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Alzheimer's and Autism

Herpes By Kent Heckenlively, Esq.

One of the key issues put forward by the attorneys for the families in the Omnibus Autism Proceeding was whether the measles virus could survive for years in children with autism without being eradicated by the body.

Recent research from the University of Manchester points to the continued persistence of viruses in the body where they may be responsible for the amyloid plaques which are the hallmark of Alzheimer’s disease. (“Herpes Simplex Virus Type 1 DNA is Located within Alzheimer’s Disease Amyloid Plaques”, The Journal of Pathology, Volume 217, issue 1, pages 131-138)  The research was also highlighted in an article in Science Daily. (“Cold Sore Virus Linked to Alzheimer’s Disease, December 7, 2008)

While the virus found in the study was herpes simplex 1, the virus responsible for cold sores, I was intrigued by this finding as my own daughter had especially high titers for herpes varicella-zoster, the virus which causes chicken-pox in children, or shingles in adults.  Other researchers have suggested the involvement of the cytomegalovirus (another of the herpes virus family) in autism.

The research was so convincing that the lead sentence to the Science Daily article boldly stated, “The virus behind cold sores is a major cause of the insoluble protein plaques found in the brains of Alzheimer’s disease sufferers.”

During my review of testimony from the Omnibus Autism Proceeding I was struck by the lack of specific knowledge about so many aspects of viral pathology.  Even the witnesses for the defense stated that the process by which viruses were “attenuated”, or “weakened” was akin to putting the viruses in a “black box” and then trying to figure out how they were different when they came out.

The connection between viral exposure and genetics that many believe underlies autism was also present in the findings relating to herpes simplex 1 and Alzheimer’s.  From the Science Daily article, “The team had discovered that the virus is present in brains of many elderly people, and that in those people with a specific genetic factor, there is a high risk of developing Alzheimer’s disease.”  The researchers noted that the virus is widespread in the general population, often remaining for life in the peripheral nervous system, causing cold sores for approximately 20-40% of those infected.

In fact, the regression which so many people link to vaccinations might be explained by a process similar to what Dr. Itzhaki, one of the paper authors, describes as their explanation for the progression of Alzheimer’s disease.  “We suggest that HSV 1 (herpes simplex virus) enters the brain in the elderly as their immune systems decline and then establishes a dominant infection from which it is repeatedly activated by events such as stress, immunosuppression, and various infections.”

Another striking similarity is that the researchers have used acyclovir, an anti-viral drug used by many children with autism as a way to ameliorate some of the more severe features of autism, “in preliminary experiments they have shown that acyclovir reduces the amyloid deposition and reduces also certain other features of the disease.”

Could research involving Alzheimer’s give some clues about the possible connection between viruses, immune-suppression, and genetics?  Will the pieces of this puzzle ever form a coherent picture?

The search for the cause of autism often reminds me of the tale of the six blind men who are asked to describe an elephant using only their sense of touch.  One feels the leg and says the elephant is like a pillar.  Another feels the tail and says the beast is like a rope.  The third blind man feels the trunk and says it’s like a tree branch. The fourth feels the ear and says it’s like a hand fan.  The next feels the belly and says it’s like a wall.  The last feels the tusk and proclaims the elephant is definitely like a pipe.

Each one is correct, but they need to combine their observations to form an accurate picture.  I imagine that to truly understand autism we’re all going to be presented with a similar challenge.

Kent Heckenlively is Legal Editor of Age of Autism

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Kent who wrote this article has his daughter on the ketogenic diet and said he was amazed at how well it was working.

Jon Poling neurologist and former FDA employee, father to Hannah Poling that was damaged by a vaccine that said that her mitrochondia disorder was made worse by vaccines and who also won a large settlement from the vaccine compensation court:::: IS ON THE 15 CARB a Day Dr. Atkin's Diet to control her seizures.

Rob;
Some history on epilepsy diets might help you decide what to do. I hope this helps.

Probably since the beginning of agriculture there the cure of epilepsy was starvation. This cure was mentioned in the Bible and by both Greek and Roman physcians.

Diet and the immune system are tied together.
That is why famine was often followed by plague.
That is why measles was nothing disease in a well feed child (a new born or in the womb - still having mother's antibodies) did okay. However; measles in a refugee camp or concentration camp turned deadly.

