Censorship continues apace

USA Today reports that Facebook will extend its censorship to anti-vaccine news. USA Today states:

‘Facebook is considering making anti-vaccination content on its site less visible amid a measles outbreak that has reignited a conversation about preventative shots.

The social media giant that’s been criticized for spreading fake news told USA TODAY it’s “taken steps to reduce the distribution of health-related misinformation on Facebook, but we know we have more to do.”

Facebook has been fighting misinformation on its platform since the 2016 presidential election after fake accounts and news stories aimed at sowing discord among users were discovered.’

Facebook, YouTube, Amazon and others announce censorship plans

Not only are social media censoring left political ideas but, now, extending this censorship to medical issues regarding vaccines and other unpopular ideas. The victims of this censorship is the left, natural medicine, and those pointing to deficiencies in current vaccines. It should be noted that we now have the technology and knowledge to make safer and more effective vaccines. Among those censoring are Facebook, YouTube, Amazon and other social media.

Those voices who normally raise concerns about censorship and demand free speech are strangely and cowardly absent today.

Small molecule nicotinamideN-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle

[**Biochemical Pharmacology**][Biochemical Pharmacology]

Available online 10 February 201

**Abstract**

Aging is accompanied by progressive declines in skeletal muscle mass and strength and impaired regenerative capacity, predisposing older adults to debilitating age-related muscle deteriorations and severe morbidity. Muscle stem cells (muSCs) that proliferate, differentiate to fusion-competent myoblasts, and facilitate muscle regeneration are increasingly dysfunctional upon aging, impairing muscle recovery after injury. While regulators of muSC activity can offer novel therapeutics to improve recovery and reduce morbidity among aged adults, there are no known muSC regenerative small molecule therapeutics. We recently developed small molecule inhibitors of nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed with aging in skeletal muscles and linked to impairment of the NAD\\+ salvage pathway, dysregulated sirtuin 1 activity, and increased muSC senescence. We hypothesized that NNMT inhibitor (NNMTi) treatment will rescue age-related deficits in muSC activity to promote superior regeneration post-injury in aging muscle. 24-month old mice were treated with saline (control), and low and high dose NNMTi (5 and 10 mg/kg) for 1-week post-injury, or control and high dose NNMTi for 3-weeks post-injury. All mice underwent an acute muscle injury (barium chloride injection) locally to the tibialis anterior (TA) muscle, and received 5-ethynyl-2’-deoxyuridine systemically to analyze muSC activity. *In vivo*contractile function measurements were conducted on the injured TA muscle and tissues collected for ex-vivo analyses, including myofiber cross-sectional area (CSA) measurements to assess muscle recovery. Results revealed that muscle stem cell proliferation and subsequent fusion were elevated in NNMTi-treated mice, supporting nearly 2-fold greater CSA and shifts in fiber size distribution to greater proportions of larger sized myofibers and fewer smaller sized fibers in NNMTi-treated mice compared to controls. Prolonged NNMTi treatment post-injury further augmented myofiber regeneration evinced by increasingly larger fiber CSA. Importantly, improved muSC activity translated not only to larger myofibers after injury but also to greater contractile function, with the peak torque of the TA increased by ∼70% in NNMTi-treated mice compared to controls. Similar results were recapitulated *in vitro* with C2C12 myoblasts, where NNMTi treatment promoted and enhanced myoblast differentiation with supporting changes in the cellular NAD\\+/NADH redox states. Taken together, these results provide the first clear evidence that NNMT inhibitors constitute a viable pharmacological approach to enhance aged muscle regeneration by rescuing muSC function, supporting the development of NNMTi as novel mechanism-of-action therapeutic to improve skeletal muscle regenerative capacity and functional recovery after musculoskeletal injury in older adults

[Biochemical Pharmacology]: https://www.sciencedirect.com/science/journal/00062952
[In Press_ Accepted]: https://www.sciencedirect.com/science/journal/aip/00062952
[What]: https://service.elsevier.com/app/answers/detail/a_id/22799/supporthub/sciencedirect/
[HarshiniNeelakantan]: https://www.sciencedirect.com/science/article/abs/pii/S0006295219300462?via%3Dihub#!
[https]: https://doi.org/10.1016/j.bcp.2019.02.008
[Get]: https://s100.copyright.com/AppDispatchServlet?publisherName=ELS&contentID=S0006295219300462&orderBeanReset=true

Make Vaccines Safe

  • Vaccines contain chemicals and other ingredients that are carcinogenic.

  • The biggest class of carcinogenic additives in vaccines are heavy metals with mercury being the most dangerous. Even minute amounts of mercury affect every system of the body: the endocrine, the neurological system, the digestive system, the epithelial tissue.

