Re: drug Lipitor and parkinson's disease any relationship anyone might know of?

the following is an english translation of a letter that appeared in a
German Medical Journal, February, 2003. the author, Thomas Muller,
also published in annals of neurology 2 case reports of individuals
who developed parkinson's that was said to have been "unmasked" by
statins. that report is referenced in the list for the translated
letter; it is #2.


Der Nervenarzt
Publisher: Springer-Verlag Heidelberg
ISSN: 0028-2804 (Paper) 1433-0407 (Online)
DOI: 10.1007/s00115-002-1445-6
Issue: Volume 74, Number 2
Date: February 2003
Pages: 115 - 122
Fibrat-/Statin-Myopathie


J. Finsterer A1


A1 Neurologische Abteilung,KA Rudolfstiftung,Wien
Letter in response with case study of statin-unmasked Parkinsons
"To the excellent review about the development of
myopathies following long-term medication of cholesterol
level decreasing fibrates and statins, there should be
considered additional differential diagnostic possibilities.


Because of the similar clinical symptomatology with muscle
aches and increased stiffness, the diagnosis of statin-
induced aggravated Parkinson Disease Syndrome should
be discussed. The development of such muscular side
effects is seen more with statins than with fibrates.
The case report in Table 1 indicates the history of a 60 year
old patient with statin-induced Parkinson Syndrome
occurring over a long time.


On the other hand, with central effective statins, a possible
neuro-protective effect in neuro-degenerative diseases has
been considered, especially in dementia. But long term use
of statins, especially Lovastatin, leads to the reduction of
coenzyme Q10 and can cause damage of the mitochondrial
breathing chain. Co Q-10 is an electron receptor in the
mitochondrial complexes 1 and 2 and very effective
absorber of radicals. This antigen substance increases the
complex 1 activity. Co-Q10 shows a certain therapeutic
effect with encephalomyopathy where there is a lack of
various enzyme functions of the breathing chain.


Dysfunction of various parts of the mitochondrial breathing
chain is also considered in the pathophysiological
mechaism of idiopathic Parkinson's disease. Treatment
with Co-Q10 in patients who are not treated with Dopamine
for Parkinson patients, caused less disease symptomatology
and progression than patients treated with placebo, though
placebo treatment can cause stimulation of dopaminergic
neurotransmission. Therefore, the long-term treatment with
Co-Q10 possibly is neuroprotective in idiopathic morbid
Parkinson, though new evidence shows it appears to cause
mild symptomatic effect.


Under these circumstances treatment with prophylactic
medication of Co-Q10 which has been well tolerated in
doses up to 1200mgm in patients with neurodegenerative
diseases should be considered for statin myopathy or statin-
induced Parkinson syndrome in addition to discontinuation
of the cholesterol decreasing medication.


The Table 1 summarizes a patient with Parkinson
syndrome.


1996: start of therapy with Fluvastatin 40 mg.


1997: increasing weakness with shoulder and hip pain on the
right


1999: diagnosis of right sided Parkinson syndrome of
akinetic dominance type. Careful induction of Pergolid with
daily doses of 3 mg and Salagen 7.5 mgm


2000: complaints about increasing edema development in
legs, loss of hair, start of a potas.sium sparing diuretic and
increasing of Pergolid medication from 4.5 mg in June 2000
to 6 mgm in December.


March 2001: discontinuation of Fluvastatin, continuation of
Pergolid 6 mg


June 2001: reduction of Pergolid to 4 mgm


Sept 2001 Pergolid 3 mgm. Improvement of edema


December 2001 discontinuation of Pergolid and diuretics


March, 2002 discontinuation of Salagen"


Dr. Th. T. Muller


1.Finsterer J (2003) Fibrat-/Statin-Myopathie. Nervenarzt
:115-122


2.Müller T, Kuhn W, Pohlau D, Przuntek H (1995) Parkinsonism
unmasked
by lovastatin. Ann Neurol 37:685-686


3.Simons M, Schwarzler F, Lutjohann D, von Bergmann K, Beyreuther K,
Dichgans J et al. (2002) Treatment with simvastatin in
normocholesterolemic patients with Alzheimer's disease: A 26-week
randomized, placebo-controlled, double- blind trial. Ann Neurol
52:346-350


4.Folkers K, Langsjoen P, Willis R, Richardson P, Xia LJ, Ye CQ et al.
(1990) Lovastatin decreases coenzyme Q levels in humans. Proc Natl Acad


