Usage Of Gv971 To Treat Ad And The Case For Using A Related Compound Fucoidan
The study by Cairns et al. strongly supports the use of antiviral treatment for AD patients, and a clinical trial of VCV to treat AD patients is ongoing at Columbia university. Another clinical trial treating AD patients, described by Cummings et al. , is yielding encouraging results: a phase 2 trial of GV971, a compound derived from brown algae which consists of polysaccharideslinear sodium oligomannate moleculesof a range of sizes. This, they suggest, may reduce brain inflammation as well as systemic inflammation through effects on the gut microbiome, and very recently, the positive results of a phase 3 trial of GV971 have been reported by Xiao et al. . The latter authors stated that GV971 demonstrated significant efficacy in improving cognition, with sustained improvement across all observation periods of a 36-week trial, and it was safe and well-tolerated. However, an alternativeor perhaps additionalmechanism might operate via the drug acting as an antiviral agent against HSV1 . Marine-derived polysaccharides have been shown to have a variety of bioactivities, including antiviral effects , and anti-bacterial effects.
The next section deals with links between COVID-19. HSV1, and APOE.
The Link Between Alzheimers And Herpes
A growing amount of research has found a clear link between Alzheimers and different strains of herpes. In fact, over 100 research papers have described a correlation between HSV-1 and Alzheimers risk.
Scientists are quick to note, however, that correlation doesnt equal causation. Most of the researchers involved in these tests pose a number of theories about why the two illnesses may be linked.
One of the most recent studies on the subject at the Icahn School of Medicine at Mount Sinai looked at brain tissue from healthy people and people who had died from the disease to see what differences and similarities they could find. They were surprised to find that the viruses HHV-6A and HHV-7 showed up twice as often in the brain tissue of people with Alzheimers as they did in normal brain tissue. These strains of herpes are extremely common but remain inactive in the brain for decades, so the research suggests their presence plays some role in increasing the risk of Alzheimers.
Relationship Of Apoe And Of Infection And Infectious Burden To Cognition
Adjusted linear and logistic regressions estimated the association between IBI and cognition, with a term included for the interaction between APOE-4 and IBI. The data revealed interactions between IBI and APOE-4 , and HSV1 and APOE-4 for processing speed in those subjects who had full neuropsychological test results. IBI was associated with slower processing speed among non4 carriers, but not among APOE 4 carriers. HSV1 seropositivity was associated with slower processing speed among non4 carriers, but not among APOE 4 carriers. Two intriguing features of the study were discussions on the relevance of differences in APOE-4 frequency amongst the different ethnic groups, and the relevance of the pleiotropy of APOE-4 , with APOE-4 acting as a modifier of the association between IBI and cognition, and in turn being modified to some extent by ethnicity. The authors, however, seemed unaware that APOE modulates the consequences of infection in a number of infectious diseases , not just in the cited protective action of 4 in HCV-infection of liver . In addition, in AD patients, their suggestion that APOE-4 carriers might have increased susceptibility to HSV1 is unlikely to be correct, in view of the very high proportion of people infected with HSV1.
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Exposure Gwas Data Set
For infections, we used the GWAS summary statistics data from 23andMe cohort . Individuals were included in this GWAS analysis using a set of strict self-reported questionnaires about their history of infection diseases to define phenotypes . Participants were selected for having> 97% European ancestry as determined through an analysis of local ancestry. We focused on four infections all caused by members of the human herpesvirus that were discussed in association with AD . The detailed descriptions of the GWAS data are presented in Table .
Table 1 Description of the GWAS studies used in the primary analysis
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What The Research Says About Herpes And Alzheimers
In the study, the 15 researchers analyzed data from 622 postmortem from a dead body brains of people who once exhibited symptoms of Alzheimer’s, along with brains of people seemingly untouched by this devastating disease. They found nearly two times the level of herpesvirus, HHV-6A and HHV-7, in the Alzheimer’s brains when compared with the “normal” brains. The findings were replicated in two additional independent cohorts, or groups of people, the researchers said.
It’s important to note that because the researchers found viruses in both Alzheimer’s and non-Alzheimer’s brains, we can’t assume that herpes infections alone caused the devastating brain disease to develop.
According to a news release, researchers from the Icahn School of Medicine at Mount Sinai “identified previously unknown gene networks that will both offer new testable hypotheses for understanding Alzheimers pathology and reveal novel potential targets for new drugs that may arrest Alzheimer’s disease progression, and could potentially prevent the disease if administered early enough.”
Vaccination Protection Against Risk Of Ad And Of Hsv1 Reactivation
Whichever viruses are involved in AD, one would assume that to prevent their action, specific vaccines would be needed against each one. However, vaccinesin particular Bacillus Calmette Guérin , which was designed to protect against tuberculosishave been known since the early years of the 20th century to induce diverse non-specific effects . These effects include reduction of infant mortality independently of its effect on tuberculosis, e.g., in West Africa a 50% reduction in overall mortality was demonstrated in children vaccinated with BCGtoo large an effect to be explained by protection against tuberculosis alone . More recently, these findings have been validated in randomized controlled trials and in a meta-analysis of three RCTs investigating mortality reduction amongst low birth-weight infants . The mortality reduction in infants by BCG was attributed to protection against unrelated infectious agents, particularly against respiratory tract infections, and to protection against neonatal sepsis .