In the 1930s John Hopkins was studing diets for diabetics.
During this time the Ketogenic diet came about for a cure for epilespsy. It cured a little more than 30 percent of the those with epilepsy; but the other 60 percent were all greatly improved too.
The Ketogenic diet was a difficult diet to follow. Even water was measured. You start it off with fasting for a couple of days, and then they drink a lot of cream, some measured amount of protien and nuts all measured out. You can get books on it. It is suppose to be under the supervision of a doctor (But good luck in getting one to help you toward that end).This diet was suppose to help the body prolong the starvation type diet. The diet was not a life long diet but one only for 2 years.

In the 1950's when soldiers went off to WWII, and they discoverd that coconut oil could be used in the place of IVs --- a new discovered medium chain triglycerides (MCT oil) made from coconut oil was added to the Ketogenic diet.
When they added the MCT oil it allowed more carbohydrates to be added to the Ketogenic diet. But best of all it increased the cure rate almost up to 40 percent!

A little after this, drugs for epilespy came into play and they threw out this baby and bath water. What a shame!

Why it works: We think!!!
Our bodies have have two pathways to make energy.
1) carbohydrates metabolizes into glucose
2) Fats into ketones
and then there is protein. Protein is used by the body for so much other things than energy it is seldom wasted to that purpose. But if a lot of protein is eaten in huge quanities the body will turn it into glucose.

The fat to Ketones do not come into play as long as there are carbs in the body. You can get rid of Carbs in your body in less than 24 hours.

Maybe?????? The immune system the ones that produce IgG -- is made from carbohydrates.

It reminds me of the story of Cain and Abel at the beginning of the Bible. At the beginning of Agriculture.
Two different men sacrificing two different things to the God (perhaps meaning the best for the human body?). Perhaps it is a metaphor for two different pathways -- and when agriculture won out -- the sign on the forehead and hand (in the Bible sign on head means thinking and hand meant not good control of hands).
But I getting off topic.

Back in the 1980s Dr. Atkins was working on a good diet for diabetics. Dr. Atkins had a three step program. The first step lasted two weeks at least, and no more than 20 carbs a day would be consumed. Then there was a second stage were more carbs were consumed but slow released ones; and finally a third stage -- were the dieter has learned to slow release carbs and healthy ones at that. I learned that berries are slow release; were as oranges and apples are faster. Eating one apple as day was 20 carbs and blew the rest of the day for carbs!!

In 2005 in an "The Epilespy Magazine" there was an article about John Hopkins doing research on Dr. Atkin's diet. It said that epilespy could be controlled by a modified Atkin's diet of no more than 15 carbs a day. Kind of blows eating an apple -- for a while anyway.

John Hopkins-- also did some other research on slow release carbs and if they have the right types of foods up to 30 to 60 carbs can be consumed a day -- that would work too!

Recently some research has come out that some women with a genetic prone to breast cancer had taken two days out of the week and eat no carbs at all. And it appeared to work.

What we did was bought an Atkin's diet book went through the diets at the back of the book, and recipes --- we were on the 20 carbs for about a year, and then went to slower release carbs. Now we always watch our carbs, make sure they are slower release/ try to substitue wheat flour, soy flour, soy protien, whey protein, wheat bran, oat bran, oatmeal, brown rice flour, millet flour, cornmeal, dried-gound chick peas and on and on--instead of just white processed flour. . I bought some nice large mouth glass cansistors for all of this.

And two days a week we try to stay under 15 carbs.

Also Atkin's does not care what kind of fats you use. I care. I threw out margarine and use only butter, coconut oil, olive oil, canola oil.

Hope this helps and it is not too much information.

I have been researching on line about nutritional therapy , vitamins and other recognised nutritional suppliments that may have an influence on persons who are afflicted with autism and or alzheimers in their family. I recently heard and red about the use of coconut oil on a daily basis that helps those with alzheimers, My reason for this interest is my 6 yr old nephew has autism and my mother at 90 years of age was diagnosed with alzheimer's before she died at age 95. Has anyone else found similar nutritional research on this subject ? If so please share it with me and others , who knows we may have found a cure that is NON pharmaceutical or chemical .

Some parents of autistic kids, for instance, claim that heavy-metal poisoning is a cause of autism ... There is no medical evidence to support that claim.

Hi i read the article with interest.

Autism is complex and depending on the person, i suppose, can lead to mis-diagnosis. I’d be grateful if you can provide us with the source of your information (i.e. research paper for Namenda). As a father with a ASD kid, i’m inetrested in learning all avenues of research.

