Is There A Risk Of Being Infected
Science is still working on determining what really causes Alzheimer’s disease. We know that risk factors like age, genetics, family history and lifestyle are all part of the picture. It’s also possible that an infectious property such as prions may be involved in Alzheimer’s disease, but this potential is unproven at this time and is based only on preliminary research with mice.
If it turns out that prions do play a role in Alzheimer’s disease, it’s important to remember that prion diseases are not spread through casual or even intimate physical contact with others. So, go ahead and hug that person with Alzheimer’s. Their disease is not contagious in any way, and they could experience some of the benefits related to appropriate physical touch for people with dementia, including lowering blood pressure, reducing pain and reducing challenging behaviors in dementia.
Evasion And Establishment Of Latent And Chronic Infection
The ability of spirochetes and C. pneumoniae to evade destruction by host immune systems and establish chronic infection is well known. HSV-1 can also remain in a latent state and persist throughout life in human tissues. In the latent state, the viral genome is present, but no viral particles are produced. Viral gene expression during latency is limited to one locus the gene encoding the latency-associated transcript .
Existing Evidence Suggests An Infectious Aetiology Of Neurodegenerative Diseases
The neurodegenerative diseases AD and AMD are complex multifactorial diseases that share modifiable and non-modifiable risk factors as well as common pathological mechanisms, including inflammation and oxidative stress .
Figure 1. Schematic diagram of risk factors and mechanistic events that underlie the pathogenesis of Alzheimer disease and age-related macular degeneration . The question sign indicates an unknown, potentially infectious contributor to the downstream immunopathological cascades that are common in both AD and AMD.
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Agents That Cause Infectious Diseases
Infectious diseases can be caused by several different classes of pathogenic organisms . These are viruses, bacteria, protozoa, and fungi. Almost all of these organisms are microscopic in size and are often referred to as microbes or microorganisms.
Although microbes can be agents of infection, most microbes do not cause disease in humans. In fact, humans are inhabited by a collection of microbes, known as the microbiome, that plays important and beneficial roles in our bodies.
The majority of agents that cause disease in humans are viruses or bacteria, although the parasite that causes malaria is a notable example of a protozoan.
Examples of diseases caused by viruses are COVID-19, influenza, HIV/AIDS, Ebola, diarrheal diseases, hepatitis, and West Nile. Diseases caused by bacteria include anthrax, tuberculosis, salmonella, and respiratory and diarrheal diseases.
Research About How Alzheimers Disease Spreads
While Alzheimers disease is not spread through contact with others, some research with mice seems to indicate that it could have some type of an infectious component, possibly related to prions . In prion diseases, including Creutzfeldt-Jakob disease, prion proteins begin to fold abnormally and then infect other healthy prions they encounter within the body, causing cells to die in the brain and dementia to develop. Although the unhealthy prions spread within a person, there is virtually no risk of the disease affecting other people around that individual, including family members or those caring for that person.
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How Can Non Infectious Diseases Be Prevented
Reduce the major modifiable risk factors, such as tobacco use, harmful use of alcohol, unhealthy diets, and physical inactivity. Develop and implement effective legal frameworks. Orient health systems through people-centred health care and universal health coverage. Promote high-quality research and development.
What Is The Most Effective Way To Prevent Viral Infections
Good hygiene: the primary way to prevent infections
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Evidence For A Causal Role Of Pathogens In Ad
Astrocytes and microglia infected in vitro with C. pneumoniae display inclusions that are indistinguishable from those characteristic of active infection of the standard HEp-2 host cell line . It was reported that chronic or persistent infection of CNS cells with C. pneumoniae can affect apoptosis in AD, in both a pro- and antiapoptotic manner . Furthermore, infection of BALB/c mice by intranasal inhalation of C. pneumoniae initiated A142 deposits in the brain that resembled senile plaques . Antibiotic treatment following C. pneumoniae infection limited the number of induced amyloid plaques in vivo .
The glycoprotein B of HSV-1 has a highly homologous sequence to a fragment of A . Synthetic peptides derived from this region accelerate fibrillar aggregation of A in vitro. They can self-assemble into fibrils, which are ultrastructurally indistinguishable from A and are neurotoxic at a similar dose to A. It was proposed that HSV-1 might act as a seed for senile plaque formation . It was also shown that HSV-1 is associated with APP during its anterograde transport, which might affect APP degradation and synaptic function .
Check Your Knowledge Can You:
provide examples of non-infectious and infectious diseases including the global conditions that increase the risk of disease occurrence?
list the steps required for a normal cell to become a cancer cell and explain the difference between a benign and malignant tumor?
outline how hormones regulate blood sugar, explaining the relationship of blood sugar to type I, type II, and gestational diabetes?
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Neuroinflammation And Tlr Signalling
Persisting, poorly degradable bacterial remnants in mammalian tissues act as chronic inflammatory stimuli . Lipopolysaccharides , PGN and various bacterial lipoproteins elicit a variety of proinflammatory responses and might represent an important source of inflammation in AD. Complex interactions between the innate and adaptive immune systems have a major role in infection . The functions of innate immunity allow host cells to recognise most microorganisms, execute proinflammatory defences and start adaptive immune responses.