  • Antibodies that are stimulated by the body from vaccines are not always enough to provide lifelong protection from a disease. For example, people who had Chicken Pox often still get Shingles later in life.

  • Vaccines include foreign RNA and DNA from animals, aborted fetal tissue, formaldehyde, antifreeze-like compounds. If you added these same ingredients to a baby’s bottle you would be charged with attempted murder.

Gonorrhea Protection From Vaccine

Serogroup B meningococcal vaccine Bexsero reported to elicit antibodies to Neisseria Gonorrhea

December 21st, 2018 – New research indicates that the meningococcal B vaccine Bexero may offer cross-protection against gonorrhea.

Bexsero, which is FDA-approved to prevent invasive disease caused by Neisseria meningitidis serogroup B, for individuals 10 to 25 years of age, includes the MeNZB OMV component plus 3 recombinant antigens, NadA, fHBP-GNA2091 and NHBA-GNA1030.

This research found there is a high level of sequence identity between MeNZB OMV and Bexsero OMV antigens, and gonococcal proteins in test rabbits.

This study’s conclusion said ‘the anti-gonococcal antibodies induced by MeNZB-like OMV proteins could explain the previously seen decrease

And, the high level of anti-gonococcal-NHBA antibodies generated by Bexsero vaccination in humans may result in additional cross-protection against gonorrhea.

Gonorrhea is the 2nd most commonly reported notifiable disease in the USA.

Gonorrhea is a sexually transmitted disease caused by infection with the Neisseria gonorrhoeae bacterium.

N. gonorrhea infects the mucous membranes of the reproductive tract, including the cervix, uterus, and fallopian tubes in women, and the urethra in women and men, according to the US Centers for Disease Control and Prevention (CDC).

This new study builds on a 2017 report that the outer membrane vesicle (OMV) meningococcal B vaccine, MeNZB, was reported to be associated with reduced rates of gonorrhea following a mass vaccination campaign in New Zealand.

To probe the basis for this protection we assessed cross-reactivity to N. gonorrhea of serum raised to the meningococcal vaccine Bexsero, which contains the MeNZB OMV component plus three recombinant antigens (NadA, fHBP-GNA2091, and NHBA-GNA1030).

This new information is important since gonorrhea is becoming increasingly difficult due to widespread antibiotic resistance, says the CDC.

In 2017, 555,608 cases of gonorrhea were reported to CDC.

While vaccines are routinely used for N.meningitidis, no vaccine is available for N.gonorrhea.

“We have all the knowledge and technology to make a real gonorrhea vaccine,” said the producer of Bexero, GSK, in an interview during November 2018.

This study’s results may lead to human clinical trials.

These Australian researchers included Evgeny A Semchenko, Aimee Tan, ay Borrow, and Kate L Seib, Institute for Glycomics, Griffith University, Gold Coast, Australia.

Study links frequent red meat consumption to high levels of chemical associated with heart disease

NEWS RELEASES
Monday, December 10, 2018

Findings reveal tripling of blood levels of TMAO from red meat diet, but dietary effects can be reversed

Researchers have identified another reason to limit red meat consumption: high levels of a gut-generated chemical called trimethylamine N-oxide (TMAO), that also is linked to heart disease. Scientists found that people who eat a diet rich in red meat have triple the TMAO levels of those who eat a diet rich in either white meat or mostly plant-based proteins, but discontinuation of red meat eventually lowers those TMAO levels.

TMAO is a dietary byproduct that is formed by gut bacteria during digestion and is derived in part from nutrients that are abundant in red meat. While high saturated fat levels in red meat have long been known to contribute to heart disease—the leading cause of death in the United States—a growing number of studies have identified TMAO as another culprit. Until now, researchers knew little about how typical dietary patterns influence TMAO production or elimination.

The findings suggest that measuring and targeting TMAO levels—something doctors can do with a simple blood test—may be a promising new strategy for individualizing diets and helping to prevent heart disease. The study was funded largely by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health. It will be published Dec. 10 in the European Heart Journal, a publication of the European Society of Cardiology.

“These findings reinforce current dietary recommendations that encourage all ages to follow a heart-healthy eating plan that limits red meat,” said Charlotte Pratt, Ph.D., the NHLBI project officer for the study and a nutrition researcher and Deputy Chief of the Clinical Applications & Prevention Branch, Division of Cardiovascular Sciences, NHLBI. “This means eating a variety of foods, including more vegetables, fruits, whole grains, low-fat dairy foods, and plant-based protein sources such as beans and peas.”

