Acetyl L-Carnitine retards some aspects of the aging process in the skin:
ALC improves the reaction times of persons afflicted with Cerebral Insufficiency.
ALC (2-4 grams per day) improves walking distance without pain in persons afflicted with Intermittent Claudication.
ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the brain.
ALC enhances the ability of Macrophages to function as Phagocytes. to order
ALC improves athletic performance [ALC given prior to Exercise increased the maximum running speed of animals].
ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).
ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).
ALC inhibits the damage caused by hypoxia.
ALC transports Lipids into the Mitochondria of Cells.
ALC improves mood and memory in people with Age Associated Memory Impairment.
ALC improves Mental Function where Alcohol (Ethanol) induced cognitive Impairment exists.
ALC increases alertness.
Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [persons afflicted with Alzheimer's Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].
ALC increases alertness in persons afflicted with Alzheimer’s Disease – 2,500-3,000 mg per day for 3 months].
ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.
ALC improves Attention Span in persons afflicted with Alzheimer’s Disease.
ALC improves Short Term Memory in persons afflicted with Alzheimer’s Disease.
High concentrations of ALC are naturally present in various regions of the brain.
ALC reverses the age-related decline that occurs in Cholinergic receptors (i.e. the receptors that receive Acetylcholine).
ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].
ALC improves the Interhemispheric flow of information across the Corpus Callosum of the brain.
ALC retards the decline in the number of dopamine receptors that occurs in tandem with the aging process and (more rapidly) with the onset of Parkinson’s Disease.
ALC enhances the release of dopamine from dopaminergic neurons and improves the binding of dopamine to dopamine receptors.
ALC can prevent the destruction of dopamine receptors by MPTP (a neurotoxin capable of causing Parkinson’s Disease via Dopaminergic Receptor death.
ALC improves Attention Span and Memory in persons with Down’s Syndrome.
ALC retards the inevitable decline in the number of Glucocorticoid receptors that occurs in tandem with the aging process.
ALC enhances the recovery of persons afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.
ALC retards the age-related deterioration of the Hippocampus [research - rats].
Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].
ALC improves both Short-Term memory and Long-Term memory .
ALC improves Mood [ALC improves Mood in 53% of healthy subjects].
ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the aging process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].
ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) receptors that occurs in tandem with the aging process.
ALC stimulates and maintains the growth of new Neurons within the brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the brain].
ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.
ALC rejuvenates and increases the number of N-Methyl-D-Aspartate receptors (NMDA receptors) in the brain [even a single dose of ALC increases the number of functional NMDA receptors]:
ALC protects the NMDA receptors in the brain from the natural decline that occurs in tandem with the aging process [research - animals].
ALC is presently being researched as a treatment for Parkinson’s Disease.
ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).
ALC improves the quality of sleep and reduces the quantity of sleep required.
ALC improves the function of (reduces the over-excitability of) Motor Nerves in persons afflicted with Spasticity.
ALC improves Spatial memory (an aspect of short Term memory that involves remembering one’s position in space).
ALC inhibits the excessive release of Cortisol in response to stress and inhibits the depletion of Luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.
ALC improves Verbal Fluency.
ALC enhances the function of Cytochrome Oxidase (also called Complex IV) – an essential enzyme of the Electron Transport System.
ALC normalizes Beta-Endorphin levels.
ALC reduces Stress-induced Cortisol release [research - animals].
ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.
ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the aging Process.
ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].
ALC increases the body’s levels of circulating Thyrotrophin.
ALC facilitates the production of Adenosine Triphosphate (ATP) [research - animals].
ALC “shuttles” Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.
ALC facilitates both the release and synthesis of Acetylcholine.
ALC’s ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.
ALC increases the brain’s levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine receptors.
De Falco, F. A., et al. Effect of the chronic treatment with L-acetylcarnitine in Down’s syndrome. Clin Ther. 144:123-127, 1994.
Bowman, B. Acetyl-carnitine and Alzheimer’s disease. Nutr Rev. 50:142-144, 1992.
Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord (USA). 9(3):128-131, 1995.
Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Annals of the New York Academy of Sciences (USA). 663:483-486, 1993.
Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer’s Disease? Annals of the New York Academy of Sciences (USA. 640:228-232, 1991.
Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the efficacy of a pharmacological aid. Drugs under Experimental and Clinical Research. 14(11):715-718, 1988.
Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. International Journal of Clinical Pharmacology Research. 10(1-2):75-79, 1990.
Pettegrew, J. W., et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging . 16:1-4, 1995.
Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine in patients with Alzheimer’s dementia. Current Medical Research and Opinion. 11(10):638-647, 1989.
Sano, M., et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol. 49:1137-1141, 1992.
Sinforiani, E., et al. Neuropsychological changes in demented patients treated with acetyl-L-carnitine. International Journal of Clinical Pharmacology Research. 10(1-2):69-74, 1990.
Spagnoli, A. U., et al. Long-term acetyl-l-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732, 1991.
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