Common Infections Linked to Cognitive Decline in Older Adults

 Is your competent? doctor preventing these infections to not make your cognitive problems worse?

Common Infections Linked to Cognitive Decline in Older Adults

Exposure to certain common infections, particularly cytomegalovirus and herpes simplex virus type 2, was linked to poorer executive function in older adults, indicating that chronic infectious exposures may accelerate cognitive aging. Exposure to common infectious agents is associated with domain-specific cognitive impairment among community-dwelling older adults, according to study findings published in Alzheimer’s & Dementia Evidence regarding the effects of individual pathogens on specific cognitive domains is limited. Researchers from Columbia University and the University of Miami analyzed data from the Northern Manhattan Study to examine whether serologic evidence of infection with 5 common pathogens (herpes simplex virus [HSV]-1, HSV-2, cytomegalovirus [CMV],Chlamydia pneumoniae The study included 593 participants (mean [SD] age, 71 [8] years; 39% men; 69% Hispanic) who were free of stroke and dementia at baseline. Participants underwent serologic testing for infectious exposures and completed neuropsychological assessments clustered into 4 cognitive domains: memory, language, processing speed, and executive function. Over a mean follow-up of 7.8 years, 30% of participants developed cognitive impairment, and 17% were diagnosed with dementia.…[C]ommon infectious exposures may contribute to cognitive aging and dementia in late life. After adjusting for demographic, vascular, and psychosocial confounders, CMV and HSV-2 seropositivity were significantly associated with poorer executive function (β = -0.29; 95% CI, -0.51 to -0.08;P= .007 and β = -0.19; 95% CI, -0.36 to -0.02;P= .03, respectively), whileC pneumoniae seropositivity was linked to reduced language performance (β= -0.17; 95% CI, -0.32 to -0.01;P=.03). In unadjusted models, CMV seropositivity was associated with increased risk for incident MCI (hazard ratio [HR], 1.22; 95% CI, 1.09-1.36;P=.0005) and dementia (HR, 1.18; 95% CI, 1.02-1.37;>P= .024). However, these associations were no longer significant after adjustment. Study limitations include reliance on serologic titers, which indicate exposure rather than active infection or reactivation, possible misclassification of infection status over time, and limited power due to few dementia cases. “Taken together, we provide evidence that CMV exposure is associated with decreased executive function and possibly increases risk for cognitive impairment and dementia, adding to a growing body of evidence that common infectious exposures may contribute to cognitive aging and dementia in late life,” the researchers concluded. Disclosures: This research was supported by the National Institutes of Health. Please see the original reference for a full list of disclosures

Herpesvirus Infections May Accelerate Dementia

 Your competent? doctor is still responsible for preventing your higher risk of dementia.

Specific herpesvirus infections and associated diseases: 
Herpes Simplex Virus (HSV): HSV-1 primarily causes oral herpes (cold sores). 

HSV-2 primarily causes genital herpes. 

Varicella-Zoster Virus (VZV): Causes chickenpox (varicella) and shingles (herpes zoster). 

Epstein-Barr Virus (EBV): Causes infectious mononucleosis (mono) and is linked to certain cancers. 

Cytomegalovirus (CMV): Can cause serious infections in newborns and immunocompromised individuals. 

Other Human Herpesviruses: HHV-6, HHV-7, and HHV-8 can cause various conditions, including roseola infantum and Kaposi's sarcoma. 

Your risk of dementia, has your doctor told you of this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Herpesvirus Infections May Accelerate Dementia

Summary: A new study finds that prior herpesvirus infections are linked to a faster age-related increase in blood biomarkers associated with dementia, even in cognitively healthy women. Researchers measured five key biomarkers in 167 women and found that seropositivity for HHVs doubled the rate of biomarker accumulation compared to those without prior infection.

The strongest viral associations were seen for Epstein-Barr virus and HHV6, with amyloid-beta and phosphorylated tau levels most affected. These findings support the hypothesis that chronic viral infections may accelerate neurodegeneration and raise dementia risk independently of genetic factors.

