The effects on brain function by statins have been of particular concern to me. Pfreiger has documented the effect of cholesterol deprivation on synaptic formation and function. We think much of the amnesia, forgetfulness, disorientation and confusion with statin drug use results from this synaptic effect.
The collateral damage to the vital CoQ10 and dolichol metabolic pathways, branching off beyond statin drugs' reductase block, cannot be denied and surprisingly, both pathways can be tied to neuronal function. The side effects of CoQ10 inhibition range from the energy lack of altered mitichondrial function and the loss of cell wall integrity.
Meske found in his neuron cell cultures that blocking the usual cholesterol dependent pathway with lovastatin (Mevacor) evoked not only degeneration of the neuritic network of the neurons under study but also a transient increase of tau phosphorylation. To refresh your memory, Tau is that protein so prominently deposited in the brains in Alzheimers patients and also has been observed in other of the neuro-degenerative diseases.
While blocking cholesterol, statins appear to block the more natural mevalonate pathways resulting in activation of abnormal Tau phosphorylation. I cite this evolving research area only to document the existence of yet another means by which statin drugs can cause such diverse central nervous system side effects in susceptible individuals.
A large number of people have reported persistent short-term memory loss associated with statin drug use. One of the most widely publicized cases was the Hope case wherein a former CEO was reduced to an unemployable status due to negligible ability for short-term recall following prolonged use of Lipitor. Smart Money magazine carried this story.
Only by frequent cell phone calls with his wife, notepads, and other mechanical and electronic aids to memory was he able to be trusted with even the most menial of tasks. A complete array of medical and psychological testing revealed only short-term memory loss with no evidence of pathology. Even the most skeptical of medical specialists, of the dozens with whom he came in contact in several years of follow-up, finally had to admit probable statin causality.
This case and many others has challenged physicians to devise a reasonable treatment plan for such statin damaged people. Hope is not alone; there are many more like him and the list is growing steadily. To my knowledge, no one has significant experience in this area of persistent short-term memory impairment following statin use to advise, so one must resort to theory.
1. Balestreri R, Fontana L, Astengo F. A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction. J Am Geriatr Soc. 1987;35:425-430.
2. Burtsev EM, Savkov VS, Shprakh VV, Burtsev ME. 10-year experience with using Cavinton in cerebrovascular disorders. Zh Nevropatol Psikhiatr Im S S Korsakova 1992;92(1):56-60.
3. Hindmarch I, Fuchs HH, Erzigkeit H. Efficacy and tolerance of vinpocetine in ambulant patients suffering from mild to moderate organic psychosyndromes. Int Clin Psychopharmacol. 1991;6:31-43.
4. 4. Hitzenberger G, Sommer W, Grandt R. Influence of vinpocetine on warfarin-induced inhibition of coagulation. Int J Clin Pharmacol Ther Toxicol. 1990;28:323-328.
5. Kiss B, Karpati E. Mechanism of action of vinpocetine. Acta Pharm Hung 1996 Sep;66(5):213-24.
6. Olah VA, Balla G, Balla J, et al., An in vitro study of the hydroxyl scavenger effect of Vinpocetine. Acta Paediatr Hung, 30: 309-316, 1990.
7. Osawa M, Maruyama S, Effects of TCV-3B (Vinpocetine) on blood viscosity in ischemic cerebrovascular disease. Ther Hung, 33: 7-12, 1985.
8. Otomo E, Atarashi J, Araki G, et al., Comparison of Vinpocetine with ifenprodil tartrate and dihydroergotoxine mesylate treatment and results of long-term treatment with Vinpocetine. Curr Ther Res, 37: 811-821, 1985.
9. Sauer et al (1988) Vinpocetine prevents ischaemic cell damage in rat hippocampus. Life Sci 1988, 43, 1733-39.
10. Szakall S, Boros I, Balkay L, Emri M, Fekete I, Kerenyi L, Lehel S, Marian T, Molnar T, Varga J, Galuska L, Tron L, Bereczki D, Csiba L, Gulyas B. Cerebral effects of a single dose of intravenous vinpocetine in chronic stroke patients: a PET study. J Neuroimaging 1998 Oct;8(4):197-204
11. Tamaki N, Kusunoki T, Matsumoto S, The effect of Vinpocetine on cerebral blood flow in patients with cerebrovascular disease. Ther Hung , 33: 13-21. 1985.
12. Thal LJ, Salmon DP, Lasker B, et al. The safety and lack of efficacy of vinpocetine in Alzheimer's disease. J Am Geriatr Soc. 1989;37:515-520.
13. Meske V and others. Blockade of HMG-CoA reductase activity causes change in microtubule-stabilizing- protein, tau, via suppression of geranylgeranylpyrophosphate formation: implications for Alzheimer's Disease. European J of Neuroscience 17(1):93, January 2003
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor