This case report discusses a patient with co-occurring neuroborreliosis and Alzheimer's disease (AD). Although no claim is made for causality nor is there objective evidence that spirochetes are involved in AD, co-infection may exacerbate the symptoms of either neuroborreliosis or AD. Much is to be learned about the role of spirochetes in degenerative central nervous system disease.
PMID: 16528463
I've often thought Pres. Ronald Regan likely had lyme...horseback riding, vacations to wooded areas, etc.
And now this:
Whereas horse owners repeatedly asked for examination of their horses, and some veterinarians asserted equine Lyme borreliosis to be an underestimated problem in the horse population, others stated the disease was often enough misdiagnosed.
PMID: 16524771
With Alzheimer's on the rise and the costs (financially and emotionally), perhaps now some attention will be made!
You can't let Mg-ATP levels drop. Mg is needed to make all proteins. If not enough = bad proteins.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Worthless tests & labs, a dangerous vaccine, insurance companies refuse to pay, undertreatment the norm, all about money. MO. Posts: 281 | From CT | Registered: Oct 2005
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mlkeen
Frequent Contributor (1K+ posts)
Member # 1260
posted
our llmd has recently started treating his Alzhiemer patients as having lyme. I haven't been in a while to know if they are improving.
It makes sense because we already know there is a connection between aluminum and Alzheimers and metal toxicity and lyme. It could be any one of the 7+ TBIs that triggers Alzheimers. It is certainly worth trying abx/ diflucan on these patients and looking for improvement.
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map1131
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posted
Marnie, I often had a gut feel on Ronnie too. The only thing about the alzhemiers I don't understand is...why do they die on average of 8 yrs after onset of sx?
Many on this board have gone years and years with no treatment. Lymetoo for example. So what makes these alz patients different?
Any ideas?
Pam
-------------------- "Never, never, never, never, never give up" Winston Churchill Posts: 6478 | From Louisville, Ky | Registered: Jan 2002
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posted
As for horses and Lyme. I got my bite and rash when I was an exercise rider for thorobred racehorses in N. Cal.. I was in an urban area. I know the odds are very , very high , I got a tick off of a horse. I was a professional athlete, in my prime physically. I watched in horror as I lost my body over the ensuing months. Nothing was more frustrating than the docs telling me it was in my head or it was "female strees", hysteria. Hell, I crawled out of ambulances after falls and spills, and these whankers are telling me I was faking It? I lost the thing I loved best in the world, riding. A pox on all their houses.
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Areneli
Frequent Contributor (1K+ posts)
Member # 6740
posted
< So what makes these alz patients different?
They are old
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mlkeen
Frequent Contributor (1K+ posts)
Member # 1260
posted
TBI is a trigger for ALZ as they are suspected for other diseases like MS, lupus, RA and Parkinson's.... Clearly we don't get all of those things, just like we don't get all of the symptoms for lyme or other TBIs.
There are genetic, physiological, immune system, dietary, enviromental and other factors that come into play for each individual.
We are just touching the tip of the ice-berg with our understanding that bacterial, viral and fungal issues may be triggers for many diseases that we didn't know the cause of in the past.
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david1097
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posted
My position on this is a bit different. A lot of investigation has gone into looking for a relationship between spirocheetes and brain disorders. I think this focus is primarily a result of the long history and known effects of syphillis.
There are a lot of other infections that can go neuro. Richesettia diseases are a notable in this regards. What is known about these very tiny bacteria and their variants... Almost nothing.
They are know to be sometimes be associated with odd skin lessions (sounds familiar), they do not culture well if even at all, they are intracellular, they grow slowly and they can go dormant for a while. They also multiply in both the cytoplasm and the nucleus of cells. (Does this means that some of the plasmids from the bacteria can be inducted into the DNA of the host cell??? At least the posibility exists....)
I really think that if they did very close examination of autopsy brians they would find a whole pile of "living" things that are not expected. Wether or not these things cause fatal disease I think is to a significant degree dependant on the genetics of the person affected. Now that people are living so much longer the problem becomes more apparent as the infection has more time to do its damage as the immunue system gradually wears down.
Most animals and earlier human generations don't have such apparent brain degeneration, mainly becuase they died of other things much earlier in life.
Along the same lines, I think in the next 30 years there will be a lot of discoveries about the relationship between living pathogens and human ailments, an area that lyme seems to be a forfront of at this time.
