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Medical Forum / Diseases and Disorders / Alzheimer's / April 2005

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Cognition / oxidative stress

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ironjustice@aol.com - 18 Apr 2005 06:18 GMT
Neurology. 2005 Apr 12;64(7):1152-6. Links

Evidence of increased oxidative damage in subjects with mild cognitive
impairment.

Keller JN, Schmitt FA, Scheff SW, Ding Q, Chen Q, Butterfield DA,
Markesbery WR.

Department of Anatomy, University of Kentucky, Lexington 40536-0230,
USA. Jnkell0@pop.uky.edu

OBJECTIVE: To determine if increased levels of oxidative damage are
present in the brains of persons with mild cognitive impairment (MCI),
a condition that often precedes Alzheimer disease (AD). METHODS: The
authors assessed the amount of protein carbonyls, thiobarbituric
acid-reactive substances (TBARS), and malondialdehyde in the superior
and middle temporal gyri (SMTG) and cerebellum of short postmortem
interval and longitudinally evaluated normal subjects and those with
MCI and early AD. RESULTS: Elevated levels of protein carbonyls
(approximately 25%), malondialdehyde (approximately 60%), and TBARS
(approximately 210%) were observed in the SMTG of individuals with MCI
and early AD vs normal control subjects. The elevation in TBARS was
associated with the numbers of neuritic but not diffuse plaques. Levels
of protein carbonyls increased as delayed verbal memory performance
declined. CONCLUSION: Oxidative damage occurs in the brain of subjects
with mild cognitive impairment, suggesting that oxidative damage may be
one of the earliest events in the onset and progression of Alzheimer
disease.

PMID: 15824339 [PubMed - in process]

--------------------------------------------------------------------------------

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://herbivore.7h.com
ironjustice@aol.com - 19 Apr 2005 01:51 GMT
Mult Scler. 2005 Apr;11(2):191-7. Related Articles, Links

Pattern of neuropsychological impairment in the early phase of
relapsing-remitting multiple sclerosis.

Olivares T, Nieto A, Sanchez MP, Wollmann T, Hernandez MA, Barroso J.

Facultad de Psicologia, Universidad de La Laguna, La Laguna 38205,
Tenerife, Islas Canarias, Spain.

To investigate the neuropsychological profile in the first few years
post-onset of relapsing-remitting multiple sclerosis (MS) we carried
out a comprehensive neuropsychological evaluation of 33 patients
characterized by very short evolution of this disease, minimal levels
of neurological disability and preserved general cognition.
Thirty-three individually pair-matched controls were also evaluated.
Patients performed as well as controls on many of the cognitive
exploration measures. Nevertheless, the group of patients evinced a
general slowness that affected motor execution and cognitive
processing. Memory functions were characterized by preservation of
working memory, retrieval or storage of information and a deficit at
the acquisition phase in (verbal and visual) supraspan tasks. In
addition, significant correlations were observed between some measures
of information processing speed and memory. These results highlight the
importance of studying cognitive deficits not only in the different
subtypes of MS but also in different phases of the disease.

PMID: 15794394 [PubMed - in process]

--------------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore
DEADPEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking
Michael - 19 Apr 2005 03:50 GMT
There's no mention whatsoever of oxidative stress here, Tom.

If you're hallucinating again, you must have forgotten your meds.

> Mult Scler. 2005 Apr;11(2):191-7. Related Articles, Links
>
[quoted text clipped - 35 lines]
> DEADPEOPLE WALKING
> http://pages.ivillage.com/ironjustice/deadpeoplewalking 
Sharon Hope - 20 Apr 2005 04:28 GMT
Yes, and this is also understood to be the mechanism for cognitive damage
from statin drugs (Lipitor, Crestor, Zocor, Pravachol, Lescol, Mevacor, and
Baycol).

Statin drugs depelete body of CoQ10, an antioxidant that is normally
manufactured in the body, but statins interrupt that process.

