I've been following the research story of Dr. Ruth Itzhaki for years

who partially made me one of her believers on her strong belief that

many Alzheimer's are caused by the herpes simplex virus based on her studies.

This article reviews the full story of infection hypothesis as direct causes of

Alzheimer's which is most interesting, to say the least as in the case of

H. Pylori, the etiology of peptic ulcer.

Prof Ruth Itzhaki

Emeritus Professor

• Affiliations:
• Division of Neuroscience & Experimental Psychology (L5)Division of Neuroscience & Experimental Psychology

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24

• Overview
• Publications
• Research and projects
• Media contributions and coverage

Overview

Alzheimer’s disease (AD) is a major brain disease, afflicting about 18 million elderly people worldwide. This figure will rise with increasing longevity, so there is an urgent need for effective treatment. The brains of AD sufferers contain many abnormal deposits called plaques and tangles, which are thought to play a crucial role in the disease. However, the causes of their formation and of the disease itself are unknown. We have been investigating whether a common virus has a role in AD. We found that many elderly people harbour this virus within their brain but only those who have a specific genetic factor are at risk of developing AD. Subsequently we discovered that the viral DNA is located specifically within plaques; also, infection with this virus causes production of the main components of plaques and tangles (called beta-amyloid and abnormal tau), indicating that the virus might be a cause of these abnormal deposits. Our recent experiments with antiviral agents indicate that they might be an effective treatment to slow AD progression in that they decrease the levels of beta-amyloid and abnormal tau which the virus induces. Also, the future possibility exists of prevention of the disease by vaccination against the virus.

Biography

I was educated at St Paul's Girls' School in Hammersmith, where I was a junior and senior Foundation Scholar. Afterwards, I studied for a BSc in physics, then worked for an MSc in Biophysics - being awarded one of the only two studentships then available in that subject - and finally proceeded to a PhD in Biophysics - all London University degrees.

I then moved to Cambridge, working in the University Department of Radiotherapeutics. I held a Beit Memorial Fellowship for Medical Research and the Wheldale-Onslow Memorial Fellowship (and Praelectorship) at Newnham College. One paper I published in Cambridge became a "citation classic". My next move was to Manchester where I worked initially in the Paterson Laboratories and subsequently in the Department of Optometry and Neuroscience, UMIST.

My research topics have been diverse: iron-binding in plasma; effects of ionising radiation on natural and synthetic macromolecules; chromatin structure (I was the first to use polylysine and a nuclease to investigate this); effects of irradiation on chromatin; carcinogens and chromatin; viruses and neurological disease. More recently I have been studying Alzheimer's disease, in particular defective DNA repair, aluminium, and in most detail, the role of viruses acting with a genetic factor in dementia. For the virus work (see Research) I won an Investigator award from the Lancet, a Wellcome Trust Innovative award, two Olympus Foundation awards, an Alzheimer's Research Forum award and a Manchester City Council award. Our other research topic, which stems from the Alzheimer's disease work, is on the role of the same genetic factor in determining outcome of infection by pathogens.

Thank you, Professor, for your invaluable comments on vasculitis and

Buerger's disease. That is another fascinating story, indeed.

Over the years whenever I read Dr. Itzhaki's published report, she has made me

a believer in her theory. Some years ago, I started taking herpes simplex seriously 

and would treat it with acyclovir like they did in a Taiwan study.

I believe she's been on the right track for decades.

We will know the truth soon, hope.

After having read the linked article, I am frustrated about why hasn't anything been done so far? 

Why Dr. Itzhaki has not done anything further? Do something and get the damn Nobel Prize!!

Have something like the following been done?? (Just my personal thought)

1. Immunization (by vaccination) against HSV1 virus infection (Herpes Simplex Virus Type1)?
Is HVS-2, HPV, or HIV have any connection to Alzheimer's? (very similar viruses)
2. Rx with anti-herpetic drugs, e.g. Valacyclovir, acyclovir, and famciclovir. (Like in a N.Y. study)
3. People with APOE4 gene (I guess studies had been done already)
4. Study on patients on post-corona virus infection (not being done yet??)
5. Beta-amyloid may be actually protective (or claimed to be) to the Alzheimers??
And some researchers are trying to remove beta-amyloid (What the hell is that !! ??)
6. Why not hire some pharmaceutical company to work on this?
Let them develop HSV vaccines and develop better medications.
Don't leave the task to the poor researcher like Ruth Itzhaki who just keeps doing nothing more

than waiting research grant that seemed to have never come.

Hire some rich research organization instead. 
7. How about Shingles or Chicken Pox vaccinations. Will it help?

The following is the only trial mentioned in the article,

Three decades after her initial investigations, Itzhaki hopes we will now see the development of more clinical trials testing new treatments, in a bid to replicate the observations of the HSV1 patients receiving antiviral medication in Taiwan.

