The Link Between the Herpes Virus and Alzheimer's

More than 30 million people in the world are currently suffering from Alzheimer's disease, and to date, there is still no cure for it, only treatments that help reduce its symptoms. However, scientists are now working on different ways to cure the disease, and as a result of various experiments and observations, they get to know more about it, including the factors that may predict it even before its familiar symptoms appear.

In a recent October 2018 study at Oxford University, evidence was found that the herpes virus was closely linked to Alzheimer's disease and that a drug that treated the virus could also help treat the devastating nerve disease. Because of the great importance of the issue and its impact on the health of adults today and ourselves in the future, it is recommended that you continue reading to learn more about the relationship between herpes and Alzheimer's.

What is the herpes virus?

Herpes is a whole family of viruses. Herpes simplex is manifested in the form of blisters in the skin, lips, eyelids, or genitals. Herpes simplex is also divided into 2 types, with herpes simplex 1 being the most common type and causing blisters on the lips, while herpes simplex 2 is considered to be a sexually transmitted disease.

Herpes simplex is a very contagious disease, and it passes through skin to skin contact or contact with objects that are infected from shared use, such as lipstick. When infected, the hereditary material is stored in the nervous system and tends to erupt with its familiar symptoms when the body is under stress, during transitional seasons, during illnesses accompanied by fever, and during periods of hormonal changes in the body.

What is the relationship between herpes and Alzheimer's?

As noted, the herpes virus attacks the nervous system and remains dormant until it erupts. In 1991, a study in Manchester found that in many elderly people the virus was also found in the brain and in 1997 it was found that there was a link between its presence in the brain and the risk of Alzheimer's in people with a gene called APOE4, which is known to increase the risk of Alzheimer's disease.

According to the experts' hypothesis, the presence of the virus in the brain and its recurrent eruption cause cumulative damage, because the chances of suffering from Alzheimer's according to the observations are 12 times higher for APOE4 carriers who also suffer from herpes simplex 1, compared to people who do not have both cases together.

However, another study conducted at the University of Manchester and a study in Chile found that people suffering from the herpes virus suffer from increased production of amyloid beta-protein and a very high amount of tau protein, which also endanger the brain and body in Alzheimer's disease.

Researchers believe that when the body gets older and the immune system weakens, the herpes virus can penetrate the brain through the nervous system, where it creates a dormant infection that is activated in stressful situations or when the brain suffers from other infections. Repeated outbreaks of the virus cause cumulative damage to the infected cells of the brain, leading eventually to Alzheimer's in people who have inherited the disease. People with a family history of Alzheimer's disease, who are also carriers of the herpes virus, may be particularly likely to suffer from Alzheimer's disease, even in their youth. It is therefore important to know the warning signs of Alzheimer's disease so that it can be identified in time and treated appropriately.

The significance of the findings regarding innovative treatment for Alzheimer's disease

Although all these findings sound very worrisome, they are also somewhat encouraging, because recent research indicates that Alzheimer's disease can be treated, or at least delayed, with treatment for the herpes virus. Fortunately, research has already been done on the subject in Taiwan and it shows promising results - anti-herpes drug treatment has indeed helped to prevent Alzheimer's disease in the subjects. More research is underway, but Alzheimer's disease may be avoided in the near future with a simple herpes virus vaccine.

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Developing Alzheimer's diseases could be due to disrupted sleep

Losing a night's sleep can be the reason behind developing Alzheimer's, study reveals.

The interrupted sleep schedule for even a night increases the level of tau protein in a young male's body thus increasing the chances of developing Alzheimer's disease.

According to CNN, the report was published on Wednesday in Neurology, the medical journal of the American Academy of Neurology

"Our study focuses on the fact that even in young, healthy individuals, missing one night of sleep increases the level of tau in blood suggesting that over time, such sleep deprivation could possibly have detrimental effects," said study author Dr Jonathan Cedernaes, a neurologist at Uppsala University in Sweden.

As defined by the Alzheimer's Association, tau is the name of a protein that helps in stabilizing the internal structure of the brain's nerve cells. An abnormal build-up of tau protein in the body can end up in causing interior cells to fall apart and eventually developing Alzheimer's.

"When you get more of that deep sleep and you get the REM sleep in the normal amounts, that improves clearance of abnormal proteins which we think is good," said Mayo Clinic neurologist Dr Donn Dexter, not the study author but a fellow of the American Academy of Neurology.