Key Facts

• Biomarker Acceleration: HHV-seropositive women showed a 2.15× faster rise in dementia-related blood biomarkers with age.
• Viral Impact: The strongest associations were seen with HHV4 (Epstein-Barr) and HHV6.
• Genetic Independence: The effects of HHV infection on biomarkers were independent of APOE4 genotype.

Source: Neuroscience News

New research sheds light on a possible connection between common herpesvirus infections and the early biological changes that precede dementia.

Scientists found that cognitively healthy women who tested positive for human herpesviruses (HHVs) showed a significantly steeper age-related increase in blood biomarkers associated with Alzheimer’s disease compared to those without prior viral exposure.

The discovery that viral infection correlates with faster biomarker accumulation strengthens the hypothesis that infections act as a trigger or accelerator for Alzheimer’s and other dementias. Credit: Neuroscience News

These findings support growing evidence that infections may accelerate neurodegenerative processes — long before cognitive symptoms appear — highlighting the importance of understanding infection’s role in dementia risk.

The study analyzed blood samples from 167 cognitively unimpaired women aged 26 to 98, measuring levels of key dementia biomarkers — amyloid-beta 40 and 42 (Aβ40, Aβ42), the Aβ42/Aβ40 ratio, and phosphorylated tau proteins (pTau181, pTau217).

While all markers except the Aβ42/Aβ40 ratio increased with age overall, the increase was more than twice as high in women who were seropositive for one or more HHVs.

Among the viruses, Epstein-Barr virus (HHV4) and HHV6 were most strongly associated with elevated biomarker trajectories, followed by herpes simplex virus (HHV1). The APOE4 genetic risk factor did not significantly influence these patterns, suggesting that viral effects may operate independently of genetic predisposition.

Why does this matter? These biomarkers — detectable years before symptoms — are considered indicators of underlying neurodegeneration. The discovery that viral infection correlates with faster biomarker accumulation strengthens the hypothesis that infections act as a trigger or accelerator for Alzheimer’s and other dementias.

Interestingly, researchers note that while amyloid-beta and tau are central to dementia pathology, they also have antimicrobial properties, raising the possibility that their buildup in infected individuals may initially serve as a protective response against persistent viruses — a response that eventually becomes pathological.

These findings add weight to calls for broader research into the infectious origins of dementia and could even open avenues for preventive strategies, such as vaccines or antiviral therapies, in at-risk individuals.

Further studies are needed to determine if these findings extend to men and to other populations, and whether targeting chronic infections could slow or prevent dementia onset.

About this neurology and dementia research news

Author: Neuroscience News Communications
Source: Neuroscience News
Contact: Neuroscience News Communications – Neuroscience News
Image: The image is credited to Neuroscience News

Original Research Open access.
“Human herpes viruses are associated with steeper age-dependent increases of serum biomarkers for dementia in cognitively unimpaired women” by Lisa M. James et al. Scientific Reports

Scientists Confirm: Herpes Virus Implicated in Alzheimer’s Disease

You'll want your doctor to know what to do with this to prevent your getting dementia.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

