[olsen]

http://tinyurl.com/3c3zh5

Coenzyme Q treatment of neurodegenerative diseases of aging

Wendy R. Galperna, , and Merit E. Cudkowiczb
aNational Institute of Neurological Disorders and Stroke, National Institutes of Health, 6001 Executive Blvd., Room 2225, Bethesda, MD 20892, USA
bMassachusetts General Hospital East, Neurology Clinical Trials Unit, CNY Building 149, Room 2274, Charlestown, MA 02129, USA
Received 26 October 2006; accepted 29 January 2007. Available online 27 March 2007.

Abstract

The etiology of several neurodegenerative disorders is thought to involve impaired mitochondrial function and oxidative stress. Coenzyme Q-10 (CoQ10) acts both as an antioxidant and as an electron acceptor at the level of the mitochondria. In several animal models of neurodegenerative diseases including amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease, CoQ10 has shown beneficial effects. Based on its biochemical properties and the effects in animal models, several clinical trials evaluating CoQ10 have been undertaken in many neurodegenerative diseases. CoQ10 appears to be safe and well tolerated, and several efficacy trials are planned.

Keywords: Amyotrophic lateral sclerosis; Parkinson’s disease; Huntington’s disease; Coenzyme Q; Clinical trial



Corresponding author. Tel.: +1 301 496 9135; fax: +1 301 480 1080.

Mitochondrion
Volume 7, Supplement 1, June 2007, Pages S146-S153
The Role of Coenzyme Q in Cellular Metabolism: Current Biological and Clinical Aspects

[olsen]

http://www.lef.org/whatshot/index.html#rfcs

July 16, 2007

Review finds coQ10 safe and well tolerated by patients with neurodegenerative diseases

A review published in the June, 2007 issue of the journal Mitochondrion concluded that coenzyme Q10 (coQ10) is safe in relatively high doses and may be prove to be an effective treatment for amyotrophic lateral sclerosis (ALS), Huntington's disease, and Parkinson's disease, which are neurodegenerative diseases associated with aging.

Wendy R. Galpern of the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, and Merit E. Cudkowicz of Massachusetts General Hospital East in Charlestown selected 1 ongoing trial and 1 completed study of ALS, 5 trials of Huntington's disease patients, 7 Parkinson's disease trials, and 1 ongoing trial of Alzheimer's disease and 2 of progressive supranuclear palsy (PSP) for their review.

For ALS patients, 3000 milligrams per day coQ10 was safe and well-tolerated. The ongoing trial included in the review will be evaluating preliminary signs of efficacy for 1800 milligrams or 2700 milligrams coQ10 compared with a placebo.

Among patients with Huntington disease, coenzyme Q10 was discovered to lower brain lactate levels, which are elevated in this disease. Doses of up to 3600 milligrams daily were found to be safe and well tolerated. A phase III trial is being planned to determine whether the compound has the ability to slow the disease's progression.

Coenzyme Q10's benefit in Parkinson's disease has been demonstrated in several studies. Plasma levels of coQ10 have been shown to plateau when between 2400 and 3600 milligrams per day were consumed.

Although lower doses of coQ10 may be helpful for healthy individuals, high doses may be needed to improve symptoms for those with neurodegenerative diseases. The current review has shown that these doses are generally safe and well tolerated, however, more research needs to be conducted in the area of efficacy to confirm laboratory research and preliminary clinical findings.

—D Dye

[ZucchiniFlower]

I'm looking foward to MitoQ (Mitoquinone):

http://www.antipodeanpharma.com/inde...d=14&Itemid=28

http://www.otago.ac.nz/news/news/200...s_release.html

# The antioxidant part was modeled on a naturally occurring antioxidant found in the body, Coenzyme Q. Laboratory tests have shown that MitoQ is 1000 times more effective in preventing oxidative damage than Coenzyme Q.
# The "targeting component" is a positive electrical charge that delivers MitoQ by electrical attraction to the negatively charged mitochondria.
# As a result MitoQ is uniquely able to travel through the cell membrane and position itself in the mitochondria to prevent the chemical oxidation that leads to damage to the mitochondria and dopamine nerve cell death.
# Additionally, MitoQ can accumulate and recycle in the mitochondria, extending its therapeutic effect.

[olsen]

Complex-1 activity and 18F-DOPA uptake in genetically engineered mouse model of Parkinson's disease and the neuroprotective role of coenzyme Q10

Sushil K. Sharmaa, Hesham El ReFaeyb and Manuchair Ebadia, b, c, ,
aDepartment of Pharmacology, University of North Dakota School of Medicine and Health Sciences, 501 North Columbia Road, Grand Forks, ND 58203, United States

Received 26 October 2005; revised 13 November 2005. Available online 27 December 2005.





Abstract

Regional distribution of coenzyme Q10 and mitochondrial complex-1 activity were estimated in the brains of control-(C57BL/6), metallothionein knock out-, metallothionein transgenic-, and homozygous weaver mutant mice; and human dopaminergic (SK-N-SH) cells with a primary objective to determine the neuroprotective potential of coenzyme Q10 in Parkinson's disease. Complex-1 activity as well as coenzyme Q10 were significantly higher in the cerebral cortex as compared to the striatum in all the genotypes examined. Complex-1 activity and coenzyme Q10 were significantly reduced in weaver mutant mice and metallothionein knock out mice, but were significantly increased in metallothionein transgenic mice. The reduced complex-1 activity and 18F-DOPA uptake occurred concomitantly with negligible differences in the coenzyme Q10 between in the cerebral cortex and striatum of weaver mutant mice. Administration of coenzyme Q10 increased complex-1 activity and partially improved motoric performance in weaver mutant mice. Direct exposure of rotenone also reduced coenzyme Q10, complex-1 activity, and mitochondrial membrane potential in SK-N-SH cells. Rotenone-induced down-regulation of complex-1 activity was attenuated by coenzyme Q10 treatment, suggesting that complex-1 may be down regulated due to depletion of coenzyme Q10 in the brain. Therefore, metallothionein-induced coenzyme Q10 synthesis may provide neuroprotection by augmenting mitochondrial complex-1 activity in Parkinson's disease.