“This study shows for the first time what a dramatic effect changing your diet has on levels of TMAO, which is increasingly linked to heart disease,” said Stanley L. Hazen, M.D., Ph.D., senior author of the study and section head of Preventive Cardiology & Rehabilitation at the Cleveland Clinic. “It suggests that you can lower your heart disease risk by lowering TMAO.”

Hazen estimated that as many as a quarter of middle-aged Americans have naturally elevated TMAO levels, which are made worse by chronic red meat consumption. However, every person’s TMAO profile appears to be different, so tracking this chemical marker, Hazen suggested, could be an important step in using personalized medicine to fight heart disease.

For the study, researchers enrolled 113 healthy men and women in a clinical trial to examine the effects of dietary protein—in the form of red meat, white meat, or non-meat sources—on TMAO production. All subjects were placed on each diet for a month in random order. When on the red meat diet, the participants consumed roughly the equivalent of about 8 ounces of steak daily, or two quarter-pound beef patties. After one month, researchers found that, on average, blood levels of TMAO in these participants tripled, compared to when they were on the diets high in either white meat or non-meat protein sources.

While all diets contained equal amounts of calories, half of the participants were also placed on high-fat versions of the three diets, and the researchers observed similar results. Thus, the effects of the protein source on TMAO levels were independent of dietary fat intake.

Importantly, the researchers discovered that the TMAO increases were reversible. When the subjects discontinued their red meat diet and moved to either a white meat or non-meat diet for another month, their TMAO levels decreased significantly.

The exact mechanisms by which TMAO affects heart disease is complex. Prior research has shown TMAO enhances cholesterol deposits into cells of the artery wall. Studies by the researchers also suggest that the chemical interacts with platelets—blood cells that are responsible for normal clotting responses—in a way that increases the risk for clot-related events such as heart attack and stroke.

TMAO measurement is currently available as a quick, simple blood test first developed by Hazen’s laboratory. In recent published studies, he and his colleagues reported development of a new class of drugs that are capable of lowering TMAO levels in the blood and reducing atherosclerosis and clotting risks in animal models, but those drugs are still experimental and not yet available to the public.

The study was supported by grants from the NHLBI and the Office of Dietary Supplements (HL103866, HL126827, HL106003, HL130819) and the National Institute of Diabetes and Digestive and Kidney Diseases (DK106000). The study was also supported by UCSF Clinical and Translational Science Unit.

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases and other materials are available online at https://www.nhlbi.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892

Guillain-Barré Syndrome

Medically reviewed by Debra Sullivan, PhD, MSN, RN, CNE, COI

What is Guillain-Barré syndrome?


Guillain-Barré syndrome is a rare but serious autoimmune disorder in which the immune system attacks healthy nerve cells in your peripheral nervous system.

This leads to weakness, numbness, and tingling. It can eventually cause paralysis.

The cause of this condition is unknown, but it’s typically triggered by an infectious illness, such as the stomach flu or a lung infection.

Guillain-Barré is rare, affecting only about 1 in 100,000 Americans, according to the National Institute of Neurological Disorders and Stroke.

There’s no cure for the syndrome, but treatment can reduce the severity of your symptoms and shorten the duration of the illness.

There are multiple types of Guillain-Barré, but the most common form is acute inflammatory demyelinating polyradiculoneuropathy (AIDP). It results in damage to myelin.

Other types include Miller Fisher syndrome, which affects the cranial nerves.

What causes Guillain-Barré syndrome?
The precise cause of Guillain-Barré is unknown.

According to the Centers for Disease Control and Prevention (CDC), about two-thirds of people with Guillain-Barré develop it soon after they’ve been sick with diarrhea or a respiratory infection.

This suggests that the disorder may be triggered by an improper immune response to the previous illness. Learn more about autoimmune disease here.

Campylobacter jejuni infection has been associated with Guillain-Barré. Campylobacter is one of the most common bacterial causes of diarrhea in the United States. It’s also the most common risk factor for Guillain-Barré.

Campylobacter is often found in undercooked food, especially poultry.

The following infections have also been associated with Guillain-Barré:

influenza
cytomegalovirus, which is a strain of the herpes virus
Epstein-Barr virus infection, or mononucleosis
mycoplasma pneumonia, which is an atypical pneumonia caused by bacteria-like organisms
HIV or AIDS
Anyone can get Guillain-Barré, but it’s more common among older adults.

In extremely rare cases, people can develop the disorder days or weeks after receiving a vaccination.