One study in New York is already investigating the use of the anti-herpetic medication valacyclovir on patients with mild Alzheimer's disease. The participants are set to undergo a series of cognitive tests after 52 and 78 weeks. If those receiving the drug experienced a slower decline in performance than those receiving a placebo, it will provide some compelling evidence for the efficacy of the treatment – and the infection hypothesis more generally. "It's the first trial of its kind," says Itzhaki.

If antiviral drugs do prove to be effective, they could offer protection to an enormous number of people. Itzhaki calculates that around 18% of people aged 30-40 have the APOE4 gene variant, and also carry a latent HSV1 infection, putting them at the much-heightened risk of Alzheimer's in the decades ahead.

The success of anti-herpetic drugs could also spur efforts to treat the many other kinds of infections that may also contribute to Alzheimer's risk in certain patients. Eventually, doctors may be able to screen people according to the many different microbes they may be carrying in their brains – and control the infections before they have time to cause serious damage.

During our conversation, Itzhaki repeatedly expresses her frustration that progress hasn't come sooner. If these treatments help a fraction of the seven million people developing Alzheimer's disease every year, they would have an enormous impact on world health. 

"After these 30 years of difficulties getting funding and getting published, it strikes me very often how many people might have benefited if these treatments had been tested earlier," she says. "I feel so strongly about that."

https://link.springer.com/article/10.1007%2Fs13311-018-0611-x

https://pubmed.ncbi.nlm.nih.gov/32034019/

The problem of Alzheimer's seems to be a super-urgent-emergency problem facing us.

Why were she and her associates dragging their feet for three decades?

I could not believe what has happened or not happened for so long.

I have a few people I know who are in the nursing home under Alzheimer's disease.

Let's get things going so that we don't die or are disabled by the disease.

It is pretty convincing revelatin. My wife often gets herpes simplex infection 

around her lips. She takes Acylclovir whenever it is bad. But it always comes back.

It seems to me that there is no way to get rid of it permanently. Is there?

Is it easy to know if she has APOE4 gene? Thank you very much for sharing

valuable information, Dr. Lee!

Alzheimer's Organization: Genetic Testing
The ApoE Genetic Test For Alzheimer's Risk

Price: $125.00

DESCRIPTION

The ApoE genetic test for Alzheimer’s will tell you which version of the ApoE gene you have. 

The test is mailed to you, performed by yourself at home, and then mailed in pre-paid packaging to a laboratory. Results are returned to you in two weeks by electronic mail. Alzheimer’s Organization technicians will answer any questions you may have during the test or after when you are reviewing your results.

​

ApoE is a gene that can dramatically increase your risk for Alzheimer’s. It is important that Individuals with the ApoE 4 gene take measures to reduce their risk of Alzheimer’s. Learn more about the ApoE gene and how it affects you: Alzheimer's Risk and The ApoE Gene.

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TEST KIT CONTENTS

​1. Test Instructions 

​2. (3) Three cotton-tipped swabs (used for swabbing the inner cheek)

​3. Educational Information

​3a. How Genetic Testing Works

​3b. Information about ApoE

​4. Pre-Paid Fedex Return Envelope

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AFTER TEST SERVICES

1. Approximately two weeks after the lab receives your test you will receive your ApoE status as well as what your status means for you.

​2. When you order your test kit you will be contacted by one of our technicians who will answer any questions you may have along the way and any questions you may have about your results.

​TESTING PROCEDURES

​1. The Test Kit is mailed to your address.

​2. You administer the test by rubbing three cotton-tipped cheek swabs on your inner cheek. 

​3. You replace the cotton swabs back in the test kit.You mail the test kit in a pre-paid, pre-addressed envelope to our laboratory.

​4. After approximately two weeks you will receive your ApoE status and explanation via electronic mail.

​5. Testing includes unlimited online consultations with our trained technicians whom can answer any questions you may have along the way and can explain your results and what they mean for you.

You are welcome, Dr. Ohn.

​Personally I've had acyclovir readily available and have used it

​at the first sign of blisters for me and my wife until it goes away.

​Taking it long term in case you have family history and the apoe4 gene

may well be worthwhile as Dr. Itzhaki believes, but we don't have the data.

You have to be your own guinea pig.

Here is the answer and more,

Herpes Simplex Virus: HSV-1 & HSV-2

Herpes simplex viruses -- more commonly known as herpes -- are categorized into two types: herpes type 1 (HSV-1, or oral herpes) and herpes type 2 (HSV-2, or genital herpes). Most commonly, herpes type 1 causes sores around the mouth and lips (sometimes called fever blisters or cold sores). HSV-1 can cause genital herpes, but most cases of genital herpes are caused by herpes type 2. In HSV-2, the infected person may have sores around the genitals or rectum. Although HSV-2 sores may occur in other locations, these sores usually are found below the waist.

https://www.cdc.gov/std/herpes/stdfact-herpes.htm

Thanks, buddy, Speedy Gonzales!!!