> Neurology. 2005 Apr 12;64(7):1152-6. Links
>
[quoted text clipped - 34 lines]
> Jesus Was A Vegetarian!
> http://herbivore.7h.com
Robert - 20 Apr 2005 07:36 GMT
> Yes, and this is also understood to be the mechanism for cognitive damage
> from statin drugs (Lipitor, Crestor, Zocor, Pravachol, Lescol, Mevacor, and
> Baycol).
Understood mechanism for cognitive damage?
Maybe it's the milk they are drinking?
Here's the proven understood mechanism. The milk causes your lungs to glue
together and causes depletion of oxygen and in so doing your body is forced
into making ROS causing the damage.
That's been understood for many years now.

> Statin drugs depelete body of CoQ10, an antioxidant that is normally
> manufactured in the body, but statins interrupt that process.

Everybody knows that. There's a million people with muscle damage and renal
failure and cognitive damage.
Sharon Hope - 21 Apr 2005 05:00 GMT
>> Yes, and this is also understood to be the mechanism for cognitive damage
>> from statin drugs (Lipitor, Crestor, Zocor, Pravachol, Lescol, Mevacor,
[quoted text clipped - 14 lines]
> renal
> failure and cognitive damage.

Actually, there is measurable evidence of cognitive damage after only 6
months of statin use.  See Dr. Muldoon's studies.

Randomized trial of the effects of simvastatin on cognitive functioning in
hypercholesterolemic adults.
Am J Med. 2004 Dec 1;117(11):823-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=15589485

Effects of lovastatin on cognitive function and psychological well-being.
Am J Med. 2000 May;108(7):538-46.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=10806282


BTW, CoQ10 affects quite a bit of the body, and a deficiency caused by
statin drugs can impact the body in many ways.  See the presentations from
last weekend below:

Programme of the 4th Conference of the International Coenzyme Q10
Association

Beverly Hilton, Los Angeles, April 14-17 2005

Thursday, April 14th

14.00 - 19.00 Registration

19.00 Welcome reception

Friday, April 15th

8.30 - 8.50: Introductory remarks:

Bioenergetics and Biosynthesis
Chairpersons: G. Lenaz and E. Cadenas

8.50         G. Lenaz The existence of supercomplexes of the mitochondrial
respiratory chain:

         the role of Coenzyme Q diffusion and implications in human
pathology

9.10   G. Dallner Regulation of coenzyme Q synthesis by endogenous modified

         intermediates

9.30         C. Clarke Genetic and Physical Evidence for a Coenzyme Q
Biosynthetic Complex

9.50    J. Olsson  Reduction of coenzyme Q10 by thioredoxin reductase. A
reaction

dependent on the selenium concentration.

10.10 - 10.30          Discussion

10.30 - 10.50          Coffee break

10.50  P. Navas Q biosynthesis during development and aging
11.10  M. Kawamukai  Prenyl diphosphate synthases from higher eukaryotes

11.30 - 11.40          Discussion

                   Non mitochondrial electron transport and antioxidant
aspects

Chairpersons: T. Kishi and L. Packer

11.40  T. Kishi  Extra-mitochndrial CoQ redox cycle and cellular defense
mechanism

12.00  J. Villalba  Interference of cell cycle checkpoint by quinone
reductase inhibitors.

12.20  J. Morrè  CoQ/CoQH2 ratios from plasma membrane electron transport
ceramide

         and shingosine-1-phosphate levels during  GL arrest and apoptosis.