Scientists Confirm: Herpes Virus Implicated in Alzheimer’s Disease

A coalition of scientists from the Icahn School of Medicine in New York City and Arizona State University, collected over 2,000 post-mortem tissue samples from 944 brains held at several brain banks funded by the US National Institute of Aging, which also provided money for the study. Some of the brain samples had the tell-tale amyloid plaques and tau buildups found in Alzheimer’s disease and some had signs of other cognitive impairments. Others were “control” patients with healthy brain function. What they discovered is groundbreaking news for scientists and any lives touched Alzheimer’s disease. They published their results in the science journal, Neuron, last week.
The herpes viruses
There are 9 herpes viruses known to man but when people think of herpes, they usually think of sexually transmitted diseases and unsightly cold sores erupting from infected lips. Those are the herpes viruses, HSV1 and HSV2. The peculiar thing about any herpes virus is its ability to go dormant in the body only to reawaken later and begin reproducing all over again causing diseases like shingles. In fact, the name herpes is derived from the Greek word meaning, “to creep” because of their ability to creep up nerves and plant themselves on our spines and in some instances, even our brains, probably having an effect on Alzheimer’s disease.
Although the research team found over 500 types of viruses present in those 2,000 brains, the two forms of herpes virus – HHVA6 and 7 – were found in particularly high concentrations in the brains of individuals with Alzheimer’s. After their dormant stage, they start actively reproducing and appear to speed up the Alzheimer’s-related protein build ups that ultimately lead to the brain’s system failure. Although not causative, they are described as “putting gas on the flame,” by Joel Dudley, a geneticist at the Icahn School of Medicine at Mt. Sinai in New York City, who described the virus as accelerating the disease. The study offers strong evidence that viral infections can influence its course.
Just an accident
Like the discovery of penicillin, many scientific discoveries are made by accident and this discovery is no different. The goal for this study was to identify new targets for drugs by using genetic data to look for differences between healthy brain tissue and brain tissue from those who had developed Alzheimer’s. Dudley says that, “Viruses were the last thing we were looking for.” But when they began to analyze the differences, “it just sort of came screaming out at us from the data.” The two human herpes viruses HHV6 and HHV7 were twice as high in brain tissue from people with Alzheimer’s!
Once they knew this, the next step was to find out how the viruses could affect the course of a brain disease. In order to do this, they set about identifying interactions between virus genes and other genes in the brains cells by mapping out a kind of social network between the two. Dudley wanted to know, “If the viruses are tweeting, who’s tweeting back?”
What they found were that the herpes virus genes were interacting with genes known to both increase a person’s risk for Alzheimer’s and to make a person’s brain more vulnerable to infection with HHV6 and HHV7. Just having the virus present in the brain isn’t enough to cause Alzheimer’s. Something needs to activate the virus out of its dormancy. To date, that activating factor has not been found but Dudley is hopeful and suspects some internal function of the brain cells is the cause. Still, because of the importance of this finding, we are two steps closer to finding a way to slow and maybe even stop the progression of the disease.

---

Research
1. Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus. Neuron.
https://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5
2. Herpes Viruses Implicated in Alzheimer’s Disease. The Scientist. June, 21, 2018
https://www.the-scientist.com/news-opinion/herpes-viruses-implicated-in-alzheimer-s-disease-64246
3. Researchers Find Herpes Viruses In Brains Marked By Alzheimer’s Disease. NPR. June 21, 2018.
https://www.npr.org/sections/health-shots/2018/06/21/621908340/researchers-find-herpes-viruses-in-brains-marked-by-alzheimers-disease

Unusually High Levels of Herpes Viruses Found in the Brains of Patients With Alzheimer’s Disease

You'll have to hope there is some human followup with this testing. Will your doctor be doing that followup? OR just sit on their asses and wait for  SOMEONE ELSE TO SOLVE THE PROBLEM and deliver a protocol!

When the Taiwanese authors looked at subjects who suffered severe herpes infection and who were treated aggressively with antiviral drugs, the relative risk of dementia was reduced by a factor of 10.

http://dgnews.docguide.com/unusually-high-levels-herpes-viruses-found-brains-patients-alzheimer-s-disease?