Cheers

Dear all, A beta amyloid causes a number of secondary events. Peroxide release, stimulation of an imflamatory response by microglea, etc. The bottom line is that inflamation is already a know predisposition to activation of latet herpes virus!!! Sun,injury, irretati, other infection, all predispose to cold sores. A correlation of finding HSV in the inflamatory cells associated with plaq is just that an association. Perhaps what im saying is lost - in translation. Cities have lots of high tension power lines - cities also have lots of care accidents. This is an association every bit as valid as the results that are published. In science we publish associations sometimes. The only invalid thing here is to conclud the power lines cause traffic accidents - or that HSV causes alzheimers. (it is trivial to demonstrate that there are hsv seronegative individules who develop alzheimers.) So it is possible to lay people and scientists to draw incorrect conclusions. This is usually caught in the review process. Sorry for the spelling errors.

I wanted to respond to Lillian (the first poster after the article)... I find it so interesting that the nurse practitioner from the VA said that. I read in a Psychology Today article from a few years ago (highlighting a young woman with Aspergers) that Autistic/Asperger people usually have a characteristic round face with round eyes and are very pretty. I have noticed these features as well when I see someone with either syndrome.

My Dad has been recently diagnosed with Alzheimer's Disease so I am new to all this research data etc. One thing that interested me greatly was when a nurse practitioner who has worked in a VA hospital (mostly male patients) for many years (she is age 75 and still works!) asked me if my Dad was a handsome man. When I told her yes....that when he was younger, he was extremely handsome. She shook her head knowingly, as if she knew my answer before I gave it. She said in all her years experience in the medical field she had noticed that autistic children are usually extremely beautiful children and Alzheimer's patients were extremely handsome men (she didn't know much about female Alz. patients). She said she couldn't help but notice that for many many years. After I started thinking about it, I too, realized that every man I know/knew that had/has Alz. disease was/is very handsome!
Also she stated she thinks there is some correlation in the children's autism and Alzheimer's disease. Just thought I'd pass this along. Enjoyed all the postings. I have a LOT to learn. Thanks, Lillian

Hi

I am a mom of a nine year old boy who was diagnosed with Autism at the age of 5. I came across your website doing some digging looking for a connection between herpes type 1 and Autism. My son had his initial outbreak of herpes type 1 at age 2 and has been on Acyclovir daily since the age of 3. He is know beginning to outgrow his dose and testing has begun to try to figure out why these outbreaks are continuing. I thought your posting was interesting and I would love it if you could share any further information with me. I swear there is a connection and I'm desperately looking for answers. Thank you.


Vijendra K. Singh has written several articles on Alzheimer's and autism.

The latest one is........

Serum Analysis of Amyloid Beta Protein in Healthy Subjects, Autistic Children and Alzheimer's Patients

which I have an attachment that I can send to those interested at RayGallup@optimum.net

The article referenced one article in 1977 on Alzheimer's and neuroautoimmunity.

Swedish studies (Ilback et al) have shown many interesting correlations between viral infections and increased uptakes of heavy metals during infection, as well as their redistribution to the brain.

One of their studies concluded that "...Enteroviral infections may therefore be an underlying factor regarding the changes in ... potentially toxic trace elements in the brain."

On the other hand the same team also experimented by exposing mice to mercury prior to infecting them with a common virus, and found that "..virus persistence tended to be influenced by MeHg in a direction compatible with the development of chronic disease..." and that "placental and lactational transfer of MeHg does adversely affect the developing immune system of the rat... (Natural killer (NK) cell activity was reduced by 42% in mercury exposed mice)."

Kathy, thank you for your comment about Lyme! My husband, myself, and our two kids, ages 7 and 2 years, were recently diagnosed with chronic Lyme disease. We have never lived on the east coast. My kids have gestational Lyme disease, meaning they got Lyme disease from me, in utero.

We all have low CD57. My husband has very high HHV6 and a horrible yeast problem (I and my kids haven't been tested for HHV6 yet).

I am SO THANKFUL that I never vaccinated my kids! I truly believe that they would be autistic if I had vaccinated them. I also never gave them Tylenol, or any drug at all. I am not afraid of fevers and have never lowered them, despite my daughter's frequent previously unexplained fevers (from Lyme). Because Lyme is the only stressor in their bodies, they have been able to tolerate it without showing symptoms. They are now being treated with long term antibiotics (and probiotics)! I have always been against antibiotics, but this is one of the situations where they are truly needed.

I have many extended family members who I know have long term, chronic Lyme disease, but they refuse to get tested and treated. I know in my heart that they will get Alzheimer's from Lyme if they live long enough. It is so sad.

Although my kids narrowly escaped autism, so I am not personally affected by it, I have been following Age of Autism because I see the autism epidemic as a problem of epic proportions. It has changed the world and will continue to change the world and I just cannot believe that the majority of people are blind to that! Every day I wonder when it will all explode to the point where nobody can deny it.