Earlier studies have also shown that getting deprived of sleep can allow higher tau development and accumulation. Thus that poor sleep can hasten the development of cognitive issues.

Researchers caution that the study is small and inconclusive, and acknowledged they were not able to determine what the increased levels might mean.

"This study raises more questions than answers," agreed Dexter on a concluding note, sharing, "What this is telling us is that we have to dig more deeply. Despite something we do for a third of our lives, we know so little about sleep and we're learning every day, particularly when it comes to sleep and dementia."

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Thousands of Alzheimer’s cases misdiagnosed?

Hundreds of thousands of Alzheimer’s cases worldwide may not be responding to treatment simply because they are not Alzheimer’s disease, according to recent data.
 
Alzheimer’s disease, as well as the numerous other kinds of dementia are becoming a global health issue. Increases in life expectancy the globe over have placed millions of people into the over-65 bracket, after which dementia rates increase exponentially on a year by year basis.
 
India is no exception to this. Two decades ago, the condition was considered to be rare, though to some extent this may be accounted for by lower life expectancies combined with low rates of diagnosis. Current estimates place the number of patients with dementia in India at around 4 million.  This may be a conservative estimate as countless numbers of people in rural communities may be living with the condition, still without a diagnosis.

Worldwide numbers of dementia cases are estimated to hit 131.5 million by 2050. India is unlikely to avoid this rapid increase in disease cases.

Unprepared, and unknown

Alzheimer’s disease has no cure. Current treatments aim to slow the progression of the disease as well as manage the symptoms, but even these often have very little impact. A key issue currently faced in addressing the Alzheimer’s problem is the fact that we have only a fractional understanding of the causes of the disease. 

Recent data from an international team of scientists  have discovered that many cases of dementia- predominantly those occurring in  individuals aged 80 or above- may not be Alzheimer's at all.
Rather, these cases are a form of dementia that mimics the symptoms of Alzheimer’s disease so closely they are all but indistinct.

This form of dementia, “limbic-predominant age-related TDP-43 encephalopathy” or “LATE”, has much the same pathology as Alzheimer’s disease, and even to some extent a similar mechanism. Specifically, aggregates of the TDP-43 protein affect areas of the brain, in a similar way amyloid protein aggregates affect an individual.

“This is a disease that really attacks the very latest portion of the human aging spectrum,” said the study's co-author.

One major drawback of the studies findings is that the condition can only be picked up after death. 

There are, as of yet, no clinical tests outside of an autopsy that can determine whether a patient has this form of dementia. As such, it remains indistinct from Alzheimer’s until after death. This leaves little option but to use the limited tools available to medicate against Alzheimer’s disease, now knowing they may have no effect.

Current working models have not translated into effective treatment

This creates further issues when it comes to the already ineffective means of managing Alzheimer’s disease.

The current working model of Alzheimer's disease is the amyloid hypothesis. In short, this considers that the amyloid protein — usually involved in neuronal growth and repair — is the primary cause of the disease. Amyloid protein is also potentially involved in communication between synapses — an electrical/chemical junction between neurons. It is thus thought to be a vital part of brain function. However, the hypothesis dictates that the protein can be broken down into smaller molecules that can bind to themselves, forming plaques that can damage the brain.

Amyloid plaques have been found in autopsies of patients known to have severe Alzheimer’s disease, and there are a number of genes implicated in increasing amyloid burden. These include mutations to the APP gene, Presenilin-1 as well as APOE-ε4. All of these have been inserted into transgenic mouse models to study the disease, producing excess amyloid plaques, resulting in Alzheimer’s symptoms.

The use of these genes in genetic testing has not resulted in many treatments. The genetic cause of Alzheimer’s represents around two to three percent of all Alzheimer’s cases in humans.

The amyloid hypothesis likely does not paint the full picture of Alzheimer’s disease. Other explanations have been put forward and tested, such as tangles within the tau protein, influence of prions, or simply damage to the brain over time. No current model fully explains non-familial — or sporadic — Alzheimer’s disease.

Explanation of the limited effectiveness of treatment?
At the very least, the new discovery may explain why studies are not being transformed into treatments. Of the 97 to 98 percent of sporadic cases, any number could be LATE, meaning that treatment would not work.