12.40 - 13.00          Discussion

13.00 - 14.30          Lunch

                                               Plasma and tissue
concentrations

Chairpersons: GP Littarru and T. Menke

14.30  M. Miles Serum levels in children, adults and in metabolic syndrome

14.50  P. Palan  Serum levels in pregnancy and menopause

15.10     T. Menke   Measurement of CoQ10 in plasma and blood cells in
childhood: Age

         related reference values,   disease related changes and
comparison of values in

         plasma and blood cells after oral supplementation

15.30  Lili Miles CoQ10 content of skeletal muscle

15.50     RB. Singh Effect of oral coenzymeQ10 dosages on serum Q10 and MDA
levels among healthy men.

16.10 - 16.30          Discussion

16.30 - 16.50          Coffee break

                                     Effect of CoQ10 in gene expression

Chairpersons: C. Clarke and  G. Dallner

16.50     D. Groneberg Coenzyme Q10 affects expression of genes involved in
cell signalling, metabolism and transport in human CaCo-2 cells

17.10     H. Nohl  Ubiquinol and the papeverine derivative caroverin prevent
the

        expression of tumor-promoting factors involved in
coloncarcinogenesis induced by

        dietary-fat nutrition

17.30 -17.50           Discussion

17.50 - 18.30          Poster Session - R. Kalpravidh (beta-thalassemia), De
Luca-Korkina

                            (Coenzyme Q10 treatment in burns)

18.30 - 19.30 Meeting of participants involved in the Q-Symbio trial

Saturday, April 16th

Neuromuscular and neurodegenerative diseases
Chairpersons: C. Shults and A. Naini

8.30         F. Beal  Preclinical Studies of CoQ in Neurodegenerative
Diseases and Clinical Trials

8.50         Geng Li Volume MRI Study: The effects of Coenzyme Q10 in
Transgenic Mouse Models of Alzheimer's Disease and Cerebral Ischemia

9.10    R. Artuch  Familiar cerebellar ataxia caused by primary coenzyme Q10
deficiency

9.30    C. Shults Clinical Trials of Coenzyme Q10 in Neurological Diseases

9.50        Y. Yamamoto Redox status of CoQ in neurodegenerative syndromes

10.10-10.30            Discussion

10.30 -10.50           Coffee break

                                     Role in aging mechanisms

Chairpersons: P. Navas and R. Sohal

10.50  R. Sohal Effects of coenzyme Q intake on the aging process

11.10  J. Quiles  Coenzyme Q supplementation in aging

11.30  S. Hekimi  Multiple ubiquinone-dependent processes as revealed by
clk-1 mutants

11.50   C. Santos Ocana  Yeast YML125C, a Q-dependent  PM reductase and
aging

         control

12.10  -12.30          Discussion

12.30 - 14.30          Lunch break

                                               Cardiovascular diseases

Chairpersons: SA. Mortensen and R. Belardinelli

14.30     B. Golomb Clinical follow-up after stopping statin treatment

14.50  P. Langsjoen  Adverse consequences of HMG-CoA reductase inhibitors in

          clinical cardiology and their response to supplemental CoQ10

15.10  M. Silver  Lipitor/CoQ10/Diastolic Dysfunction study

15.30  H. Mabuchi   Reduction of Serum Ubiquinol-10 and Ubiquinone-10 Levels
by

           Atorvastatin in Hypercholesterolemic Patients

15.50  K. Adarsh Atorvastatin alone/in combination with coenzyme Q10 in 103
cases of

          heart failure (HF) due to ischemic cardiomyopathy (ICM).