If this is true than us lyme sufferes can acutually be regardsed as pioneers in the field...Nice thought but higly unlikely..... Posts: 1184 | From north america | Registered: Feb 2003
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posted
on alzheimers, lyme, gray matter(brain's cortex) and white matter(under gray matter cortex).
paraphrasing a blurb by a lyme expert psychiatrist, an actual memory itself is in the gray matter, and most, if not all association with a memory is supposed to be in the white matter of the brain.
in alzheimer's dis., the memory is gone, and in lyme, for one thing, a memory is difficult to retrieve.
borrelia have a preference for subcortical structures of the brain, and white matter comprises many subcortical structures of the brain.
i don't know if, and how Bb affects gray matter.
thats as far as i can go with this.
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GiGi
Frequent Contributor (5K+ posts)
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posted
"Does this means that some of the plasmids from the bacteria can be inducted into the DNA of the host cell??? At least the posibility exists....)"
From Gitte Jensen's research (read her publications) we know that to be so. From knowledge that we have, RBC's do not have DNA - they do not have a nucleus with DNA in it. She simply looked for DNA in the Red Blood Cells; when she finds it, we know that it is foreign. It is alien. She found that over a lifetime the DNA in our RBC's is in a linear progression, more and more toward the end of life.
Another study she published (which should have been on the cover of Time Magazine!!!): that there is a direct relationship between the subjective feeling of wellness and the amount of foreign DNA found in our Red Blood Cells. It simply shows that illness is nothing but an accumulation of foreign bugs in us.
She also found that the DNA in white cells and other body cells, which do have a nucleus and have DNA in them, is twice as long when we die as it was when we were born. That means, as Dr. K. puts it, that at the end of our life we are only half "us" and half "them". Dr. K. calls it a huge discovery. Lyme Disease of course is just one of the many bugs that contribute to that.
I have become convinced that with some luck and with the help of a doctor that understands all this, we can clean up our body to the extent that residing in our body is just not attractive for them any longer. Right now, most of us are so toxic; the microbes in their quest for survival that is threatened by our pesticide mentality and our could-care-less attitude at our environment have become so aggressive, and more so every year, that they are getting the upper hand.
Lyme microbes are not the last ones that threaten us, I suspect, it is probably going to be even tougher as we move along in our SUV's and our plastic clothing, pots and pans.
Too bad many do not live long enough to comprehend the damage of our attitude and the attitude of the politicians we elect to office.
The only way out of this dilemna is - detox your body with every means at your disposal, just as we did. Both my husband and I got well that way.
Did you ever have a course of antibiotics in your life? That should clarify it for everyone, because all the experiments done on the spirochete/cyst form confirm: you give one patient one pill, and immediately you have the cysts appearing everywhere in the body. Obviously it's not the solution.
Dr. K.'s motto: Bring your body back up to snuff, so that the cysts will no longer want to hatch. The proof comes with every patient that has gotten well -- "change the inner environment, the milieu, so that the cyst does not feel like hatching."
Take care.
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bettyg
Unregistered
posted
quote:Originally posted by map1131: Marnie, I often had a gut feel on Ronnie too. The only thing about the alzhemiers I don't understand is...why do they die on average of 8 yrs after onset of sx? Pam
Pam, my late sister-in-law died at age 40, yes 40, after her early-onset alzheimer's illness of between 8-14 years. Again, 8 yrs. was very prominent from when we figured out what was going on with her brain.
She was treated for SEVERE DEPRESSION the entire time. Spent 1 wk. at Mayo Clinic going thru every test they had.
When she died, they got her brain & took almost 5 months to conclude it was Alzheimer's eliminating everything else including mongoloids.
They kept her brain tissue for any newer developments to give my brother's kids any results if this WAS the inheritable type or not; apparently NOT; thank God.
NO, Alzheimer's is NOT an old person's disease. There are about 10% plus young folks!
When my sister-in-law was dying, I had about a 24 year old!
Back to 8 years. All depends on their health prior to this & complications. They don't die of Alzhemer's but the complications:
pneumonia, choking since they forget how to swallow/chew, etc.
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Sorry, the following is long, but critical to understanding!
It is a choline deficiency that is triggering this whole mess (including the drop in other nutrients to try to counter).
Now, the KIND of choline to rebalance, does apparently make a difference.
Okay, for those of you who are interested in the choline links to Parkinson's, Alzheimer's, etc. here is some research:
You might reasonably conclude from this that all we need to do to slow down brain aging or Alzheimer's disease is supply more choline to the brain, but you'd be only partly right. The problem is that choline transport into the brain is not especially efficient and tends to decline with age.