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Alzheimers And Herpes: It Isnt Just What You Think
A lot of people have come to associate the word herpes with the STI thats just one of many versions of the infection. In fact, the medical community has identified a number of strains of the infection many of which are extremely common.
Nearly two-thirds of all people have been infected with HSV-1, a herpes strain that causes cold sores for some, but lies dormant in the body for many. HHV-6, a version of herpes most commonly associated with the childhood skin rash roseola, infects nearly everyone. VZV or , the virus responsible for chicken pox and shingles, is yet another prevalent strain. Those are just three of the most common versions of herpes.
In short, most people have some version of herpes long before they reach their adult years and no one should view any of the strains as something shameful. Theyre merely a part of life.
Disparities In The Literature
Ben Readhead, a data scientist at Arizona State University specializing in neurodegenerative diseases who wasnt involved in the new research but has collaborations with two of its coauthors, says he is puzzled by its findings. Hes a coauthor of the 2018 study, which detected an abundance of several viral species, including HHV6, across the brain and linked them to different facets of Alzheimers disease pathology.
I think it is difficult to draw a strong conclusion from this study about whether HHV-6A/B is associated with Alzheimers disease.
Ben Readhead, Arizona State University
Although that study was based on much of the same RNA sequencing data used by Jacobsons group, the two teams report disparate results. Whereas in the RNA data from the Mount Sinai Brain Bank, Readheads team found HHV6A frequencies ranging from 18 percent to 35 percent of samples and HHV6B frequencies between 15 percent and 31 percent, Jacobsons team found HHV6A or HHV6B frequencies ranging from 0 percent to 2.2 percent. Another surprising finding is the absence of reported detection of several other very common, neurotropic viruses within the analysis of the RNA-sequence data sets, Readhead notes in an email. .
M.A. Allnutt et al., Human Herpesvirus 6 detection in Alzheimers disease cases and controls across multiple cohorts, Neuron, doi:10.1016/j.neuron.2019.12.031, 2020.
Katarina Zimmer is a New Yorkbased freelance journalist. Find her on Twitter .
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Assessment Of Global Cognition And Cognitive Domains
Participants underwent a battery of cognition tests at the baseline examination visit as well as the next follow-up examination. The tests included Mini Mental State Examination , Word Learning Test , Letter-Digit Substitution Task , Verbal Fluency Task , Stroop Test , and Purdue Pegboard Task . For global cognition, we calculated the g-factor as a standardized compound score using principal component analysis with LDST, Stroop color-word interference subtask, VFT, WLT delayed recall, and PPB sum of both hands. On each test, a higher score indicates a better performance apart from the Stroop test. Data on cognition was collected at baseline and at subsequent examination rounds between 2009 and 2011 to track cognitive decline.
Link Between Herpes Virus Infections Alzheimers Refuted
Researchers at Baylor College of Medicine and Texas Children’s Hospital report today in the journal Neuron evidence that refutes the link between increased levels of herpes virus and Alzheimers disease. In addition, the researchers provide a new statistical and computational framework for the analysis of large-scale sequencing data.
About 50 million people worldwide are affected by Alzheimers disease, a type of progressive dementia that results in the loss of memory, cognitive abilities and verbal skills, and the numbers are growing rapidly. Currently available medications temporarily ease the symptoms or slow the rate of decline, which maximizes the time patients can live and function independently. However, there are no treatments to halt progression of Alzheimers disease.
Like all types of dementia, Alzheimers disease is characterized by massive death of brain cells, the neurons. Identifying the reason why neurons begin and continue to die in the brains of Alzheimers disease patients is an active area of research, said corresponding author Dr. Zhandong Liu, associate professor of pediatrics at Baylor and the at Texas Childrens Hospital.
Presence of elevated levels of genetic material of herpes viruses indicated active infections, which were linked to Alzheimers disease. In less than a year, this study generated a flurry of excitement and led to the initiation of several studies to better understand the link between viral infections and Alzheimers disease.
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Assessment Of Incident Dementia And Alzheimers Disease
Screening for dementia was done at baseline and throughout the study via examination visits and digital medical records. Participants underwent multiple steps before being diagnosed with dementia. The first step was the MMSE and the Geriatric Mental Schedule . If participants screened positive in either test then it was followed by an examination with the Cambridge Examination for Mental Disorders of the Elderly and, if believed to have dementia, consequent neuropsychological examinations. Any participant who was unable to visit the center was followed via digital medical records through general practitioners and the Regional Institute for Outpatient Mental Health Care. The final diagnosis was made by a consensus panel in accordance with standard criteria Alzheimers disease and vascular dementia ,. Follow-up was until January 1, 2016 with 95.5% of participants. Participants were censored at date of dementia diagnosis, death, or loss to follow-up.