Bacteria attach to host cells through a variety of cell-surface components, including surface amyloid proteins, which interact with host proteases . Proteolysis of the extracellular matrix allows bacteria to penetrate the basement membrane and invade host cells.
Complex interactions between pathogen-associated molecular patterns , PRRs and TLR signalling pathways have a major role in linking innate and adaptive immunity and maintaining pathogen-free host tissues . TLRs activate two major signalling pathways . The core pathway activated by most TLRs leads to the activation of transcription factor nuclear factor-kappa B and the mitogen-activated protein kinases p38 and Jun kinase . The second pathway is activated by TLR3 and TLR4 and results in the activation of both NF-B and interferon regulatory factor-3 , allowing the induction of another set of inflammatory genes, including the antiviral interferon- gene .
Caregivers Are Being Misinformed About The Risks Associated With Alzheimers Disease And Creutzfeldt
Surgical instruments infected with prions, for example, are impossible to sterilize. Hospitals throw them away. Prions are in the blood, saliva, urine, feces, mucus, and bodily tissue of its victims. Many factors are contributing to the epidemic. Prions are now the X factor. Industry and government are not accounting for prions or regulating them. They are ignoring the threat completely, which violates the Bioterrorism Preparedness and Response Act of 2002 in the United States. Other nations also are ignoring laws developed to protect food, air and water.
Wastewater treatment plants are collecting points for prions from infected humans. The sewage treatment process cant stop prions from migrating, mutating and multiplying before being discharged into the environment where they can kill again. Wastewater treatment plants are spreading infectious waste far and wide because they are incapable of stopping prions. As such, all by-products and discharges from wastewater treatment plants are infectious waste, which are contributing to the global epidemic of neurodegenerative disease among humans, wildlife and livestock.
Since its unlikely that the sewage treatment process can effectively deactivate prions, adopting measures to prevent the entry of prions into the sewer system is advisable, said the Toronto Department of Health, November 2004.
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Retrospective Study With Humans
In a study followeing up on more than 6,100 people who had been previously injected with human growth hormones, researchers tested those hormones and found that , they contained small amounts of the tau and beta amyloid proteins that are present in the brains of people who have Alzheimer’s. These people have since been monitored to determine if they have developed Alzheimer’s disease. Thus far, none of the participants have developed Alzheimer’s disease, although most are still fairly young for a typical onset of dementia.
The Possible Role Of Systemic Infections In Alzheimer’s Disease And Other Dementias
In addition to the possibility that neurotropic agents might directly infect the brain and cause later-life neurologic sequellae, another mechanism by which infections could promote the genesis of AD is through the varied effects of systemic infections on the brain. Among children, for example, studies show that those with recurrent systemic infections demonstrate significant cognitive impairments in later childhood or adult life , and those surviving severe sepsis demonstrate significantly worse cognitive function than the general population .
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A Protein That Transmits Its Defect
In 2006, a team of researchers headed by Walker and Mathias Jucker, from the University of TÃ¼bingen , demonstrated that the defective beta-amyloid is capable of seeding the appearance of plaques by spreading its defect to other healthy copies. In other words, the Alzheimers protein would behave like a prion, the agent responsible for mad cow disease. This pathology became famous in the late 1990s when researchers began to detect cases of transmission to humans through the ingestion of products from sick cows. The cause is an abnormal prion protein that transmits its defect to other normal proteins. As a result, the affected proteins become sticky, clumping together to form deposits that cause the death of neurons. We found that this molecular mechanism is virtually identical for amyloid-beta and the prion protein, Walker summarises.
National Institutes of Health
Walker and Juckerâs finding ushered in a new approach for research into Alzheimers and other neurodegenerative ailments, which came to be seen as unconventional infectious diseases. But as with the human variant of mad cow disease, a contagion is something that would only occur in very rare cases. According to Walker, there is still no evidence for the transmission of Alzheimers disease under everyday circumstances.Spontaneous mutation would continue to be the main origin of the disease.
Is Mad Cow Disease Infectious
Is Mad Cow Disease Infectious? Neither vCJD nor BSE is contagious. This means that it is not like catching a cold. A person cannot catch it from being near a sick person or cow. Also, research studies have shown that people cannot get BSE from drinking milk or eating dairy products, even if the milk came from a sick cow.
Is mad cow disease infectious or noninfectious? Scientists examined two different forms of a prion-forming protein domain by means of NMR spectroscopy and found that the infectious and noninfectious forms differ markedly in their molecular structure. Infectious proteins known as prions have been identified as the cause of mad cow disease .
Can mad cow disease be passed from human to human? There is no evidence that people can get mad cow disease or vCJD from eating muscle meatwhich is used for ground beef, roasts, and steaksor from consuming milk or milk products. People with vCJD cannot spread it to others through casual contact.
How is mad cow disease transmitted? They can be spread to humans who eat the beef of an infected animal or come into contact with tissues of infected animals. The cattle themselves become infected with BSE by eating feed contaminated with the BSE organism. The cattle develop brain disease that results in death.