There are two choline-based supplements that can do the trick--CDP-choline (cytidine 5'-diphosphocholine) and alpha GPC (alpha glycerophosphorylcholine).
Both are natural, water-soluble compounds that achieve similar results in very different ways. CDP-choline is an essential intermediate in the biosynthesis of phosphatidylcholine and the better studied of the two compounds.
Cells make CDP-choline out of choline and some other precursors before further processing it into PC. (If you're eager for the biochemical details, an enzyme catalyzes PC synthesis by transferring the phosphocholine part of CDP-choline to diacylglycerol. Diacylglycerols are glycerine molecules with two fatty acids attached.)
In contrast alpha GPC works at the opposite end of PC metabolism. Unlike CDP-choline, alpha GPC is a metabolic breakdown product of PC rather than a PC precursor.
You might say that whereas CDP-choline is an ``anabolic'' product, alpha GPC is a ``catabolic'' one.
When phosphatidylcholine is metabolized and stripped of its fatty acids, what's left behind is alpha GPC-a glycerine molecule bound to phosphocholine.
As such it's a source of choline in the same form that a cell would obtain from scavenging its own membranes, and therefore a form of choline that neurons prefer to use for synthesizing acetylcholine during times of choline scarcity.
Despite the fact that CDP-choline and alpha GPC are chemically distinct from each other and operate at opposite ends of the metabolic spectrum, both of them do pretty much the same thing.
For example, both alpha GPC and CDP-choline have been shown to improve performance on behavioral and psychological tests among patients with mild to moderate Alzheimer's disease 9, 10.
Both can also counteract the amnesia induced by scopolamine, a compound which blocks acetylcholine receptors 11, 12, thus confirming the role of the cholinergic system in the cognitive enhancing effects of alpha GPC and CDP-choline.
And both can promote cognitive recovery from a recent stroke 13, 14.
More generally, a review of all relevant, controlled clinical trials concluded that CDP-choline is beneficial for treating cognitive and behavioral deficits caused by chronic brain disease in the elderly 15.
This is in striking contrast to a similar review cited earlier that found no benefit for treating cognitive decline with choline in the form of lecithin 8. The superiority of CDP-choline over lecithin as a choline source should be evident.
Unfortunately, however, there's no comparable large-scale overview of the effects of alpha GPC as a cognition enhancer because alpha GPC is a newer product than CDP-choline and fewer studies have been done with it.
Nevertheless, as the following selected examples show, the effects of alpha GPC and CDP-choline are remarkably similar on the molecular and cellular levels and are therefore likely to be similar on the cognitive and behavioral levels as well:
� When incubated with brain tissue from rats, CDP-choline stimulates the activity of acetylcholinesterase (AChE), an enzyme involved in choline metabolism 16. Similarly, high-dose oral alpha GPC restores decreased AChE activity to more youthful levels in the brains of aged rats 17.
� Chronic administration of high-dose oral CDP-choline also restores the numbers of acetylcholine receptors in rat brain which otherwise decrease with normal aging 18. High-dose oral alpha GPC does the same 19.
� Both CDP-choline 18 and alpha GPC 19 decrease the viscosity (stiffness) of cell membranes, an effect almost certainly due to increased phosphatidylcholine synthesis.
Another useful property shared by alpha GPC and CDP-choline is that oral administration of either one increases the release of the neurotransmitter dopamine in the brain 20, 21.
It's worth recalling that defective dopamine signaling is associated with Parkinson's disease in much the same way that defective acetylcholine signaling is associated with Alzheimer's disease.
There is evidence of enhanced PC metabolism in Parkinson's, perhaps as a result of brain cells trying to compensate for the neurodegenerative process 22.
In this sense there may be an increased demand for CDP-choline or alpha GPC in Parkinson's disease, where they may be needed to rebuild damaged cell membranes and to facilitate dopamine release as well.
L-DOPA is an amino acid precursor to dopamine that is widely used in treating Parkinson's.
Animal studies have shown that oral CDP-choline treatment enhances the effects of L-DOPA by increasing the release of dopamine newly synthesized from it 23.
In human trials, a combination of CDP-choline with L-DOPA was able to improve neurological symptoms with a smaller effective dose of L-DOPA than patients had previously received without CDP-choline 24, 25.
This result is important because chronic use of L-DOPA eventually results in neurotoxicity and loss of clinical effectiveness.
The hope is that by combining CDP-choline with smaller doses of L-DOPA, it may be possible to prolong the period during which L-DOPA remains effective.
