- CARNTINE:
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. 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 alleviates Age
Associated Memory Impairment (AAMI): ALC improves Creativity in persons
afflicted with AAMI. ALC improves Memory in persons afflicted with AAMI.
ALC improves Mood in persons afflicted with AAMI. 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 afflicted 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. References De Falco, F. A., et al. Effect of
the chronic treatment with L-acetylcarnitine in Down’s syndrome.
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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
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design pilot study of acetyl levocarnitine in patients with Alzheimer’s
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