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Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimers disease, Parkinsons disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy. The operative word is transmissible. Even the global surge in autism appears to be related.
Neuroinflammation In Ad Pathogenesis
Inflammation is a biological response of the body to different types of damages within the cells and tissues caused by chemical, physical and biological factors . An acute inflammatory response can be beneficial as an immune response to tissue injury or infections, and the proper inflammatory reactions are characterized by an advantage of processes of restoring homeostasis over the destructive processes. However, these reactions might be impaired during aging, thus resulting in increased susceptibility to infection. If the activity of stimulating factors and the mechanisms of the proper development of inflammation are dysregulated, the body still receives a signal of health hazard and switches from the acute to a chronic inflammatory state . Chronic inflammation results in a response that leads to tissue degeneration and development of autoimmune or circulatory system diseases, arthritis and CNS disorders . The inflammation hypothesis of AD proposed more recently by Krstic and Knuesel is one of three important hypotheses on the etiopathogenesis of AD along with the cholinergic hypothesis by Bartus and colleagues then amyloid cascade hypothesis by Hardy and Allsop .
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Is Bacterial Worse Than Viral
While bacteria and viruses can both cause mild to serious infections, they are different from each other. This is important to understand, because bacterial and viral infections must be treated differently. Misusing antibiotics to treat viral infections contributes to the problem of antibiotic resistance.
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Eventually Doctors May Be Able To Screen People According To The Many Different Microbes They May Be Carrying In Their Brains
This could just be another consequence of the overall assault on the body, including the increased inflammation that comes with the disease. But some animal studies and analyses of human autopsies suggest that the coronavirus can invade the brain. And laboratory experiments suggest that this infection may, in turn, trigger neural damage. In one striking study, Jay Gopalakrishnan at Heinrich-Heine-University in Dusseldorf and colleagues created a series of “cerebral organoids” miniature, lab-grown brain tissue and then exposed them to the virus. They saw some marked changes in the tau proteins that are associated with Alzheimer’s, and increased neural death, after infection from the virus.
Such findings ring alarm bells for Fulop. “Sars-Cov-2 may act exactly as HSV-1,” he proposes. Others including Gopalakrishnan are more cautious, however. “We have demonstrated that the virus can infect human neurons, and it can cause some sort of neuronal stress,” he says. “And this may have some unexpected effects.” Much more research will be necessary to assess any long-term risks for neurological disease.
An elderly women with dementia is vaccinated against Covid-19 by a team of volunteers
Three decades after her initial investigations, Itzhaki hopes we will now see the development of more clinical trials testing new treatments, in a bid to replicate the observations of the HSV1 patients receiving antiviral medication in Taiwan.
Analogies Between Ad And Other Age
Epidemiological studies have confirmed that several of these chronic inflammatory disorders are associated with AD . In addition, they are all linked to periodontal polybacterial disorders, which are primarily caused by Gram-negative bacteria . Spirochetes and herpes viruses are predominant periodontal pathogens , and C. pneumoniae is a major upper respiratory tract pathogen. An infectious origin might give a comprehensive explanation of the common cellular and molecular mechanisms, inflammatory processes and common inflammatory gene polymorphisms involved in these chronic inflammatory disorders and AD .
Does Alzheimer’s Make The Brain More Susceptible To Infection
The blood-brain barrier protects the brain by controlling what substances can pass from the blood into brain tissue. In Alzheimer’s disease, the blood-brain barrier is damaged, particularly in the brain region affected by Alzheimer’s.
Evidence suggests that inflammation, the Alzheimer’s hallmark amyloid protein and the ApoE4 gene, which are all linked to Alzheimer’s disease, can contribute to the breakdown of the blood-brain barrier. Once it has been weakened, bacteria, viruses, and other harmful substances can get through into the brain more easily. This may explain why certain viruses and bacteria, such as herpes and spirochetes, are more common in the brains of people with Alzheimer’s.
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Caregivers Exposed To Prion Contagion
Neurodegenerative disease is the fastest-growing cause of death in the world. Alzheimers disease alone is taking the lives of 50-100 million people now. Despite millions of Alzheimers-related fatalities annually, experts suggest that the prevalence of the disease among the living will quadruple by 2050, if not sooner. Some advocates are warning that the surging epidemic could bankrupt entire nations.
Unfortunately, there is a growing stack of evidence that Alzheimers disease is a transmissible disease, which means that millions of caregivers, friends and family members are at risk.
The epidemic is more widespread than anyone knows. A groundbreaking study suggested that Alzheimers disease causes six times as many deaths than official statistics indicate. The Centers for Disease Control and Prevention estimated that, in 2010, Alzheimers disease caused almost 84,000 deaths in the United States, a number derived from death certificates in which Alzheimers disease was listed as the main cause. In reality, the study said Alzheimers disease was the underlying cause in more than 500,000 deaths in 2010 that were often attributed to conditions, such as pneumonia, caused by complications of Alzheimers. Those numbers make Alzheimers disease the third-leading cause of death in the United States, behind heart disease and cancer. The study was led by researchers at the Rush University Medical Center in Chicago and published in 2013 in the medical journal Neurology.