In view of the known ability of alpha GPC to enhance dopamine release as well 20, a similar therapeutic enhancement of L-DOPA activity is also likely to occur with alpha GPC, but there aren't any clinical data available yet to confirm this suggestion.
Since chronic cocaine abuse is likewise associated with dopamine depletion and increased turnover of cell membranes, the choline-dopamine connection predicts that CDP-choline and alpha GPC should each be effective for treating cocaine addiction.
This has indeed been verified for CDP-choline 26 but not yet for alpha GPC.
In addition, I will personally go out on a limb here and predict that CDP-choline, alpha GPC, or both should be helpful in treating attention deficit hyperactivity disorder (ADHD), either as an adjunct to stimulants like Ritalin or as stand-alone supplements.
I base my conclusion on the known involvement of dopamine metabolism in ADHD 27 as well as on the dopamine-releasing and cognitive enhancing effects of CDP-choline and alpha GPC discussed in previous paragraphs.
Finally, there at least one more important anti-aging property shared by CDP-choline and alpha GPC-they're both growth hormone (GH) sensitizers 28, 29.
As you probably know, GH levels decline with age, resulting in age-related decreases in bone mass and in muscle mass and strength 30.
You may not be aware, however, that GH decline is also associated with age-related cognitive impairment 31.
The cholinergic system is an important part of the mechanism that regulates GH release stimulated by GHRH 32. Here GHRH (growth hormone-releasing hormone) is the hypothalamic hormone that triggers secretion of GH from the pituitary.
Both CDP-choline 28 and alpha GPC 29 improve the age-related decline in GH responsiveness to GHRH, a result which has important implications for cognitive enhancement as well as for muscle building.
Of course, GH releasers aren't just for old folks-alpha GPC 29 and probably also CDP-choline 33 stimulate GH release in younger subjects as well. This suggests the use of either or both as nutrients for sports, exercise, and weight training.
At this point I think I've made my case-CDP-choline and alpha GPC are both effective choline supplements for enhancing mental and physical performance and counteracting age-related decline.
The big question is, which supplement is better?
That's a tough one to answer because there are only two published studies I'm aware of that directly compare the activities of each compound. The first study reported that the use of 1 gram per day of alpha GPC produced higher cognitive test scores in subjects with vascular dementia than did 1 gram per day of CDP-choline 34.
The second study reported that alpha GPC raised plasma choline levels substantially higher in normal subjects than CDP-choline did 35.
On the face of it, the two studies comparing alpha GPC and CDP-choline would seem to indicate that alpha GPC is the more effective of the two compounds, but things aren't quite that simple.
For one thing, both studies compared the effects of alpha GPC and CDP-choline administered intramuscularly rather than orally.
For another, an increase in plasma choline levels may not be especially meaningful as a measure of enhanced activity or bioavailability of alpha GPC, since the lower plasma choline associated with CDP-choline injection might simply reflect an increased tissue uptake.
To gain some insight into this issue, let's take a look at what happens to CDP-choline and alpha GPC after they are ingested.
Orally administered CDP-choline is broken down into its components in the intestine, absorbed individually as choline and cytidine, and subsequently put back together again in various tissues 36.
Experiments with cultured brain cells reveal that soon after the cells are incubated with CDP-choline, newly synthesized PC can be detected 37.
The same does not happen if the cells are incubated with choline itself, suggesting that either a specific mechanism for uptake of intact CDP-choline exists 37 or else that brain cells can use choline efficiently for making PC only if cytidine is also present 38.
Either way, CDP-choline gets into the brain and more phosphatidylcholine gets made.
As for alpha GPC, it's believed that intestinal enzymes known as phosphodiesterases are responsible for cutting it into its components 39, but there's no information I can find on what percentage of an administered dose of oral alpha GPC is likely to make it through the gut intact.
My best guess, however, is that a fair amount does get through and in fact makes it into the brain. The reason for this is that in animal experiments only alpha GPC-and not choline nor any other breakdown product of alpha GPC-is able to reverse age-related decreases in brain acetylcholine receptors and membrane fluidity 19.
As a result, if all of an orally administered dose of alpha GPC were to be broken down in the intestine, plasma choline levels would indeed be elevated but you still wouldn't get the same beneficial effects that alpha GPC is known to provide.
Therefore, some of the alpha GPC must make it to the brain intact, otherwise there'd be no difference between taking alpha GPC and choline...and clearly there is a difference.
So if you're trying to decide between CDP-choline and alpha GPC as a cognitive enhancer, my advice is: choose either.
