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.
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).
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".
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.
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.
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