The CDC and the U.S. Food and Drug Administration (FDA) have systems in place to monitor the safety of vaccines, detect early warning signs of side effects, and record any cases of Guillain-Barré that develop following a vaccination.

Sabin oral polio vaccine prevents the acute flacid paralysis caused by Entrovirus through cross protection.

“As shown here, poliovirus vaccination may have an impact on subsequent severity of HFMD disease. Cross-reactivity between EV71 A3 epitope and the A3v epitope of poliovirus 3 Sabin strain, may lead to the stimulation of protective, cross-reactive T cell responses, limiting the severity of subsequent HFMD.”

Wei et al. on A Dominant EV71-Specific CD4+ T Cell Epitope Is Highly Conserved among Human Enteroviruses

Another study:

2018 Jun 29;20(9):34. doi: 10.1007/s11908-018-0641-x.

Acute Flaccid Paralysis and Enteroviral Infections.

Abstract

PURPOSE OF REVIEW:

The focus of this review is on enterovirus (EV)-associated acute flaccid paralysis (AFP) due to spinal cord anterior horn cell disease. Emphasis is placed on the epidemiology, pathogenesis, diagnosis, treatment, and outcome of AFP caused by polioviruses, vaccine-derived polioviruses, EV-D68, and EV-A71.

RECENT FINDINGS:

Since the launch of The Global Polio Eradication Initiative in 1988, the worldwide incidence of polio has been reduced by 99.9%, with small numbers of poliomyelitis cases being reported only in Afghanistan, Pakistan, and Nigeria. With the planned phaseout of oral polio vaccine, vaccine-associated poliomyelitis is also expected to be eliminated. In their place, other EVs, chiefly EV-D68 and EV-A71, have emerged as the principal causes of AFP. There is evidence that the emergence of EV-D68 as a cause of severe respiratory disease and AFP was due to recent genetic virus evolution. Antiviral medications targeting EV-D68, EV-A71, and other EVs will likely be available in the near future. An effective EV-A71 vaccine has been developed, and preliminary investigations suggest an EV-D68 vaccine could be on the horizon. The eradication of poliomyelitis and vaccine-associated poliomyelitis is near, after which other EVs, presently EV-D68 and EV-A71, will be the principle viral causes of AFP. Moving forward, it is essential that EV outbreaks, in particular those associated with neurologic complications, be investigated carefully and the causal strains identified, so that treatment and prevention efforts can be rapidly developed and implemented.

KEYWORDS:

Acute flaccid myelitis; Acute flaccid paralysis; Enterovirus A71; Enterovirus D68; Poliomyelitis; Poliovirus; Vaccine-derived poliovirus

The Remedy for hope is Action

The following is the Epilogue from Jeffrey St. Clair’s and Joshua Frank’s new book The Big Heat: Earth on the Brink, available now from CounterPunch Books.

In the spring of 2017, the carbon dioxide readings at the Mauna Loa observatory in Hawai’i cracked 410 parts per million, an all-time record and a frightening one. On Earth Day, climate marches took place in cities across the world. Trump’s policies didn’t drive the spiking CO2 levels, but they did propel tens of thousands onto the streets for a few hours of fun. Where were those people during eight years of Barack Obama, an oil and gas man of some distinction? Where were they during eight years of Bill Clinton, one of the greatest environmental con men of our time?

Has Donald Trump finally shattered our illusions, so that we can see clearly the forces—economic, political and technological—that are plunging the planet toward a man-made heat death? Is he, in fact, a kind of clarifying agent for the real state of things?

One can hope so.

Except one mustn’t hope.

As Kafka, the High Priest of Realism, admonished his readers, “There is hope. But not for us.”

Hope is an illusion, an opiate, an Oxycontin for the masses. Instead of hope, we need a heavy dose of realism. A realism as chilling as reality itself.

Twenty-five hundred years ago, the Buddha instructed us that the world is suffering, and indeed it is. He also advised us that the cure for suffering is empathy, especially for those living beings—among which we would include redwood trees, sea coral and saguaro cacti—which have no defense against the forces that are inflicting that globalized torment.

That’s where we come in. Defenders of the Earth need to abandon all hope before entering the fray. Hope is a paralytic agent. Hope is the enemy.

The antidote is action.