NEW YORK -- June 26, 2018 -- Researchers have discovered that 2 strains of human herpesvirus -- human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) -- are found in the brains of people with Alzheimer’s disease at levels up to twice as high as in those without Alzheimer’s.
In a study published in Neuron, Benjamin Readhead, Icahn School of Medicine at Mount Sinai, New York, New York, and colleagues described how they used evidence from postmortem brain tissue to identify previously unknown gene networks that will offer new testable hypotheses for understanding Alzheimer’s pathology and reveal novel potential targets for new drugs that may halt Alzheimer’s disease progression.
The researchers initially performed RNA sequencing on 4 brain regions (superior temporal gyrus, anterior prefrontal cortex, inferior frontal gyrus, and parahippocampal gyrus) in over 600 samples of postmortem tissue from people with and without Alzheimer’s to quantify which genes were present in the brain, and whether any were associated with the onset and progression of Alzheimer’s.
Through a variety of computational approaches, the team uncovered a complex network of unexpected associations, linking specific viruses with different aspects of Alzheimer’s biology. They examined the influence of each virus on specific genes and proteins in brain cells, and identified associations between specific viruses and amyloid plaques, neurofibrillary tangles, and clinical dementia severity.
Notably, the study found an abundance of HHV-6A and HHV-7 across the anterior prefrontal cortex and the superior temporal gyrus.
To evaluate the robustness of their findings, the researchers incorporated over 800 additional RNA sequencing samples from 2 additional, independent cohorts and were able to replicate their main findings.
“This study represents a significant advancement in our understanding of the plausibility of the pathogen hypothesis of Alzheimer’s,” said Joel Dudley, PhD, Icahn School of Medicine at Mount Sinai. “Our work identified specific biological networks that offer new testable hypotheses regarding the role of microbial defense and innate immune function in the pathophysiology of Alzheimer’s. If it becomes evident that specific viral species directly contribute to an individual’s risk of developing Alzheimer’s or their rate of progression once diagnosed, then this would offer a new conceptual framework for understanding the emergence and evolution of Alzheimer’s at individual, as well as population, levels.”
The findings could translate to the identification of virus, or virus-related, biomarkers that may improve patient risk stratification and diagnosis, noted Dr. Dudley. It could also imply novel viral targets and biological pathways that could be addressed with new preventative and therapeutic drugs. As with any complex set of findings, they will need to be confirmed in additional patient cohorts, and further studies to specifically address a causal role for viruses are now being conducted.
“This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer’s,” added Sam Gandy, MD, Center for Cognitive Health and NFL Neurological Care at Mount Sinai, New York, New York. “A similar situation arose recently in certain forms of Lou Gehrig’s disease. Viral proteins were discovered in the spinal fluid of some patients [with Lou Gehrig’s disease], and patients with positive viral protein tests in their spinal fluid showed benefit when treated with antiviral drugs.”
Reference: https://doi.org/10.1016/j.neuron.2018.05.023
SOURCE: Mount Sinai Health System

Study Finds Link Between Alzheimer's and Herpes

I had two forms of the virus as a kid; chicken pox and cold sores. Should I be taking these antiviral drugs as a precaution?

