If your dog is old, on statins and you care for him/her beyond words, you may want to

[HysteryDiagnosis]

be looking at this, of course with animals we all know it is just placebo effect at work.

http://www.ncbi.nlm.nih.gov/pubmed/21763754

Neurosci Lett. 2011 Aug 26;501(2):92-5. Epub 2011 Jul 8.
Coenzyme Q10 and cognition in atorvastatin treated dogs.
Martin SB, Cenini G, Barone E, Dowling AL, Mancuso C, Butterfield DA, Murphy MP, Head E.
Source

Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536, United States.
Abstract

Statins have been suggested to protect against Alzheimer's disease (AD). Recently, however, we reported that aged dogs that underwent chronic statin treatment exhibited cognitive deficits compared with age matched controls. In human studies, blood levels of Coenzyme Q10 (CoQ10) decrease with statin use. CoQ10 is important for proper mitochondrial function and is a powerful antioxidant, two important factors for cognitive health in aging.

Thus, the current study tested the hypothesis that CoQ10 levels in the serum and/or parietal cortex are decreased in statin treated dogs and are associated with poorer cognition. Six aged beagles (>8 years) were administered 80mg/day of atorvastatin for 14.5 months and compared with placebo-treated animals. As predicted, serum CoQ10 was significantly lower in statin-treated dogs. Parietal cortex CoQ10 was not different between the two groups.

However, poorer cognition was correlated with lower parietal cortex CoQ10. This study in dogs suggests that serum CoQ10 is reduced with atorvastatin treatment. CoQ10 levels in brain may BE linked to impaired cognition in response to atorvastatin, in agreement with previous reports that statins may have a negative impact on cognition in the elderly.

[Lunabelle]

1. Interesting that statins have this effect

I wonder how it correlates to human beings and the plaque build up in their brains?

[HysteryDiagnosis]

2. How about statin induced diabetes?? Like that? Want that?? As far as the plaque in the

brain goes I don't have anything... however brain function and statins does have a laundry list of honorable mentions.

http://www.ncbi.nlm.nih.gov/pubmed/20847439
Changes in cognition and amyloid-β processing with long term cholesterol reduction using atorvastatin in aged dogs.
Murphy MP, Morales J, Beckett TL, Astarita G, Piomelli D, Weidner A, Studzinski CM, Dowling AL, Wang X, Levine H 3rd, Kryscio RJ, Lin Y, Barrett E, Head E.
Source

Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 405360230, USA. [e-mail]
Abstract

Human studies suggest either a protective role or no benefit of statins against the development of Alzheimer's disease (AD). We tested the hypothesis that statin-mediated cholesterol reduction in aged dogs, which have cognitive impairments and amyloid-β (Aβ) pathology, would improve cognition and reduce neuropathology. In a study of 12 animals, we treated dogs with 80 mg/day of atorvastatin for 14.5 months.

We did not observe improvements in discrimination learning; however, there were transient impairments in reversal learning, suggesting frontal dysfunction. Spatial memory function did not change with treatment. Peripheral levels of cholesterol, LDLs, triglycerides, and HDL were significantly reduced in treated dogs. Aβ in cerebrospinal fluid and brain remained unaffected. However, β-secretase-1 (BACE1) protein levels and activity decreased and correlated with reduced brain cholesterol.

Finally, lipidomic analysis revealed a significant decrease in the ratio of omega-6 to omega-3 essential fatty in temporal cortex of treated aged dogs. Aged beagles are a unique model that may provide novel insights and translational data that can predict outcomes of statin use in human clinical trials. Treatment with atorvastatin may be beneficial for brain aging by reducing BACE1 protein and omega6:omega3 ratio, however, the potential adverse cognitive outcomes reported here should be more carefully explored given their relevance to human clinical outcomes.

[Lunabelle]

3. Well, I'm no scientist,

But I thing I'd rather have diabetes than Alzheimer's. If I ever get that diagnosis like my grandmother did, I'm gonna take what people may say is the easy way out. But I don't want to die from Alzheimer's. It is the most hideous disease and I'll take the bullet instead, or the cocktail.

[HuckleB]

4. Well, old hysterical is no scientist either.

No need to bother yourself with his outbursts.

[HysteryDiagnosis]

5. Something you may want to read, there is more at the link

http://www.lef.org/LEFCMS/aspx/PrintVersionMagic.aspx?CmsID=113875


Compelling and growing evidence links inflammation and oxidative stress to Alzheimer’s disease. According to the inflammation theory (discussed in dozens of recent clinical trials), inflammatory cytokines gather at the neurons of people who have Alzheimer's. These cytokines set off an inflammatory cascade. The inflammation generates high levels of free radicals that contribute directly to the formation of beta-amyloid plaques. The result is more inflammation, free radicals, and beta-amyloid plaques. Iron has also been linked to the generation of free radicals. Studies have shown that free iron accumulates on the surface of dying neurons, where it generates oxygen-derived free radicals that hasten the spread of the disease (Mandel S et al 2006).

Supporting the inflammation theory is the fact that nonsteroidal anti-inflammatory drugs (NSAIDs), taken over the long-term, actually decrease the risk of developing Alzheimer’s disease and delay its onset. Of course, this presents a problem: long-term intake of NSAIDs is not a good idea. Over-the-counter NSAIDs, such as ibuprofen, are associated with gastrointestinal and kidney complications, while prescription COX-2 inhibitors have been shown to raise the risk of heart attack and stroke.

The inflammation theory of Alzheimer’s disease is joined by other possible causes, including the excitotoxicity theory. In this theory, high levels of the amino acid glutamate in the brain overstimulate neurons. The overstimulated neurons release inflammatory cytokines. Glutamate excitotoxicity is mediated by N-methyl-D-aspartate (NMDA) receptors.

Other possible causes include high levels of homocysteine in the brain and specific nutrient deficiencies. Although these ideas are still developing, they have opened up exciting new targets for therapy. In clinical studies, the most cutting-edge researchers are turning to therapies such as anti-inflammatory nutrients, antioxidants that reduce oxidative stress, and metal chelating agents (such as green tea) that reduce the levels of free iron in the brain.