How about cross-immunity between two subtypes? Vaccine for genital herpes does not work for oral herpes? If Type 2 should cause(?) cervical cancer, what about Type 1? Does it cause any oral cancer?

Quite curious!!!

P.S. Doesn't the oral sex contract/propagate Type 2 to the mouth and vice versa? If not, why?

P.S. since I stopped getting involved in transplant surgery for almost 20 years to concentrate on vascular malformation and lymphedema, I didn't keep up with this opportunistic viral infection among the immunosuppressed transplant patients other than cytomegalovirus so that I am sure there must have been quite a progress in this virology.

So they should have more answers to this common virus infection!

Dr. Ohn;

I used to have oral herpes often especially when I am tired.

One day, I was working in the E.R. and I told a nurse that I am about to get oral herpes

by the prodromal tingling sensation at my lip.  An E.R. nurse gave me a cold spray at the lip

for a few seconds where the tingling was. Strangely, the herpes lesion did not come afterward.

I realized that the herpes virus favors heat and hates cold. (See, it happens with fever.)

By applying cold spray (or anything cold) at the site of the lip, the virus get deactivated immediately

and the blistering will be prevented. It does not kill it but makes it dormant until next time.

When at home, I simply apply an ice cube to the tingling site for about 2-3 minutes,

and, in the mountain, I apply a cold glass, a rock, or metallic bottle to my lip at the particular site

for about 5-10 minutes cooling the lip tissue.

That will keep the virus proceeding into a full-blown blister. Complete prevention !!

It always worked without failure even today. Please tell this to your wife.

Even after the small blister starts, the cold application will still work by shortening the course.

No one else seems to know this secret recipe except me and the middle-aged nurse in the E.R.

of Rochester, N.Y.  Trust me and let your wife try this. Or else. she will suffer a week-long blister.

In the same token, this ice-cube treatment could work in genital herpes too. I have not tried though.

After all they are the same virus anyway.

Thanks a million, WM! I will try it next time she gets it.

The main thing is to apply ice when the lip tingles much (a few hours) "before" the blister.

One needs to be conscious (pay attention to) about this prodromal sensation at the lip.

But even after the blister, this still minimizes the symptoms.

However, the virus won't go away and will keep trying to come out though.

Studies Suggest Oral Diuretic Pill Could Help Prevent Alzheimer's Disease in People at Genetic Risk
https://www.genengnews.com/news/studies-suggest-oral-diuretic-pill-could-help-to-prevent-alzheimers-disease-in-people-at-genetic-risk/

I'm very familiar with this diuretic (brand name Bumex)whose potency is equal to furosemide, Lasix,

roughly Bumex 1 mg equal to Lasix 40 mg.

This is totally unexpected finding relating to AD and Apoe 4 gene, discovered by careful scientific search

as detailed in the article.

Of note,

APOE gene

apolipoprotein E

The APOE gene provides instructions for making a protein called apolipoprotein E. This protein combines with fats (lipids) in the body to form molecules called lipoproteins. Lipoproteins are responsible for packaging cholesterol and other fats and carrying them through the bloodstream. Maintaining normal levels of cholesterol is essential for the prevention of disorders that affect the heart and blood vessels (cardiovascular diseases), including heart attack and stroke.

There are at least three slightly different versions (alleles) of the APOE gene. The major alleles are called e2, e3, and e4. The most common allele is e3, which is found in more than half of the general population

The e4 version of the APOE gene increases an individual's risk for developing late-onset Alzheimer's disease. Alzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. The late-onset form of the condition occurs in people older than age 65. People who inherit one copy of the APOE e4 allele have an increased chance of developing the disease; those who inherit two copies of the allele are at even greater risk. The APOE e4 allele may also be associated with an earlier onset of memory loss and other symptoms compared to individuals with Alzheimer disease who do not have this allele.

It is not known how the APOE e4 allele is related to the risk of Alzheimer disease. However, researchers have found that this allele is associated with an increased number of protein clumps, called amyloid plaques, in the brain tissue of affected people. A buildup of amyloid plaques may lead to the death of nerve cells (neurons) and the progressive signs and symptoms of this disorder.

It is important to note that people with the APOE e4 allele inherit an increased risk of developing Alzheimer's disease, not the disease itself. Not all people with Alzheimer's disease have the APOE e4 allele, and not all people who have this allele will develop the disease.

Comment on antivirals by Dr. Itzhaki below.
https://www.contagionlive.com/view/antivirals-to-treat-herpes-infection-may-decrease-risk-of-dementia