However, this presents a situation where treatment options are simply being wasted on cases where they will inevitably have no effect. In India, there is no current government policy to address the situation of the rising numbers of Alzheimer's cases. This leaves the country vulnerable to wasting resources, as well as leaving countless others without any kind of treatment. 

More must be done to assess whether there are other conditions that may be misdiagnosed as Alzheimer’s disease, as well as research into diagnosing patients with LATE before death. 

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Abnormal proteins linked to aggressive behavior among dementia patients

In a recent study, scientists have observed an association between certain proteins and  dementia sufferers` tendency, to commit criminal acts. The research studied deceased patients who were diagnosed with Alzheimer's disease Alzheimer's disease or frontotemporal dementia. “This study is unique in that we studied deceased patients, something that means we are 100 per cent sure of the dementia diagnosis, which is not always established while the patients are alive,” said a researcher.

“In addition, we observed that the likelihood of committing criminal acts was nine times higher among patients with frontotemporal dementia who had accumulations in the brain of certain abnormal proteins, above all TDP-43, compared with those who had accumulations of tau protein. The TDP-43 proteins seem therefore to be particularly associated with developing criminal behaviour among people with frontotemporal dementia,” she added.

When a person who previously has been perceived by those around them as well-behaved starts committing criminal acts such as theft, shoplifting, sexual harassment or other aggressive behaviours, there may be a dementia disease behind these unexpected actions. Researchers in the Neuropathology team studied 220 deceased patients with Alzheimer`s disease or frontotemporal dementia (FTD), who had been monitored at the Clinic between 1967 and 2017.

Of these, 30 per cent had committed a criminal offence – 15 per cent of the total number of patients who had Alzheimer`s and 42 per cent among those who had FTD. The latter group committed repeated criminal offences to a greater extent than the Alzheimer`s group. When examining the behaviour such as excessively loud laughing or unexpected shouting, the frontotemporal dementia group is also over-represented (75 per cent), compared with the Alzheimer`s group (56 per cent). “It confirms what we have seen in previous studies.

With these patients, the damage is in the frontal part of the brain, where our personality, including impulse control and empathy, resides”, said a Dr., emphasising that dementia diseases do not exclusively affect the elderly. “Frontotemporal dementia can also occur in younger people and it can often take a long while before there is a correct diagnosis. That is why it`s important that relatives, healthcare services, the police and the entire legal system respond to altered social and criminal behaviour and provide assistance to enable these people to get medical care”, she concluded.

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Alzheimer protein can be transmitted

A study into proteins linked to Alzheimer’s disease has flagged the contamination of surgical instruments during brain operations, after researchers found that the proteins could potentially be transmitted.

The current study, done by a team, follows up on one conducted in 2015 when researchers examined brains of individuals who had died due to Creutzfeldt-Jakob Disease (CJD). These individuals had been treated with growth hormones in their childhood, and until 1985, such hormones were derived from the brains of deceased persons.

The 2015 findings found links between the growth hormone injections and deposits of beta-amyloid proteins in the individuals. Such deposits are regarded as a hallmark of the Alzheimer’s disease.

For the current study, the researchers tracked down old stocks of the growth hormone and found some of the samples to contain significant levels of beta-amyloid proteins and tau proteins — presence of both these proteins is crucial for diagnosis of Alzheimer’s disease. In further experiments, the team injected the contaminated hormones into the brain of mice that had been genetically modified. The mice brain later developed clumps of protein typical of Alzheimer’s.

Groups of the same mice that had been injected with synthetic growth hormone showed no such patterns. These findings support the hypothesis that beta-amyloid proteins were accidentally transmitted to patients through this medical treatment, which is now defunct.

"It is well known that the abnormal proteins seen in Creutzfeldt-Jakob disease have been transmitted between patients by certain medical and surgical procedures. We have been investigating whether the same can be true for amyloid beta," says one of the authors of the study.

“We have found new evidence that amyloid beta pathology may be transmissible. This does not mean that Alzheimer's disease can be transmitted, as we did not find any significant amount of pathological tau protein which is the other hallmark protein of Alzheimer's disease. Our findings relate to neurosurgical procedures done a long time ago. Nevertheless, the possibility of pathological protein transmission, while rare, should factor into reviews of sterilisation and safety practices for surgical procedures."

