CoBuHe
Janice, can you repost that link on the supplement info...I'd like to check that out.
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Neuromuscular
Disease
Carley
J. Abramson
The Ohio State University
Columbus, OH, USA
Complete
diagnostic evaluation is essential to identify a specific cause of
neuromuscular deficiency.
Treatment
should be tailored for the specific disease diagnosed. However, for
non-specific neuromuscular diseases, trial supplementation with L-carnitine
(50mg/kg BID), Coenzyme Q10(4mg/kg/day), and B-vitamins (100mg/day) have been
recommended to support the nerve and muscle metabolic
demands.
Dr. Abramson is a veterinary neurologist at Ohio State University.
This is a link to the LP forum; http://pets.groups.yahoo.com/group/LP/ You can do a search about supplements without having to be a member. The information I gave about vitamin E and fish oil came from here.
This is some information from PubMed concerning CoQ10 and neuropathies disorders;
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Coenzyme Q10 (CoQ10) is an essential cofactor of the electron transport
chain as well as an important antioxidant. Previous studies have suggested that
it may exert therapeutic effects in patients with known mitochondrial
disorders. We investigated whether it can exert neuroprotective effects in a
variety of animal models. We have demonstrated that CoQ10 can protect against
striatal lesions produced by both malonate and 3-nitropropionic acid. It also
protects against MPTP toxicity in mice. It extended survival in a transgenic
mouse model of amyotrophic lateral sclerosis. We demonstrated that oral
administration can increase plasma levels in patients with Parkinson's disease.
Oral administration of CoQ10 significantly decreased elevated lactate levels in
patients with Huntington's disease. These studies therefore raise the prospect
that administration of CoQ10 may be useful for the treatment of
neurodegenerative diseases.
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Mancuso
M, Orsucci
D, Volpi
L, Calsolaro
V, Siciliano
G.
Department of Neuroscience, Neurological Clinic, University
of Pisa, Italy.
mmancuso@inwind.it
Abstract
Coenzyme Q10 (CoQ10, or ubiquinone) is an electron
carrier of the mitochondrial respiratory chain (electron transport chain) with
antioxidant properties. In view of the involvement of CoQ10 in oxidative
phosphorylation and cellular antioxidant protection a deficiency in this
quinone would be expected to contribute to disease pathophysiology by causing a
failure in energy metabolism and antioxidant status. Indeed, a deficit in CoQ10
status has been determined in a number of neuromuscular and neurodegenerative
disorders. Primary disorders of CoQ10 biosynthesis are potentially treatable
conditions and therefore a high degree of clinical awareness about this
condition is essential. A secondary loss of CoQ10 status following HMG-Coa
reductase inhibitor (statins) treatment has be implicated in the
pathophysiology of the myotoxicity associated with this pharmacotherapy. CoQ10
and its analogue, idebenone, have been widely used in the treatment of
neurodegenerative and neuromuscular disorders. These compounds could
potentially play a role in the treatment of mitochondrial disorders,
Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis,
Friedreich's ataxia, and other conditions which have been linked to
mitochondrial dysfunction.
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This study concerns L-carnitine and antioxidants, including vitamin E;
Institute for Brain Aging & Dementia, Department of Neurology,
University of California, Irvine, CA, USA. Elizabeth.head@uky.edu
Dogs develop cognitive decline and a progressive
accumulation of oxidative damage. In a previous longitudinal study, we
demonstrated that aged dogs treated with either an antioxidant diet or with
behavioral enrichment show cognitive improvement. The antioxidant diet included
cellular antioxidants (vitamins E and C, fruits and vegetables) and
mitochondrial cofactors (lipoic acid and carnitine). Behavioral enrichment
consisted of physical exercise, social enrichment, and cognitive training. We
hypothesized that the antioxidant treatment improved neuronal function through
increased mitochondrial function. Thus, we measured reactive oxygen species
(ROS) production and bioenergetics in mitochondria isolated from young, aged,
and treated aged animals. Aged canine brain mitochondria show significant
increases in ROS production and a reduction in NADH-linked respiration.
Mitochondrial function (ROS and NADH-linked respiration) was improved
selectively in aged dogs treated with an antioxidant diet. In contrast,
behavioral enrichment had no effect on any mitochondrial parameters. These
results suggest that an antioxidant diet improves cognition by maintaining
mitochondrial homeostasis, which may be an independent molecular pathway not
engaged by behavioral enrichment.
All of the supplements I listed are safe as long as they aren't given in very large doses. B vitamins are water soluble and your dog will pass what he doesn't use.