They do pretty much the same thing and I'm not convinced that either one is superior to the other. Better yet, I suggest trying a combination of both for optimal effect, since they work from complementary ends of PC metabolism.
A good place to start might be to try one 250 mg capsule per day of either alpha GPC or CDP-choline for several days until you can gauge the effect. If you're happy with the results, stop there.
If not and you're looking for more intense cognitive stimulation, trying adding a single capsule per day of the other enhancer to your regimen, so that you're taking a total of one apiece.
You can gradually increase the dosage of either if desired, since both nutrients are reportedly well tolerated with few if any side effects.
And if you can stand taking caffeine, consider washing down your capsules of alpha GPC and CDP-choline with a strong cup of java. The caffeine acts as a nonspecific phosphodiesterase inhibitor 40 and should therefore allow more of each nutrient to be absorbed intact.
CONCLUSIONS: CDP-choline can stimulate brain AChE and Na(+), K(+)-ATPase independently of ACh and noradrenaline. This enzymatic stimulation may be due to the transformation of CDP-choline to membrane phophatidylcholine. The above data could explain in part the clinical effects of this substance in some neuronal disturbances.
PMID: 11018686
These results indicate that CDP-choline affects GH and PRL secretion from the anterior pituitary. cytidine diphosphate choline (CDP-choline), growth hormone (GH) and prolactin (PRL) PMID: 639755
These results show that long-term treatment with CDP-choline increases the K+ induced release DN and suggest, in accordance with previous research, that by providing exogenous choline and cytidine, CDP-choline modulates dopaminergic transmission.
(Helps with Parkinson's)
PMID: 11193174
These studies demonstrate that cytidine 5'-diphosphocholine can enhance basal and GHRH-stimulated GH release in the elderly, but the mechanism of action of the drug remains unclear. PMID: 2028709
A multicentre trial to evaluate the efficacy and tolerability of alpha-glycerylphosphorylcholine versus cytosine diphosphocholine in patients with vascular dementia.
Both treatments produced a definite symptomatic improvement and showed a very good tolerability. The results suggest that in most tests alpha-GPC possessed a statistical higher efficacy and an overall more satisfactory activity assessed by both patients and investigators compared with CDP.
In the liver, fat and cholesterol are packaged into lipoproteins called very low density lipoproteins (VLDL) for transport through the blood to tissues that require them.
Phosphatidylcholine is a required component of VLDL particles. Without adequate phosphatidylcholine, fat and cholesterol accumulate in the liver.
Major source of methyl groups
Choline may be oxidized in the body to form a metabolite called betaine. Betaine is a source of methyl (CH3) groups required for methylation reactions. Methyl groups from betaine may be used to convert homocysteine to methionine.
Elevated levels of homocysteine in the blood have been associated with increased risk of cardiovascular diseases.
Men and women fed intravenously (IV) with solutions that contained adequate methionine and folate, but lacked choline have developed a condition called "fatty liver" and signs of liver damage that resolved when choline was provided.
Choline is required to form the phosphatidylcholine portion of very low density lipoprotein (VLDL) particles. VLDL particles transport fat from the liver to the tissues (see Function). When the supply of choline is inadequate, VLDL particles cannot be synthesized and fat accumulates in the liver ultimately resulting in liver damage.
Because low density lipoprotein (LDL) particles are formed from VLDL particles, choline deficient individuals also have reduced blood levels of LDL cholesterol (6).
Healthy male volunteers with normal folate and vitamin B-12 nutritional status fed a choline deficient diet developed elevated blood levels of a liver enzyme called alanine aminotransferase (ALT).
Elevated ALT activity is a sign of liver damage. Liver damage appears to be the result of increased liver cell death. In cell culture, liver cells initiate programmed cell death (apoptosis) when deprived of choline.
The human requirement for choline is affected by its relationships with other methyl group donors such as folate and S-adenosyl methionine (SAM). See diagram.
The methyl group donor (SAM) is synthesized from the amino acid, methionine. Three molecules of SAM are required for the three methylations of phosphatidylethanolamine required to synthesize phosphatidylcholine.
Once SAM donates a methyl group it becomes S-adenosyl homocysteine, which is metabolized to homocysteine.
Homocysteine can be converted to methionine in a reaction that requires methyl tetrahydrofolate (THF) and a vitamin B-12-dependent enzyme.
Alternately, betaine (a metabolite of choline) may be used as the methyl donor for the conversion of homocysteine to methionine (2).