Involvement Of Vzv In Ad/dementia
Apart from in the studies described in the preceding section, VZV has not so far been suggested as a prospective cause of dementia. A possible argument against its involvement is the fact that it usually reactivates only once, rarely a second time. Recurrent reactivations seem to be a prerequisite for the development of dementia, as progression of the disease occurs over many years. However, as mentioned above, it is unknown whether or not dementia might be caused by VZV if present in brain or via inflammation caused by peripheral VZV infection leading to HSV1 reactivation in brain. In the case of herpes zoster sufferers, both Chen et al. and Bae et al. found shingles was associated with a clear but small risk of AD/dementia, and a significantly lower risk in those treated with antivirals.
As to whether an allele of APOE confers a risk of shingles is uncertain: Pirtilla et al. examined the APOE genotypes of 41 patients with HZ and found no differences in allele frequency between the patients and controls. In contrast, my group , found that women homozygous for APOE-4 had a higher-than-normal risk of shingles . However, both studies had only a small number of participants, so they need to be repeated.
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Antiviral Drug A Possible Cure For Alzheimers Disease
Dr Ruth and her team found surprising result of lower rate of Alzheimers disease among those who received antiviral drugs for their herpes infection, including chicken pox . This points towards the the future possibility of preventing Alzheimers disease with antiviral therapy. However, the effective time, dose, duration and type of antiviral drug for preventing Alzheimers still need further research. Currently, we have no idea about the usefulness of antivirals for people without severe herpes infection as well as those who already have Alzheimers disease.
Viral Infections Linked To Dementia
Infection With Common Viruses May Increase Dementia Risk
A new study shows that elderly people with evidence of infection with three common viruses viruses that cause cold sores, genital herpes, and a mono-like illness were more than twice as likely to suffer from dementia.
Researchers say the study adds new evidence to the theory that inflammation, which is part of the bodys natural response to infection, plays an important role in the development of several health problems, such as heart disease, stroke, and dementia.
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How An Outsider In Alzheimers Research Bucked The Prevailing Theory And Clawed For Validation
Neuropathologist Ruth Itzhaki of the University of Manchester in England, who has studied the role of microbes in causing Alzheimers, agreed, calling the research a really important development. She said the Tufts team, by showing that HSV-1 causes the formation of structures closely resembling the characteristic AD plaques and tangles, demonstrated directly what before now had been only inferred: that the human brains response to HSV-1 and other viruses might be what gets Alzheimers disease going years before symptoms, and that the plaques and other pathology that most people thought caused the disease are instead a defensive response to the true cause.
That might seem to suggest that antivirals will never be effective against Alzheimers: The damage is long since done. Thats what Devanands clinical trial is designed to find out. But the 3D quasi-brains offer reason for optimism. When the scientists added the herpes drug valacyclovir, which GlaxoSmithKline sells as Valtrex, the brain tissue became less inflamed, eliminated many of the plaque-like deposits, and functioned better.
The Maddening Saga Of How An Alzheimers Cabal Thwarted Progress Toward A Cure For Decades
Several studies have linked HSV-1 and other herpesviruses to Alzheimers, finding, for example, high levels of viral genomes in areas of the brain ravaged by Alzheimers and donated to science. That supported the idea that the brain responds to a viral invasion by producing amyloid, which seems to be antimicrobial but may also destroy synapses.
Active infection may not be a requirement for Alzheimers disease, Kaplan and his colleagues wrote. A history of herpes infection might be sufficient to initiate Alzheimers.
But not in everyone. An estimated two-thirds of people 50 and younger are infected with HSV-1. Although nothing close to that number will develop Alzheimers from a virus or anything else, scientists arent sure what combination of genetics, lifestyle, and other factors determines who will.
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Abundance Of Nscs/npcs: A Neurogenic Niche
As demonstrated ex vivo, the hippocampus and periventricular areas of neonate mice were particularly susceptible to HSV-1 infection . The viral dissemination into these brain regions where neuronal differentiation is active suggests that dividing cells are more vulnerable to HSV-1 infection . Using organotypic hippocampal cultures, it was shown that the hippocampal DG was most vulnerable to HSV-1 infection compared to hippocampal glia and other neuronal types . Another study also showed that HSV-1 preferentially infects undifferentiated NSCs rather than mature hippocampal neurons, resulting in impaired hippocampal neurogenesis . More recent studies have shown that HSV-1 readily infects NSCs/NPCs and induces A42 accumulation, neuroinflammation and neuronal impairments, which can be prevented with valacyclovir antiherpetic treatment .
Can Treating Herpes Prevent Alzheimers
19 May, 2021
Can treating herpes prevent Alzheimers? According to recent findings, yes. In fact, treating the disease early on can reduce the risk of contracting Alzheimers and diseases like depression. But what does this really mean? Lets take a closer look below.
Many people suffer from sporadic herpes outbreaks, especially around the mouth and mucous membranes. Outbreaks can happen due to changes in weather, sun exposure, contact with an irritating substance, fatigue, stress, or hormonal changes.
Doctors regularly stress the importance of catching and treating illnesses early on, but now we know that this is even more important with herpes after the latest findings that are both surprising and interesting.
Recent evidence suggests that theres a relationship between the herpes virus and the risk of contracting depression and Alzheimers. Consequently, treating herpes is crucial in preventing these diseases.
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