One of the authors, adds in a press note: “It is most important to emphasise that there is no suggestion in our work that you can catch Alzheimer’s disease (or CJD) by contact with a person with the disease. Our findings highlight the need to do further research in this area.”

He says further: “We suggested that the human growth hormone—which prior to 1985 was prepared from human tissue—may have been contaminated with seeds of this material as well as the prions causing CJD… We have now provided experimental evidence to support our hypothesis that amyloid beta pathology can be transmitted to people from contaminated materials.

We cannot yet confirm whether medical or surgical procedures have ever caused Alzheimer’s disease itself in people, or how common it might be to acquire amyloid pathology in this way. It will be important to review risks of transmission of amyloid pathology by other medical procedures still done today, including instruments used in brain surgery, drawing on other research and what we already know about accidental CJD transmission.”

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Novel blood test may diagnose Alzheimer's disease

Scientists have developed a blood test that can accurately diagnose or even predict Alzheimer's disease  before symptoms appear. Currently the only way to definitively diagnose Alzheimer's disease in life is through brain scans and tests of cerebrospinal fluid that must be collected via lumbar puncture. 

Though cumbersome and expensive, such tests provide the most accurate diagnoses for patients.

Researchers  are working to develop a blood test that could replace these procedures.

The tau protein has long been implicated in Alzheimer's, however, tau occurs as a family of related molecules which have subtly different properties.

The team took advantage of the complexity of tau and built assays to measure different forms of tau and identified a subset of tau proteins which are specifically elevated in Alzheimer's disease.

"A blood test for Alzheimer's disease could be administered easily and repeatedly, with patients going to their primary care office rather than having to go into a hospital," said a researcher.

"Our test will need further validation in many more people, but if it performs as in the initial two cohorts, it would be a transformative breakthrough," he said .

Researchers developed tests capable of detecting different populations of tau fragments in cerebrospinal fluid and blood.

They applied these tests to participants who had donated both plasma and cerebrospinal fluid. They validated results in a second group of patients.

The team analysed five different tests for tau fragments, finding that one, known as the NT1 assay, showed sufficient ability to predict AD cases and exclude controls to pursue its use as a potential screening tool for Alzheimer's disease. This was confirmed in both sets of patients.

While performing the experiment twice - in two sets of patients with two different demographic backgrounds - provided important confirmation, the authors note that both groups of participants were small (65 participants and 86 participants, respectively).

Larger groups of participants will need to be studied. Researchers are also interested in studying patients over time to determine how tau levels in blood may change as the disease progresses and what those numbers may look like before the onset of symptoms.

"We've made our data and the tools needed to perform our test widely available because we want other research groups to put this to test," he said.

"It's important for others to validate our findings so that we can be certain this test will work across different populations," he said.

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Alzheimer’s can now be detected in early stages by looking at brain scans

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 Researchers at the University of California have found that brain scans can foretell if a person will suffer from Alzheimer's. They have proven that sticky amyloid plaques and tau protein tangles which are characteristic of the disease can be spotted and the moment they can trigger Alzheimer's.

 Scientists for long now have been trying to find a way to diagnose Alzheimer's disease early and have finally  come up with a way to do it. Researchers at the University of California have found that brain scans can foretell if a person will suffer from Alzheimer’s. They have proven that sticky amyloid plaques and tau protein tangles  which are characteristic of the disease can be spotted and the moment they can trigger Alzheimer’s. The scientists were also successful in tracking  stages of Alzheimer’s in adults who showed no symptoms. The findings suggest that people at risk  like those who carry the APOE variant gene should be regularly screened and can also reassure people who have memory problems  that they do not suffer from Alzheimer’s. 

 The study is a breakthrough especially because currently the  only way to diagnose Alzheimer’s is to look at brain scans once the patient in dead and for patients who are alive doctors only monitor cognitive and memory skills. This study will enable doctors to use as a diagnostic and staging tool.

 The new technology was tested on 53 adults, five of whom were young adults, 33 who were pensioners without any neurodegeneration and 15 who had suspected Alzheimer’s disease. The scientists were able to prove definitively which were clear, at risk and those who had the condition. The findings also shed new light on how tau protein and amyloid plaques build up as the brain ages. For many years, the accumulation of amyloid plaques was considered the main culprit in Alzheimer’s. But now the scientists believe that both tau and amyloid work together to cause the disease.The research was published in the journal Neuron.