A recent study of 21 men and women fed diets that varied in folate and choline content indicated that choline is used as a methyl group donor when folate intake is low,
and that the de novo synthesis of phosphatidylcholine is not sufficient to maintain adequate choline nutritional status when dietary folate and choline intakes are low.
A large body of research indicates that even moderately elevated levels of homocysteine in the blood increase the risk of cardiovascular diseases (7).
For more information on homocysteine and cardiovascular diseases, see Folic Acid.
Choline, when oxidized in the body to form betaine, provides a methyl group for the conversion of homocysteine to methionine by the enzyme, betaine-homocysteine methyltransferase (BHMT). See diagram.
Despite its relevance, the relationship of betaine and choline to homocysteine metabolism has been only lightly investigated in humans.
Methodological problems make betaine and BHMT difficult to measure. One study found higher urinary excretion of betaine and its metabolites in patients with vascular disease and elevated homocysteine levels than in control subjects, suggesting that elevated blood homocysteine levels were not related to reduced intake of choline or betaine or diminished activity of BHMT (8).
In preliminary studies, pharmacologic doses of betaine (1.7 to 6 grams/day) were found to reduce blood levels of homocysteine in a small number of patients with vascular disease and elevated homocysteine levels.
Although further research is indicated, convincing evidence that increased dietary intake or blood levels of choline or betaine affect homocysteine levels in humans is presently lacking (9).
Cancer
In rats, dietary choline deficiency is associated with an increased incidence of spontaneous liver cancer and increased sensitivity to carcinogenic chemicals.
A number of mechanisms have been proposed to explain the cancer promoting effects of choline deficiency:
a) choline deficiency causes liver damage and regenerating liver cells are more sensitive to the effects of carcinogenic chemicals,
b) choline deficiency results in decreased methylation of DNA, resulting in abnormal DNA repair,
c) choline deficiency results in increased oxidative stress in the liver, increasing the likelihood of DNA damage,
d) choline deficiency may stimulate changes in the programmed cell death (apoptosis) of liver cells, contributing to the development of liver cancer, and
e) choline deficiency activates the potent cell signaling molecule, protein kinase C, which creates a cascade of effects that are still being investigated (2,4).
The implications for choline deficiency on human susceptibility to cancer remain unclear.
Methotrexate, a medication used in the treatment of cancer, psoriasis, and rheumatoid arthritis, limits the availability of methyl groups donated from folate derivatives by inhibiting the enzyme, dihydrofolate reductase.
Rats given methotrexate have shown evidence of diminished choline nutritional status including fatty liver, which can be reversed by choline supplementation (2). Thus, individuals taking methotrexate may have an increased choline requirement.
posted
Brief comment and the article can speak for itself. Someone asked if this will make a difference in the attitude of the gov't toward lyme. Nope, they will not allow abx to treat the masses against borrelia. aint gonna happen, and I can see their point. As for someone who has alzheimer's like symptoms I say treat us (whether it's a patentable drug or not) or put us out of our misery. this S*^t sux. and good god get these people some medical cannabis. Just plain inhumane.
Alzheimer's disease--a spirochetosis? Miklossy J.
Division of Neuropathology, University of Lausanne, Switzerland.
The aetiology of Alzheimer's disease (AD), which affects a large proportion of the aged population is unknown and the treatment unresolved. The role of beta amyloid protein (beta A4), derived from a larger amyloid precursor protein (APP) in AD is the subject of intense research. Here I report observations that in 14 autopsy cases with histopathologically confirmed AD, spirochetes were found in blood and cerebrospinal fluid and, moreover, could be isolated from brain tissue. Thirteen age-matched control cases were without spirochetes. Reference strains of spirochetes and those isolated from brains of AD patients, showed positive immunoreaction with monoclonal antibody against the beta amyloid precursor protein. These observations suggest that spirochetes may be one of the causes of AD and that they may be the source of the beta amyloid deposited in the AD brain.
PMID: 8369471 [PubMed - indexed for MEDLINE]
Posts: 731 | From Humble,TX | Registered: Feb 2005
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map1131
Frequent Contributor (5K+ posts)
Member # 2022
posted
Yes, Betty I am very aware of the very young that die from alz. So the "because they are old", is not the real story.
It really sucks that a 40 yr old would be labeled alz and it accepted until her death. Bull!
Grrrr!!!!
Pam
-------------------- "Never, never, never, never, never give up" Winston Churchill Posts: 6478 | From Louisville, Ky | Registered: Jan 2002
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