Study Finds Link Between Alzheimer's and Herpes

A new commentary by scientists at the Universities of Manchester and Edinburgh on a study by Taiwanese epidemiologists supports the viability of a potential way to reduce the risk of Alzheimer’s disease.
When the Taiwanese authors looked at subjects who suffered severe herpes infection and who were treated aggressively with antiviral drugs, the relative risk of dementia was reduced by a factor of 10.
Manchester’s Professor Ruth Itzhaki and Edinburgh’s Professor Richard Lathe say the paper, by Tzeng et al. and published in Neurotherapeutics in February 2018, also shows that herpes simplex virus type 1 (HSV1) leads to an increased risk of developing the disease.
“This article and two others by different research groups in Taiwan provide the first population evidence for a causal link between herpes virus infection and Alzheimer’s disease, a hugely important finding,” said Itzhaki.
They publish a commentary in the Journal of Alzheimer’s Disease on the three articles, arguing that they provide the strongest evidence yet for a causal link between herpes infection and Alzheimer’s disease, backing 30 years of research by Itzhaki.
Itzhaki said: “I believe we are the first to realize the implications of these striking data on this devastating condition which principally affects the elderly. No effective treatments are yet available.
“Almost 30 million people worldwide suffer from it and sadly, this figure will rise as longevity increases.
“But we believe that these safe and easily available antivirals may have a strong part to play in combating the disease in these patients.
“It also raises the future possibility of preventing the disease by vaccination against the virus in infancy.
”Successful treatment by a specific drug, or successful vaccination against the putative microbe, are the only ways to prove that a microbe is the cause of a non- infectious human disease.”
Most Alzheimer’s disease researchers investigate its main characteristics — amyloid plaques and neurofibrillary tangles; however, despite the vast amount of research, the causes of their formation are unknown.
HSV1 infects most humans in youth or later and remains lifelong in the body in dormant form within the peripheral nervous system.
From time to time the virus becomes activated and in some people it then causes visible damage in the form of cold sores.
The Taiwanese study identified 8,362 subjects aged 50 or more during the period January to December 2000 who were newly diagnosed with severe HSV infection.
The study group was compared to a control group of 25,086 people with no evidence of HSV infection.
The authors then monitored the development of dementia in these individuals over a follow-up period of 10 years between 2001 and 2010.
The risk of developing dementia in the HSV group was increased by a factor of 2.542. But, when the authors compared those among the HSV cohort who were treated with antiviral therapy versus those who did not receive it, there was a dramatic tenfold reduction in the later incidence of dementia over 10 years.
“I believe we are the first to realize the implications of these striking data on this devastating condition which principally affects the elderly. No effective treatments are yet available,” said Itzhaki.
Professor Richard Lathe added: “Not only is the magnitude of the antiviral effect remarkable, but also the fact that — despite the relatively brief duration and the timing of treatment — in most patients severely affected by HSV1 it appeared to prevent the long-term damage in brain that results in Alzheimer’s.
Itzhaki said: “It was as long ago as 1991 when we discovered that, in many elderly people infected with HSV1, the virus is present also in the brain, and then in 1997 that it confers a strong risk of Alzheimer’s disease in the brain of people who have a specific genetic factor.
“In 2009, we went on to show that HSV DNA is inside amyloid plaques in Alzheimer’s patients’ brains.
“We suggested that the virus in brain is reactivated by certain events such as stress, immunosuppression, and infection/inflammation elsewhere.
“So we believe the cycle of HSV1 reactivation in the brain eventually causes Alzheimer’s in at least some patients.”
The study by Tzeng et al. investigated only people with severe HSV and cannot be generalized to healthy populations.
The paper, “Herpes Viruses and Senile Dementia: First Population Evidence for a Causal Link,” is published in the Journal of Alzheimer's Disease.
Source: University of Manchester

 

Yet More Evidence that Viruses May Cause Alzheimer's Disease

You better hope like hell that your doctors and hospital follow up this research. You will need it.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

I had cold sores when I was a kid, haven't had one in decades, wonder if I need to be concerned.

https://gizmodo.com/yet-more-evidence-that-viruses-may-cause-alzheimers-dis-1827511539

For decades, the idea that a bacteria or virus could help cause Alzheimer’s disease was dismissed as a fringe theory. But not so much anymore. On Wednesday, a team of researchers from Harvard Medical School reported in the journal Neuron the latest bit of evidence suggesting herpesviruses can spark the cascade of events that leads to Alzheimer’s disease, a fatal form of dementia that afflicts at least 5 million Americans.

The researchers studied how neurons in mice responded to the presence of herpes simplex 1 (HSV-1), the virus that causes cold sores. In a separate experiment involving a 3D model of the human brain grown in a dish, they also studied human herpesvirus 6 (HHV-6), the germ responsible for causing the childhood skin disease roseola. These viruses are usually caught early on in life and stay dormant somewhere in the body, but as we age, they almost always migrate up to the brain.

Some of the mice used in the experiment were genetically bred to have neurons that could create the human version of amyloid beta (or amyloid-β). Amyloid-β is a protein normally produced in the brain. But in Alzheimer’s patients, it clumps together to form the plaques that are thought by many experts to slowly destroy the brain. Many scientists had long assumed that amyloid-β was essentially a waste product, with no meaningful purpose. But the researchers had earlier shown that amyloid-β might actually serve as a first line of defense against fungal and bacterial infection.

In the current study, both viruses seemed to provoke an identical reaction. The mice’s brains grew new deposits of amyloid-β plaques practically “overnight,” according to senior author Rudy Tanzi, a geneticist specializing in the brain at Massachusetts General Hospital as well as Harvard Medical School. And the mice bred with these human-like neurons were able to better fend off brain infection than mice without them. The same effects were also seen in the petri dish.

