayne's Syndrome (CS), and Fanconi's Anemia (FA) that are characterized by increased sensitivity to the cell-destroying effects of ultra-violet radiation or agents that cause DNA interstrand cross-linking. Recently, the genes responsible for defective DNA repair in Xeroderma Pigmentosum, Cockayne's Syndrome , and Fanconi's Anemia have been cloned and characterized.

In addition to the above diseases in which defective DNA repair has been established as a causal factor, it's also been proposed that an altered response to DNA damage may, in part, be responsible for the development of a variety of of neurodegenerative diseases including Alzheimer's disease. Indeed, there is evidence that Peripheral Blood Lymphocytes (PBLs) sampled from patients with Alzheimer's disease are especially defective in the removal of single-strand DNA breaks.

A recent study conducted by scientists from the U.S., Italy, and The Netherlands sought to determine whether the addition of varying doses of L-Carnitine and Acetyl-L-Carnitine to cultured Peripheral Blood Lymphocytes exposed to several DNA-damaging agents could improve DNA repair in these cells4.

The study utilized several oxygen-radical generating agents (Xanthine Oxidase (XOD), Hypoxanthine (HYP), and the alkylating agent ENU) to mimic the conditions of DNA strand damage caused by reperfusion following ischemia (loss of oxygenated blood flow). . They discovered that these agents induced a large number of single-strand DNA breaks (SSB) in cultured peripheral blood lymphocytes. They then treated the damaged DNA strands with either L-Carnitine or Acetyl-L-Carnitine.

The researchers found that treatment with either L-Carnitine or Acetyl-L-Carnitine caused the disappearance of the vast majority of the single-strand breaks that had been induced in the cells. As they put it " . . . at 24 hours after treatment the elution curves of treated cells were practically indistinguishable from elution curves of control cells, indicating complete repair of the induced SSBs."

The scientists concluded that: "The ability to remove DNA lesions at an increased rate should be of great importance in maintaining correct cellular functioning and in ensuring survival. In particular, those DNA damages that appear to be removed at a slow rate, or seem to persist in the genome may gradually accumulate in target genes and result in the slow deterioration of essential gene functioning until cell death occurs."

L-Carnitine has been shown to protect heart tissue against ischemia, to improve cardiac performance, and to restore high-energy phosphate pools that contribute to the generation of energy molecules (ATP) in heart cells. Acetyl-l-Carnitine has been shown to increase energy within neurons, to improve learning and cognitive abilities, and to improve the condition of patients suffering from neurodegenerative diseases such as Alzheimer's disease.

Recently, Kalaria and Harik reported a 25%-to-40% decrease in t he mitochondrial enzyme (carnitine acetyl-transferease) that plays a key role in energy production within brain cells in both the frontal and temporal cortex of patients with Alzheimer's disease5. This enzymatic decrease may explain the benefits for such patients of taking Acetyl-l-Carnitine, as well as its benefits for normally aging persons.

  1. Nucleic Acids Res, 19:6301-6308, 1991 - Nature, 356:763-767, 1992
  2. J Gerontol Biol Sci, 47:B177 -B184, 1992 - J Amer Geriatr Soc, 35:532-541, 1987
  3. Neurobiol Aging, 12:367370, 1991
  4. Carcinogenesis, 14:10:L2131-2136, 1993
  5. Am Neurol, 32:583-586, 1992

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