16.10 - 16.30          Discussion

16.30 - 16.50          Coffee break

Chairpersons: P. Langsjoen and B. Golomb

16.50  SA. Mortensen Q-Symbio study status

17.10  F. Rosenfeldt  Metabolic, Physical and Mental preoperative approach
to surgery

17.30  R. Stocker  Plasma CoQ10 concentration and cardiovascular disease
outcome

17.50     R. Belardinelli  High-dose coenzymeQ10 improves the contractile
response to

         dobutamine of dysfunctional myocardium in patients with ischemic

          cardiomyopathy

18.10 - 18.30          Discussion

18.30 - 19.30          Poster session

20.00 Social dinner

Sunday, April 17th

Various clinical fields

Chairperson: Udo Hoppe and F. Beal

8.40   E. Teran  Preeclampsia and CoQ10

9.00   A. Mancini  CoQ10 levels in sperm cells and seminal plasma:

         physiopathological implications

9.20    G. Balercia Treatment of idiopathic asthenozoospermia with coenzyme
Q10

9.40   Y. Ashida (Shiseido) CoQ10 intake elevates the epidermal CoQ10 level
in adult

         hairless mice

10.00  T. Blatt  (Beiersdorf) Stimulation of the Skin`s Energy Metabolism
Provides
         Multiple Benefits

10.20-10.40            Discussion
10.40 -11.00           Coffee break

11.00   O. Gabrielli  CoQ10 trial in Down syndrome

11.40   L. Korkina Coenzyme Q in treatment of the alkali-injured rabbit
cornea

12.0            J. Feher  CoQ10 in combination with acetyl-L-carnitine and
omega -3 improves

age-related macular degeneration

12.20                     Discussion and conclusions

13.00                     Lunch
Evelyn Ruut - 21 Apr 2005 12:44 GMT
>>> Yes, and this is also understood to be the mechanism for cognitive
>>> damage
[quoted text clipped - 36 lines]
>
> Beverly Hilton, Los Angeles, April 14-17 2005

I was taking 150 mg of coenzyme Q-10 per day while I was taking lipitor, and
I still had horrible side effects of muscle pain and extreme muscle
weakness.

It may have some effect on memory, but it certainly isn't the cause of
alzheimers.  My mother in law never took a statin drug and she is dying this
moment at 84 of the disease.  My father is 92 and he is doing fine, been on
statin drugs for years.

I have seen your posts before regarding statin drugs.
Are you a troll?

Signature

Best Regards,
Evelyn

(to reply personally, remove 'sox')

Susan - 21 Apr 2005 13:13 GMT
> I was taking 150 mg of coenzyme Q-10 per day while I was taking lipitor, and
> I still had horrible side effects of muscle pain and extreme muscle
[quoted text clipped - 7 lines]
> I have seen your posts before regarding statin drugs.
> Are you a troll?

Sharon isn't a troll, she's a necessary counterbalance to all the well
heeled drug peddlers out there.

The information she presents is always useful, even if her assertions
are sometimes a tad broad.

Susan
Evelyn Ruut - 21 Apr 2005 14:38 GMT
> x-no-archive: yes

> Sharon isn't a troll, she's a necessary counterbalance to all the well
> heeled drug peddlers out there.
[quoted text clipped - 3 lines]
>
> Susan

Hi Susan,

I do respect your opinion (as you already know) and was planning to write to
you again about your regimen for alternative cholesterol control.    Please
post it again, and if you would prefer, you could write me again personally
with it.    Be sure to remove "sox" from my address.

After we last spoke, my doctor pursuaded me to give the Lipitor a second
shot.  It worked, (got down to under 200)  but the cost in quality of life,
was too high!   Been off it for a week and I already feel better!

Signature

Best Regards,
Evelyn

(to reply personally, remove 'sox')

outrider@despammed.com - 23 Apr 2005 04:58 GMT
> x-no-archive: yes
>
> > I was taking 150 mg of coenzyme Q-10 per day while I was taking lipitor, and
> > I still had horrible side effects of muscle pain and extreme muscle

> > weakness.
> >
[quoted text clipped - 10 lines]
>
> The information she presents is always useful, even if her assertions

> are sometimes a tad broad.
>
> Susan

I can attest that Sharon Hope is not a troll. Nor am I. And though I
have had cognitive damage from statins, including short term memory
loss, working memory loss (what you need to learn), aphasia (loss of
language, word loss, vocabularly loss, confusion of words, spelling and
syntax difficulties, forgetting what you want to say by the time you
get to the end of the sentence, inability to follow a conversation;
loss of memory of things one used to do for years for example driving a
car or knitting, spatial loss, becoming lost in one's own
neighbourhood, forgetting if one ate, or how to get dressed--on and on.
I have partly recovered so I can tell people: statin cognitive damage
is real. It is not Alzheimerer's although often misdiagnosed as such,
and although if caught in time one can recover, it can cause permanent
damage. I know people who will never recover from frontal lobe damage
and damage to the cerrebelum.