“The seeding of amyloid is what causes the deposition of plaque,” Tanzi told Gizmodo, “and herpesviruses and other microbes can rapidly seed amyloid-β.”

The study is the second in recent weeks to support the role of viruses in Alzheimer’s disease. That first study, also published in Neuron and led by researchers from the Icahn School of Medicine at Mount Sinai, found evidence that certain herpesviruses are more abundantly present in the brains of people who died with Alzheimer’s; it also suggested that genes belonging to these viruses directly interact with human genes that raise the risk of the disease.

The timing is no accident, Tanzi said. His team has corresponded with the Mount Sinai team for years, and they had originally planned to release their results at the same time (both will be published in the same print July edition of the journal). It was the Mount Sinai team, Tanzi notes, that suggested the Harvard team look at HHV-6 as well as HSV-1 in their experiments, since that was the virus they had started to zero in on in their work.

While Tanzi and his team acknowledge the long-ignored work by other researchers supporting the viral hypothesis of Alzheimer’s, as it’s known, he said their research takes things in a slightly different direction. It’s an attempt to reconcile various theories about what causes Alzheimer’s.

Supporters of the viral theory have often speculated that germs such as HSV-1—the most commonly blamed culprit—directly goad the brain into spiraling out of control through inflammation, with amyloid-β only being a bystander. But in Tanzi’s version, amyloid-β still is the key cog behind the disease. Neurons use the protein to either kill or safely trap viral or bacterial particles in a “nano-net,” as Tanzi put it. In Alzheimer’s disease, this process goes off the rails, leading to the uncontrolled buildup of plaques. From there, Tanzi’s work has shown, the plaques trigger the production of tangles—clumps of another brain protein called tau seen in the later stages of Alzheimer’s—which together then trigger chronic inflammation. All of these moving parts align to wither the brain, eventually causing death.

In this scenario, it’s not so much the germ, but the immune system that’s at fault. “The microbes are the prequel to the amyloid hypothesis,” Tanzi said.

Viruses are only one of the things that could set off Alzheimer’s, he pointed out. The same sort of seeding might happen in people whose genes cause them to make too much amyloid-β, in the absence of infection. And genetics might help explain why only some people’s infections cause the brain to start producing amyloid-β en masse. “Just having the virus isn’t enough,” Tanzi said.

But given the widespread failure of Alzheimer’s treatments that have focused on stopping amyloid-β production, the viral link provides a new, clear direction for future clinical trials: Preventative antimicrobial drugs or vaccines that can stop these germs from ever reaching the brain in the first place. Some recent, if observational research (meaning, not controlled trials) has already suggested that these drugs can lower the risk of dementia.

These sorts of definitive studies are likely still a while away, but there’s certainly a change in the headwinds.

“I think we’ve gotten past the point where this idea is ridiculed, but some might be still violently opposing it,” Tanzi said, referring to the 19th century German philosopher Arthur Schopenhauer’s maxim about the three stages of truth (first ridicule, then violent opposition, and finally acceptance as self-evident).

The Herpes Virus Can Affect Your Brain In Surprising Ways

I had two forms of the virus as a kid; chicken pox and cold sores. 

The Herpes Virus Can Affect Your Brain In Surprising Ways

If you’ve had mononucleosis, chicken pox, or cold sores, then you’ve had the herpes virus. Weird, isn’t it? Anna Rothschild explains in the YouTube channel Gross Science that the virus actually stays in your body for a lifetime and goes through a period where it lies dormant in neurons, hiding from the immune system. It turns out, however, it can even sneak into your brain.

Before you freak out about that, it’s important to note that this happens to about two in a million people. The virus can sneak into your temporal lobe and affect you in peculiar ways. For instance, those who survived the viral attack on the brain had specific damage that didn’t allow them to make normal class categorizations that we normally make on a daily basis, like colors or animals.

More at link.