Sci U S A 87:8931-8934


5.Shults CW, Haas RH, Pas.sov D, Beal MF (1997) Coenzyme Q10 levels
correlate with the activities of complexes I and II/III in mitochondria


from parkinsonian and nonparkinsonian subjects. Ann Neurol 42:261-264


6.Rotig A, Appelkvist EL, Geromel V, Chretien D, Kadhom N, Edery P et
al. (2000) Quinone-responsive multiple respiratory-chain dysfunction
due to widespread coenzyme Q10 deficiency. Lancet 356:391-395


7.Schapira AH, Mann VM, Cooper JM, Krige D, Jenner PJ, Marsden CD
(1992) Mitochondrial function in Parkinson's disease. The Royal Kings
and Queens Parkinson's Disease Research Group. Ann Neurol 32
Suppl:S116-S124


8.Chan A, Reichmann H, Kogel A, Beck A, Gold R (1998) Metabolic changes


in patients with mitochondrial myopathies and effects of coenzyme Q10
therapy. J Neurol 245:681-685


9.Haas RH, Nasirian F, Nakano K, Ward D, Pay M, Hill R et al. (1995)
Low platelet mitochondrial complex I and complex II/III activity in
early untreated Parkinson's disease. Ann Neurol 37:714-722


10.Shults CW, Oakes D, Kieburtz K, Beal MF, Haas R, Plumb S et al.
(2002) Effects of coenzyme q10 in early Parkinson disease: evidence of
slowing of the functional decline. Arch Neurol 59:1541-1550


11.Fuente-Fernandez R, Stoessl AJ (2002) The biochemical bases for
reward. Implications for the placebo effect. Eval Health Prof
25:387-398


12.Müller T, Buttner T, Kuhn W (2003) A mild benefit of Coenzyme Q
10
supplementation in patients with Parkinson's disease. J Neural Transm
: (P 57) XIIï�‰ï€


13.Feigin A, Kieburtz K, Como P, Hickey C, Claude K, Abwender D et al.
(1996) As.sessment of coenzyme Q10 tolerability in Huntington's
disease.
Mov Disord 11:321-323


Reply





mregan Jun 25, 6:21 pm show options

Newsgroups: sci.life-extension
From: "mregan" - Find messages by this author
Date: 25 Jun 2005 15:21:37 -0700
Local: Sat,Jun 25 2005 6:21 pm
Subject: Re: report of statin induced parkinson disease and reference for 2 case reports of patients with parkinson "unmasked" by statins
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shedding some light on function of mitochondria:
http://www.boston.com/news/glo­­be/health_science/articles/200­­4/11/02/a...


Aging: Is it a power failure?
Researchers explore the role of mitochondria
By Alice Dembner, Globe Staff | November 2, 2004


They are the power plants within our cells, crucial for life, and
concentrated in the tissues that often deteriorate the most as we age
-- the brain, the heart, the muscles, the eyes. But are the
mitochondria a driving force in aging?


Increasingly, researchers are focusing on the possibility that this
tiny element of a cell may be a factor in failing memory, increasing
weakness, thinning hair, and other symptoms of aging.


The evidence is piling up but not yet definitive. It is grounded in the


knowledge that mitochondrial function deteriorates with age, that
mitochondria generate damaging molecules called free radicals, and that


mutations accumulate in mitochondrial genes, some of them caused by
free-radical assault.


"It's one of the hottest areas of biology," said Simon Melov, director
of genomics at the Buck Institute for Age Research who reviewed recent
research in the October issue of Trends in Neuroscience.


Last spring, scientists in Sweden provided some of the strongest
evidence yet. They shortened the life of mice and created signs of old
age by injecting a small genetic defect into the mice's mitochondria.


Potentially harmful changes in mitochondria also have been discovered
in age-related diseases, such as Alzheimer's, diabetes and the
muscle-wasting condition called sarcopenia.


In addition, researchers are identifying natural changes in
mitochondria that may promote longevity and protect against some
diseases. For instance, scientists have discovered a particular
mutation in mitochondrial DNA that occurs five times more frequently in


centenarians than in younger individuals. Other researchers have
identified segments of the world's population with mutations in their
mitochondrial DNA that appear linked to both longer life and protection


against Alzheimer's.


But not everyone is convinced.


"It's a very appealing theory," said David Finkelstein, who oversees
research on metabolism at the National Institute on Aging.
"Mitochondria are a source of energy and a lot of damage. But the body
is designed to deal with a lot of this. I'd like to be a believer, but
I also have to remain skeptical until we see rigorous proof."


Some of the key researchers working on mitochondria believe these tiny
structures will turn out to be only one of several factors that explain


aging.