Alheimer's is a terrible disease. Do not accept this diagnosis without
a complete examination of ALL the possibilities.

Most of all, do not let anyone with dubious motives imply you or your
affected loved one are a "tad broad" or mentally ill.

Zee
Sharon Hope - 23 Apr 2005 03:22 GMT
>>>> Yes, and this is also understood to be the mechanism for cognitive
>>>> damage
[quoted text clipped - 45 lines]
> this moment at 84 of the disease.  My father is 92 and he is doing fine,
> been on statin drugs for years.

Evelyn,

No, the memory loss from statin drugs is real, and is just as debilitating
as Alzheimers, but does not cause death (to my knowledge) - although the
muscle damage from statins can cause death by rhabdomyolysis.

Alzheimer's is a separate and distinct condition.

Never in any of my posts will you see me confuse the two.  They are
absolutely different.

HOWEVER, there are many many MANY primary care physicians who DO confuse the
two.  Many many statin patients who are suffering cognitive damage from
statins, including extreme short-term memory loss and multiple episodes of
transient global amnesia, are at first MISDIAGNOSED as having Alzheimer's.
In this misdiagnosis, not only is there the additional stress and trauma of
being told INCORRECTLY that they have Alzheimers, but the statin drug, which
is CAUSING the damage, is continued to be prescribed, so the damage worsens
until they get Alzheimers ruled out.

I have asked several times, and have read other people ask, and they have
always been told that this is a support group for people with, and families
of people with MEMORY LOSS, and it does not have to be just Alzheimer's.

> I have seen your posts before regarding statin drugs.
> Are you a troll?

I am the wife (of 38 years) of a man who was twice a corporate CEO, who took
Lipitor 10mg/day for 4 years in his mid-50's and is now completely disabled
from Lipitor side effects.  He has been off the Lipitor for 3 years and has
worked weekly with a Cognitive Rehabilitation Therapist, struggling to
recover from these adverse effects.  His neuromuscular damage is so
debilitating that he can hardly walk - a major improvement from the day that
he stopped taking the Lipitor.  He is in constant excruciating chronic pain.
His short term memory is still in the NP-tested "Impaired" range.  His
business is gone and he is unable to conduct daily activities in any
semblance of his pre-Lipitor routine.

Since he was afflicted by these horrific side effects and has become so
thoroughly disabled and is in so much pain and distress, I have made the
discovery that many, many others are similarly affected.

Since this is a support group that welcomes families of those with horrific
memory loss, and I am one of those, I come to this group for support, as
many others do.  I also offer my experience and what I have learned up to
others who might have been misled into thinking their loved one has
Alzheimers, if it is in fact possible or even likely that the damage is
actually a side effect of the most-prescribed of all drugs in the world
right now, and in history: Statins.

So far, the tragedy of Alzheimer's is not yet preventable.

Statin Cognitive Damage is absolutely preventable - it only takes an
awareness campaign and doctors monitoring for it.  So far they do not.
There is no reason for people to suffer statin memory loss, but far too many
do experience it.  I am in contact with 2 women this month alone, whose
husbands were tested below the 10 percentile in short-term memory, DUE TO
STATINS.  I know of 3 families who have lost their homes JUST THIS MONTH due
to the economic impact of this disabling condition striking the breadwinner.

How many people asked you if there were any chance of statin adverse effects
being eliminated as the cause of memory loss in the significant person in
your family, prior to a diagnosis of ALZ?  Any?  Why not?

You can read about my husband's case at:
http://www.n3inc.com/SmartMoneyReprint_103003Web.pdf

You can read about some of his amnesia episodes in "Lipitor, Thief of
Memory" at http://www.spacedoc.net/

There are also publication-pending medical studies that contain his case.
 
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