Kent
I propose also another agent at hand that could cause autism and ALZ. If you look on google the following "DR ALAN MACDONALD SPIROCHETES", you will come to his very busy web page. I advocate all to study it in entirety. He has articles and PICTURES of amyloid plaques, that have the signiatures of borrelia lyme spirochetes on them (L forms, cysts, etc). I propose the following thought pattern...what if an adult has lyme, and placentally give the bacteria to child (very possible), and that vaccines activate that bacteria by lowering CMI, and also damaging TH1 TH2? This would allow bacteria and opportunistic fungi to spring forth. Since it has been known that syhpilis can cause autism in utero, why not cause another spirochete family member, lyme, to this fold? As I type, Dr Robert Bransfield is putting forth not only this hypothesis, but also actual clinical study from our family, this is entirely possible.

STILL, we have HIGH hhv-6, which is known to be the co infector of lyme infected people. They chum up with one another often. As well as mycoplasma F, which is found in GWS, and autistic kids (58 percent tested by Dr Nicholsen), which would cause immune collapse, low glutathione, metabolic ATP shifts causing mitochondrial disorders, etc. Most kids with lyme, have low CD 57...check it out, this is the BIOMARKER of lyme disease.


Then you put on that soup, mercury, aluminum and other heavy metals, fluoride aluminum, dioxins, PCB's, TCE's and the whole gammit, that now, you have kids with not only toxic bodies, which again, lowers immune response to pathogens, but the inability to detox, or WORK ON, the virus, therefore, the virus, the bacteria, are living day to day, proliferating colonies in the gut, brain, bone marrow, you name it.

This causes major oxidative stress, as well as ongoing inflammation in the brain. Call out the cytokine troops, more damage is being done. REduce fever during a vaccine reaction/during pregnancy with a flu, and you cause the inability to have a fever response (ever notice our kids often have low grade fevers or spike them)?. The point being...

MANKIND has caused this mess, and I blame MAN, not GOD, MAN, on this disaster.

This is why, antivirals, anti inflammation, and anti bacterials work in kids with autism (natural, and unfortunately pharma). And yes, I propose LONG TERM ABX's, because this would kill off year long colonies of lyme. This is why kids with autism deteriorate...they stop giving abx's, and the buggers mutate. Seek a lyme literate DAN doctor (www.liafoundation.org ).

It may seem, that lyme only exist in a state on the east coast...this is the big lie. For, if it is sexually transmitted, can cross into the placenta, is in breastmilk, possibly in our milk and blood supply, if not meat, then, who is safe from lyme? Biting mosquitos, yes, lyme. Biting bed bugs, yes lyme. Biring spiders, lyme. Anything that sucks your blood. FLEAS in your house? Bartonella. Answer, no one is free from this NUMBER ONE vector disease in the country...and, it is paralleling the autism epidemic. The most autism in the state, seem to also correlate with lyme incidences as well.

This does not dispute your findings, because it is possible CMV, EBV, HSV can cause all of these things too...but I look at viruses as opportunistic...they come upon our bodies when we are excreting a heck of a lot of cell poop...metabolic poisons, bacteria, fungi...

Wow, is this food for thought! You are definitely on to something. My son is recovering ASD with no viruses, but my non-ASD daughter has speech and motor issues, is high HSV 1&2 as well as HHV6. She is also high aluminum, mercury and lead. There was another study recently showing that aluminum damages the blood/brain barrier, and the Shaw study showing a link between aluminum hydroxide in vaccines and motor neuron death, linking it to ALS and Gulf War Syndrome.

Both of my paternal grandparents had Alzheimer's.

Kent,

Interesting article on HSV1 and AD, had never really thought about that. they tried a vaccine for AD called AN1792, but it triggered fatal brain inflammatory disease (ADEM) in too many of the study group and got shelved.

I have a question. So in your elephant analogy is Paul Offit touching the underbelly or does he have his head up the elephant's A$$!!?? or maybe both!

As for the problem with persistent measles virus, I've been wondering lately:
The Oral Polio Virus contained live polio virus and in some people the vaccine actually caused paralysis and death (the very symptoms it was intended to prevent), and was therefore replaced with the inactivated polio virus vaccine.