Action, however, is not marching in a parade a couple of times a year, featuring puppets, vagina hats and signs printed up by the Sierra Club©. Action is not taking selfies with a celebrity in the back of a police wagon after a designer arrest. Action is not typing your name on a MoveOn e-petition or voting for a Jill Stein-like candidate in safe states like Oregon or California. Action is standing arm-in-arm before water cannons and government snipers on the frozen plains of North Dakota. Action is hanging from a fragile perch 150-feet up in Douglas fir tree in an ancient forest grove slated for clearcutting, through howling winter storms. Action is chaining yourself to a fracking rig in rural Pennsylvania or camping out in the blast zone at a Mountain Top Removal site in the hills of West Virginia. Action is intervening when police in stormtrooper gear are savagely beating a defenseless woman on the streets of Portland. Action is jumping into the Pacific Ocean with a knife in your teeth to cut the vast trawler nets ensnaring white-sided dolphins and humpback whales. Action is stopping bad shit from going down, or trying to.

The time for protests is over.

Protests will not prick the conscience of the unmasked beast called Donald Trump. Trump has no conscience to arouse, no shame to trigger, no remorse to cultivate. Trump is a full-frontal menace, that dangerous object in the mirror that is closer than it appears. It is the old threat, coming at us faster than before and from all directions at once. An unchained beast that will not be moderated by regulations, social conventions or appeals to common decency.

We are witnessing the wet-dream of Steve Bannon—the Trump Whisperer—made manifest: the dismantling of the regulatory state. This new reality compels us—for those who are willing to look—to confront the shedding of another illusion, an illusion that mainstream environmentalists have been marinating in since the 1970s, when our most progressive president, Richard M. Nixon, cynically created the modern environmental regulatory state in order to split the anti-war movement, pacify the Left and smother a much more radical defense of the natural world.

The green regulatory state—as personified by the EPA, the Fish and Wildlife Service, the Forest Service and the BLM (Bureau of Livestock and Mining), as well as thousands of laws, administrative rules and regulations, the meaning of which can only be divined by lawyers, lobbyists and professional environmentalists—has not slowed the decimation of native forests, the extirpation of wildlife or the poisoning of our air and water. It has simply codified and systematized the destruction, allocating the looting to a coterie of well-connected corporations large enough and shrewd enough to navigate the legal labyrinth for their own bloody profits.

At the same time, the creation of the regulatory state effectively neutered the once potent environmental movement as a real threat to the System. As their budgets swell, often fattened by the largess of grants from foundations linked to the fossil fuel industry, the big DC-oriented conservation groups become more and more complicit with the political fool’s gold of neoliberalism. Try finding a lobbyist from NRDC with callouses on their hands and a trace of mud on their boots.

As Trump begins the demolition of the regulatory state, we start to see how hollow many of Gang Green’s alleged environmental victories of the past—from coal mining and air quality regulations to endangered species protections and new national monuments—really are. They are being wiped out with a slash of the pen.

As the archdruid David Brower used to say: “When we win, it’s only a stay of execution, when they win it’s forever. Thus we must be eternally vigilant.” These days the corporate environmental movement is vigilant about only one thing: claiming fake victories in their sustained barrage of fund-raising appeals.

But the days of the laptop environmentalism are numbered. Trump is creating a battlefield where professional conservationists will fear to tread, a direct, face-to-face confrontation with the machinery of ecocide.

And we know who will rise to the call. The ones who always have in the past: the indigenous, the altruists and the anarchists. Those are the ones who will fight as if their lives depend on the outcome, because, of course, they do.

If we are to believe the sociobiologists, such as E.O. Wilson, the altruistic gene may only be present in three percent of the human population—may their gene pool increase! But, hell, that’s still three times as many people as the one-percenters who are running the show! If you want hope, there’s a microdot to swallow.

Small, scruffy and unruly as it is, we’ve seen the power of our movement in the past. When our backs are—often literally—against the wall, when the battle lines are clear from the immobilizing fog of liberal rhetoric and free from the timid advice of professional compromisers. We’ve seen it emerge from the Lacandon jungle to say enough is enough and overtake the streets of Seattle to shut down the World Trade Organization. We’ve seen grandmothers and housewives expose the toxic crimes of Love Canal and corn farmers shut down nuclear power plants. We’ve taken the international timber industry to its knees on its home turf, blocked strip mines, pipelines and river-killing dams. We’ve thrown monkey-wrenches big and small into the gears of the System. It has been done and it will be done again and again. No grant applications or protest permits needed.

As Ed Abbey used to say: there’s no battle more important, no fight more fun waging, no comrades more trustworthy than those in the trenches with us when we rise up together in defense of life on Earth. To crib a line from Leonard Cohen: “we may be ugly, but we’ve got the music.”

So draw a line and take a stand—almost any place will do, since the whole shebang is under threat—and let loose an old battle cry so that others will know where to come join you: Earth First!

Frontiers in Aging Neuroscience. 2018 Dec; 10 : 324. Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease.

Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia-are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD. It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy.