In my repository of thousands of reports from statin damaged people, I have observed an unusual number of reported diagnoses of neurodegenerative diseases usually labeled as tauopathies, coming on shortly after the statin drug was first started.
By Duane Graveline, M.D., M.P.H.
In many the initial diagnosis was considered to be a curious amyotrophic lateral sclerosis (ALS) / Parkinson's disease (PD) type of condition. Others report a frontal lobe dementia / Alzheimers type of condition, while still others have a final diagnosis of multiple system abnormalities (MSA) after going through stages of being first considered multiple sclerosis or ALS.
There is not the slightest doubt in my mind that the numbers of reports I am seeing are far more than usually expected in a group the size of my reporting population. One naturally wonders about this curious relationship with statin drugs and what the possible mechanism of action might be.
Meske and others (1) has reported a very relevant study on abnormal tau protein phosphorylation induced by a statin drug. The researchers established the presence of abnormal tau protein phosphorylation by statins as a consequence of statin inhibitory effect on the usual mevalonate pathways.
The role of this abnormal tau protein in the formation of the neurofibrillatory tangles (NFTs) and the association of these statin induced NFTs with many of the neurodegenerative diseases mentioned above is under active investigation at this time ( 2,3.)
NFTs, are well known to be found in Alzheimer's disease, usually in association with deposits of beta amyloid and in some manner they appear to contribute to neuronal degeneration. What is much less well known is the presence of NFTs of tau protein origin in many other types of neurodegenerative diseases, sometimes accompanied by beta amyloid but more commonly not. This list of taupathies includes all those conditions mentioned above and many others, much less well known, at least to the public and most physicians.
Over twenty years ago, in the eagerness to inhibit the assumed villain, cholesterol, statin drugs were designed to interfere with the mevalonate pathway. Abnormal tau protein phosphorylation with secondary neuronal damage appears to be another instance of collateral damage from mevalonate tampering. Statins' inihibition of dolichol, CoQ10 and glial cell cholesterol synthesis, discussed in my book, Statin Drug Side Effects, also reflects statin induced collateral damage to mevalonate pathways, a consequence of tampering with natural physiologic processes.
Statin associated tauopathies may well be additional gross evidence of collateral damage to existing cellular chemistry that researchers were unable to predict when they originally designed the statins. All this from a class of drugs originally developed simply to inhibit the biosynthesis of cholesterol, now increasingly shown to be irrelevant to the atherosclerotic process.
The anti-inflammatory benefit of statins to reduce cardiovascular risk is fully acknowledged. In my opinion, what we really need in the challenge to reduce cardiovascular risk is a comparable anti-inflammatory class of drugs not based on mevalonate pathway corruption.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
1. Meske V and others. European Journal of Neuroscience. 17: 93, 2003
2. Lambourne S and others. Molecular & Cellular Biology, 2005 http://mcb.asm.org/cgi/content/abstract/25/1/278
3. Ferrer I and others, Current Alzheimer's Research, 2005 http://mcb.asm.org/cgi/content/abstract/25/1/278
Updated July 2011