Likewise, the MMR contains live measles virus. Wild measles virus can cause chronic encephalitis (SSPE) in 1 out of 100,000 cases (according to wikipedia). So why is it so hard for the medical community to believe that the MMR could cause autism when children with autism have chronic brain inflammation as proven by MRI's? And because measles is a neurotoxic illness why don't they use an inactivated measles vaccine, instead of injecting live measles virus into children; especially after having previously given them many shots which contain aluminum (which is known to damage the BBB; the very thing designed to protect our brains from dangerous viruses)?

I also agree with you whole-heartedly that the answers to the autism epidemic may be found by looking into AD because both of those diseases cause people to lose previously aquired skills. I've also wondered if the reason aluminum's possible causative role in AD has been so controversial is because aluminum is also in vaccines (in amounts that exceed the minimal risk level), and therefore, it wouldn't take long to make a connection between vaccines and regressive autism...

The elephant analogy is so true!

Thanks for the great article!

Aside from viruses there is the issue of
ineffective Choline transport/supply to the brain.
We won back our ASD child's memory with Alzheimer supplements - of all things!
Want to terrify a mother? Have her ASD child forget things the moment they are gone and attend a mainstream public school.
Getting to the bottom of memory issues was on the top of my list 2 years ago.
Leading me on a trail to study dementia. Low and behold there are many connecting dots, glutamate issues, metal poisoning, hormones, choline transport and plaque exist in both old and young populations managing brain toxicity.
When we tested my son he showed free radical damage (lipid peroxide) on the cell membrane making sense of why Phosphalipids gave us such great gains. Everyday before school he takes his "old people" supplements,Ginkgo,ALCarnitine,Phosphalipids,NADH.
You don't inject Mercury into old and young and escape brain damage.
I am happy to report our son's memory was restored inside of a year on Alzheimer supplements.
Paris Kidd PhD is a great read on this old-young connection as well as the Braintrust Program book.
I often say vaccines went through my kid like a hornet damaging many vital systems.
By the grace of God we will heal them all.


Hi Kent
It is increible the amount of research on Alzheimer, infections and toxic elements impact:
Some very recent manuscripts
Exp Neurol. 2008 Dec;214(2):293-300. Epub 2008 Sep 12. Links
Effects of oral aluminum exposure on behavior and neurogenesis in a transgenic mouse model of Alzheimer's disease.Ribes D, Colomina MT, Vicens P, Domingo JL.
Department of Psychology and Research Center in Behavioral Assessment (CRAMC), Rovira i Virgili University, 43007 Tarragona, Spain.

The effects of a very low oral dose of Al on spatial learning and neurogenesis were evaluated in a transgenic mouse (Tg 2576) model of Alzheimer disease. At 5 months of age, wild and Tg 2576 mice received a diet supplemented with Al lactate at 0 and 1 mg/g of diet for 120 days. The experimental groups (n=7-8) were: control wild, Al-treated wild, control transgenic, and Al-treated transgenic. After 3 months of Al exposure, activity in an open-field and learning in a water maze were evaluated. At the end of the behavioral testing, in order to study cell proliferation and differentiation in the hippocampus, mice were injected with 5-bromo-2-deoxyuridine (BrdU) and sacrificed 1 or 28 days after the last BrdU injection. Tg 2576 mice were impaired in both acquisition and retention of the water maze task, showing higher amounts of beta-amyloid fragments in brain. Aluminum exposure impaired learning and memory in wild mice and increased the total number of proliferating cells in the dentate gyrus of hippocampus. The low Al doses here experimented suggest that this element might impair cognition in the general population at doses comparable to current levels of human exposure. Although these doses are not enough to interact with the amyloidogenic pathway, an increase in cell proliferation can indicate a reactive response of the brain to Al insult. Further investigations should be performed to corroborate the effects observed at very low doses of Al and to study the potential effects derived from a longer exposure period.

Rev Lat Am Enfermagem. 2008 Jan-Feb;16(1):151-7. Links
Aluminum as a risk factor for Alzheimer's disease.Ferreira PC, Piai Kde A, Takayanagui AM, Segura-Muñoz SI.
College of Nursing, University of São Paulo at Ribeirão Preto, SP, Brazil. sininha83@yahoo.com.br

The purpose of the study was to condense existing scientific evidence about the relation between aluminum (Al) exposure and risk for the development of Alzheimer's Disease (AD), evaluating its long-term effects on the population's health. A systematic literature review was carried out in two databases, MEDLINE and LILACS, between 1990 and 2005, using the uniterms: "Aluminum exposure and Alzheimer Disease" and "Aluminum and risk for Alzheimer Disease". After application of the Relevance Test, 34 studies were selected, among which 68% established a relation between Al and AD, 23.5% were inconclusive and 8.5% did not establish a relation between Al and AD. Results showed that Al is associated to several neurophysiologic processes that are responsible for the characteristic degeneration of AD. In spite of existing polemics all over the world about the role of Al as a risk factor for AD, in recent years, scientific evidence has demonstrated that Al is associated with the development of AD.
The link to more studies
http://www.ncbi.nlm.nih.gov/pubmed/18392545?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Histol Histopathol. 2008 Apr;23(4):433-9. Links
Aluminium exposure induces Alzheimer's disease-like histopathological alterations in mouse brain.Rodella LF, Ricci F, Borsani E, Stacchiotti A, Foglio E, Favero G, Rezzani R, Mariani C, Bianchi R.
Unit of Human Anatomy, Department of Biomedical Sciences and Biotechnology, University of Brescia, Brescia, Italy. rodella@med.unibs.it

Aluminium (Al) is a neurotoxic metal and Al exposure may be a factor in the aetiology of various neurodegenerative diseases such as Alzheimer's disease (AD). The major pathohistological findings in the AD brain are the presence of neuritic plaques containing beta-amyloid (Abeta) which may interfere with neuronal communication. Moreover, it has been observed that GRP78, a stress-response protein induced by conditions that adversely affect endoplasmic reticulum (ER) function, is reduced in the brain of AD patients. In this study, we investigated the correlation between the expression of Abeta and GRP78 in the brain cortex of mice chronically treated with aluminium sulphate. Chronic exposure over 12 months to aluminium sulphate in drinking water resulted in deposition of Abeta similar to that seen in congophilic amyloid angiopathy (CAA) in humans and a reduction in neuronal expression of GRP78 similar to what has previously been observed in Alzheimer's disease. So, we hypothesise that chronic Al administration is responsible for oxidative cell damage that interferes with ER functions inducing Abeta accumulation and neurodegenerative damage.
Other aspects less mentioned are inflammation and oxidative stress in AD
Rev Neurol. 2006 Apr 1-15;42(7):433-8. Links
[Inflammation and Alzheimer's disease]de Toledo M.Sección de Neurología, Hospital Severo Ochoa, Madrid, Spain. mtoledo@hsvo.es

INTRODUCTION: Although Alzheimer's disease (AD) has not been traditionally regarded as an inflammatory process, there is an innate chronic inflammatory reaction in the affected tissues. The most important elements of this reaction are the activation of the phagocytic cells (microglia) with the production of cytokines and toxic substances, and the activation of the complement system. DEVELOPMENT: Inflammation is considered an important, although secondary, element in the pathogenesis of AD. It has been observed in epidemiological studies and in laboratory that treatment with anti-inflammatory drugs delays the appearance of AD. There are still no studies in humans that recommend the use of these drugs on a generalized way. CONCLUSIONS: The therapeutic targets given by the study of the inflammatory system in the brain are under investigation to obtain new drugs with less adverse effects. Those drugs could be used as primary and secondary prevention of AD.
Int J Exp Pathol. 2005 Jun;86(3):147-59.
Metals and amyloid-beta in Alzheimer's disease.Maynard CJ, Bush AI, Masters CL, Cappai R, Li QX.
Mounting evidence is demonstrating roles for the amyloid precursor protein (APP) and its proteolytic product Abeta in metal homeostasis. Furthermore, aberrant metal homeostasis is observed in patients with Alzheimer's disease (AD), and this may contribute to AD pathogenesis, by enhancing the formation of reactive oxygen species and toxic Abeta oligomers and facilitating the formation of the hallmark amyloid deposits in AD brain. Indeed, zinc released from synaptic activity has been shown to induce parenchymal and cerebrovascular amyloid in transgenic mice. On the other hand, abnormal metabolism of APP and Abeta may impair brain metal homeostasis as part of the AD pathogenic process. Abeta and APP expression have both been shown to decrease brain copper (Cu) levels, whereas increasing brain Cu availability results in decreased levels of Abeta and amyloid plaque formation in transgenic mice. Lowering Cu concentrations can downregulate the transcription of APP, strengthening the hypothesis that APP and Abeta form part of the Cu homeostatic machinery in the brain. This is a complex pathway, and it appears that when the sensitive metal balance in the brain is sufficiently disrupted, it can lead to the self-perpetuating pathogenesis of AD. Clinical trials are currently studying agents that can remedy abnormal Abeta-metal interactions.

I personally don´t understand why an integrative view- the role of essential metals, disruption of the normal metabolism of them (Fe, Cu, Se ) and the problem of the toxic elements management (Hg, Al, Cd, As,) is not more present on this complex topic. Kent, I do think your analogy is pertinent to many many medical conditions.
And please look at this
PLoS ONE. 2008;3(11):e3637. Epub 2008 Nov 4.
Seropositivity to herpes simplex virus antibodies and risk of Alzheimer's disease: a population-based cohort study.Letenneur L, Pérès K, et al
BACKGROUND: Herpes Simplex Virus (HSV) infection has been proposed as a possible risk factor of Alzheimer's Disease (AD) notably because it is neurotropic, ubiquitous in the general population and able to establish lifelong latency in the host. The fact that HSV was present in elderly subjects with AD suggests that the virus could be a co-factor of the disease. We investigated the risk of developing AD in anti-HSV immunoglobulin G (IgG) positive subjects (indicator of a lifelong infection to HSV) and IgM-positive subjects (indicator of primary infection or reactivation of the virus) in a longitudinal population-based cohort of elderly subjects living in the community. METHODS: Cox proportional hazard models were used to study the risk of developing AD according to the presence or not of anti-HSV IgG and IgM antibodies, assessed in the sera of 512 elderly initially free of dementia followed for 14 years. RESULTS: During the follow-up, 77 incident AD cases were diagnosed. Controlled for age, gender, educational level and Apolipoprotein E4 (APOE4) status, IgM-positive subjects showed a significant higher risk of developing AD (HR = 2.55; 95% CI [1.38-4.72]), although no significant increased risk was observed in IgG-positive subjects (HR = 1.67; 95%CI [0.75-3.73]). No modification effect with APOE4 status was found. CONCLUSION: Reactivation of HSV seropositivity is highly correlated with incident AD. HSV chronic infection may therefore be contributive to the progressive brain damage characteristic of AD.
J Alzheimers Dis. 2008 May;13(4):393-405.
Herpes simplex virus type 1 in Alzheimer's disease: the enemy within.Itzhaki RF, Wozniak MA.
Alzheimer's disease is a modern scourge and is likely to become increasingly so in the future, with increasing longevity. The disease has been investigated for over one hundred years yet its causes and that of the neuropathological characteristics seen in AD brain are still completely unknown. Evidence for a major causative role of a common virus, herpes simplex virus type 1 (HSV1), acting in combination with a genetic factor - the type 4 allele of the apolipoprotein gene, a known susceptibility factor - is presented here. The characteristics of the virus, some of which make it an especially likely candidate for this role, are described, as are the many precedents for the action of a genetic factor modulating outcome of infection. Various possible ways in which HSV1 might lead to development of AD, such as its up-regulation of various enzymes and in particular certain kinases, its effect on the cell cycle, on autophagy, and its inflammatory and oxidative effects are also discussed. It is concluded that there is strong evidence that the virus is indeed a major factor in AD and therefore there is a strong case for appropriate treatment, and possibly for prevention in the future.

http://www.ncbi.nlm.nih.gov/pubmed/18487848?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
About herpes encephalitis
Greer MK. Lyons-Crews M. Mauldin LB. Brown FR 3d.
A case study of the cognitive and behavioral deficits of temporal lobe damage in
herpes simplex encephalitis.
Journal of Autism & Developmental Disorders. 19(2):317-26, 1989
Herpes simplex viral encephalitis is a fairly common nonepidemic encephalitis
which produces severe neurological sequelae in survivors. Most viral infections of
the central nervous system produce diffuse damage, but the herpes simplex virus
demonstrates a predilection for localization in the temporal and orbitofrontal
regions of the brain. This case study illustrates the highly significant language
difficulties, marked memory deficits, and propensity for physical aggression
following temporal lobe damage brought about by herpes encephalitis, and presents
the usefulness of a new diagnostic measure in delineating such a variable cognitive
pattern.
Ku A. Lachmann EA. Nagler W.
Selective language aphasia from herpes simplex encephalitis. Pediatric Neurology. 15(2):169-71, 1996 Sep.

Van Hout A. Lyon G. Wernicke's aphasia in a 10-year-old boy.
Brain & Language. 29(2):268-85, 1986 Nov.
We report the case of a ten-year-old boy, who, after herpes simplex encephalitis,
presented a sensory aphasia having much in common with Wernicke's aphasia in adults.
...
Barbarotto R. Capitani E. Laiacona M.
Naming deficit in herpes simplex encephalitis.
Acta Neurologica Scandinavica. 93(4):272-80, 1996 Apr.
OBJECTIVES--The preferential involvement of living categories in naming impairment
is well recognised in Herpes Simplex Encephalitis (HSE)... anatomo-functional
aspects of category dissociation...
CONCLUSION--Language impairment, disproportionately severe for the naming of livinge exemplars, is frequently observed in HSE, is clinically relevant and should be
specifically investigated.