Mitochondria, present in every cell of the body except red blood cells,


are believed to have derived from bacteria that invaded more complex
cells billions of years ago, bringing their own genetic code. They
transform fat, Sugar and oxygen into energy that can be used by the
body. As a byproduct, they create free radicals, destructive oxygen
molecules that can damage the mitochondria genes as well as the
surrounding cells.


If mitochondria severely malfunction, humans eventually die -- from
lack of fuel for the brain and heart, or from signals from the
mitochondria that spur cell suicide. Inherited mitochondrial defects
cause dozens of rare illnesses, and scientists are increasingly finding


evidence of mitochondrial problems linked to more common diseases,
which may shed light on the aging process. Continued...


1 2 Next
Page 2 of 2 -- For example, scientists at Yale University reported in
Science magazine last month that they had found a mutation in
mitochondrial DNA that caused high blood pressure, high cholesterol and


low magnesium levels in four generations of an extended family. The
work follows a study last year that linked a 40 percent decline in
mitochondrial function in adults over 60 to insulin resistance, a major


contributor to adult-onset diabetes. Since the symptoms of insulin
resistance, high blood pressure, high cholesterol and obesity often
cluster in aging adults, researchers suggest there may be a common
mitochondrial cause.


"We need to explore this hypothesis directly," said Dr. Richard Lifton,


chairman of the genetics department at Yale who conducted the most
recent work.


Researchers also have found that mitochondrial mutations build up in
the muscles of monkeys and rats with sarcopenia, an age-related loss of


muscle mass. The damaged muscles have lost one-third to one-half of
their mitochondrial genes, and thus a big part of their ability to
generate energy to build muscle fiber, according to Judd Aiken, a
professor of animal health and biomedical sciences at the University of


Wisconsin in Madison who published the study last year. Aiken is now
looking for the same mutations in human muscle cells.


Animal research on Alzheimer's also has implicated mitochondrial
damage, finding that the disease's characteristic amyloid plaques
increased as destruction caused by free radicals rose. In human brains,


Douglas Wallace, a mitochondria researcher at the University of
California at Irvine, found 63 percent more mutations in the
mitochondria of those with Alzheimer's compared with healthy adults.
And in the Alzheimer's patients, more of these changes were clustered
in the portion of the mitochondria that controls its key functions.


While the links are accumulating, Finkelstein and others say there is
still a big question about whether the mitochondrial changes cause the
illnesses or are just another symptom.


That's why Dr. Nils-Goran Larsson decided to see if he could shorten
the lifespan of mice and create age-related symptoms with a simple
change in their mitochondria. The genetics professor and his colleagues


at the Karolinska Institute in Stockholm disabled the ability of mice
to correct errors in their mitochondrial DNA. As the mice aged and the
mitochondria replicated themselves, errors built up. The mice began to
show signs of premature aging, including weight loss, hair loss,
osteoporosis and heart enlargement. All were dead nearly a year earlier


than normal mice, which usually live about two years.


Looking at the reverse proposition -- extending life via changes in
mitochondria -- Gary Ruvkun, a professor of genetics at Harvard Medical


School, got roundworms to live 20 percent to 30 percent longer by
genetically halving the efficiency of their mitochondria, which he
theorized might have caused them to produce fewer damaging free
radicals. But he's found that tinkering with the genes involved in
regulating insulin, rather than mitochondria, can increase worm
lifespan 200 to 300 percent -- suggesting that mitochondria may play a
lesser role in aging.


Researchers can't experiment with human genes in the same way, but have


found links to longevity in natural mitochondrial variations. Dr.
Giuseppe Attardi, a biology professor at the California Institute of
Technology, discovered an accumulation of mutations in mitochondrial
DNA that was more prevalent -- though still not common -- in
centenarians. He suggested that these mutations may help people survive


under unfavorable conditions but can't yet explain the underlying
mechanism.


Wallace has examined patterns of mitochondrial DNA around the world and


found mutations he believes helped people adapt to living in colder
climates -- and had the unexpected byproduct of extending lifespan and
protecting against Alzheimer's and Parkinson's. According to a study he


published in Science in January, the mutations directed the
mitochondria to make more heat instead of energy, which led them to
generate fewer free radicals and cause less damage to the body.


"We're very confident that these mutations are . . . protective of
aging," he said in an interview.


Finkelstein said he finds the work of Attardi and Wallace provocative,
but said the fact that mutations can affect lifespan doesn't mean
they're the critical element.


"The bottom line: What controls aging is a big black box," he said.


Melov predicted that new research methods and a critical mass of
researchers are coming together to bring some answers quickly.


"Evidence which will answer this question definitively will be
published within the next few years."


© Copyright 2004 Globe Newspaper Company.

 

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