J Virol. 2008 Nov;82(21):10820-31.
Natural killer cells as novel helpers in anti-herpes simplex virus immune response.

Innate defenses help to eliminate infection, but some of them also play a major role in shaping the magnitude and efficacy of the adaptive immune response. With regard to influencing subsequent adaptive immunity, NK cells aided by dendritic cells may be the most relevant components of the innate reaction to herpes simplex virus (HSV) infection. We confirm that mice lacking or depleted of NK cells are susceptible to HSV-induced lesions. The quantity and quality of CD8(+) cytotoxic T lymphocytes generated in the absence of NK cells were diminished, thereby contributing to susceptibility to HSV-induced encephalitis. We demonstrate a novel helper role for NK cells, in that NK cells compensate for the loss of CD4 helper T cells and NK cell supplementation enhances the function of wild type anti-HSV CD8 T cells. In addition, NK cells were able to partially rescue the dysfunctional CD8(+) T cells generated in the absence of CD4 T helper cells, thereby performing a novel rescue function. Hence, NK cells may well be exploited for enhancing and rescuing the T-cell response in situations where the CD4 helper response is affected.
When I read this We confirm that mice lacking or depleted of NK cells are susceptible to HSV-induced lesions.
I remembered the recent Dr Ashwood group study
Brain Behav Immun. 2009 Jan;23(1):124-33. Epub 2008 Aug 14.
Altered gene expression and function of peripheral blood natural killer cells in children with autism.Enstrom AM, Lit L, Onore CE, Gregg JP, Hansen RL, Pessah IN, Hertz-Picciotto I, Van de Water JA, Sharp FR, Ashwood P.
Department of Medical Microbiology and Immunology, University of California at Davis, USA.
Immune related abnormalities have repeatedly been reported in autism spectrum disorders (ASD), including evidence of immune dysregulation and autoimmune phenomena. NK cells may play an important role in neurodevelopmental disorders such as ASD. Here we performed a gene expression screen and cellular functional analysis on peripheral blood obtained from 52 children with ASD and 27 typically developing control children enrolled in the case-control CHARGE study. RNA expression of NK cell receptors and effector molecules were significantly upregulated in ASD. Flow cytometric analysis of NK cells demonstrated increased production of perforin, granzyme B, and interferon gamma (IFNgamma) under resting conditions in children with ASD (p<0.01). Following NK cell stimulation in the presence of K562 target cells, the cytotoxicity of NK cells was significantly reduced in ASD compared with controls (p<0.02). Furthermore, under similar stimulation conditions the presence of perforin, granzyme B, and IFNgamma in NK cells from ASD children was significantly lower compared with controls (p<0.001). These findings suggest possible dysfunction of NK cells in children with ASD. Abnormalities in NK cells may represent a susceptibility factor in ASD and may predispose to the development of autoimmunity and/or adverse neuroimmune interactions during critical periods of development.

Thank you for consider the topic Kent. For me , it is an ongoing concern. My son has high titers for CMV and HSV and his answer to antivirals was very good.

Kent,
This is an excellent piece. I have had the cold sore virus since I was a very young toddler. My mother has it as well. I have always had a feeling my viral load is one of the major predisposing factors to my son's regression after vaccination. It's probably the number 1 reason I tried Valtrex as one of the 1st DAN treatments. With Valtrex my son gained some independant speech in sentence form for "wants" and fully potty trained for pee. However yeast came over his system to the point we had to stop, but I have a feeling it's still a huge factor. Personally I have tremendous results with OLE and honestly since I started taking it to stave off cold sores, my memory improved. I truely do hope that research like this continues and is related to the similarities in autism. With huge numbers of people developing alzheimer's and another huge amount developing autism, there is not going to be a population of healthy independant workers to care for them or pay into the system. Such a prospect should fire up research but instead the denial train is still over occupied.

Kent,

There is also an article on Science Daily (November 2008 ) about APOE 4 being associated with Alzheimers. Anyone who has ever heard Dr Boyd Haley has heard him speak of APOE 4 being associated with the inability to get toxins out of the brain. It would stand to reason that if the brain is full of toxins, many viruses could take up residence in the brain. I think the same mechanisms are in play with autism - too toxins, suppressing the immune system and viruses replicating and mutating causing even more problems. There is no doubt that vaccines are causing autism and alzheimers - same disease different age group.

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