Alzheimer’s and Gum Disease: Can One Bacterium Cause Both?

Gum problems affect more than half of the world’s population, but most people choose to ignore their oral health - a decision that can have dire consequences, as it turns out. An increasing number of scientific findings point out how gum disease causing bacteria can spread and affect the entire body, even your brain. In a previous article, we’ve discussed how poor oral health can contribute to heart disease and problems with episodic memory, but an even more worrying finding has been made in 2019, suggesting that a strain of bacteria that is typically involved in gum disease called Porphyromonas gingivalis may be the cause of Alzheimer’s disease.

The Science Behind Alzheimer’s Disease
For decades, beta-amyloid plaques and TAU tangles have been considered the cause of Alzheimer’s disease. These plaques and tangles bunch together causing clumps in the brain tissue that interfere with the function of our brain cells. As a result, certain brain functions, such as short term memory, executive functioning, and even emotional perception, just to name a few, become affected, making Alzheimer’s sufferers progressively less and less independent and capable of living life at its fullest.
Indeed, beta-amyloid plaques and TAU tangles are a unique and frequent finding in post-mortem studies in Alzheimer’s patients, and for decades, the reason behind their development was a mystery. One of the major hypotheses was that the cause may be due to an infection, and once again, post-mortem research suggested that it might be a strain of the herpes virus or even a fungus that trigger the condition.

However, these studies were small, and their results too unconvincing for the global medical community to recognize that infections cause the neurodegenerative condition, especially since other factors, such as genetics and age are known risk factors of Alzheimer’s.

The Link Between Gum Disease and Alzheimer’s

In 2019, a new study was published in the Science Advances journal finding a bacterium typically associated with gum disease in the brains of Alzheimer’s patients. But the researchers didn’t stop there and did a follow-up study in an attempt to find not only a cause but also a cure for the condition.
The scientists suggested that toxins called gingipains produced by Porphyromonas gingivalis bacteria were to blame for the creation of plaques and tangles, and they developed a drug they called COR388 that blocks these gingipains. During this second experiment, mice were exposed to the Porphyromonas gingivalis bacteria, and after 6 weeks, the bacteria already appeared in their brain and started causing plaques.

Then, the mice were treated with the drug the researchers had developed, which resulted in a significant reduction of plaques in the mice’s brains and halted neurodegeneration. The researchers conclude that Alzheimer’s disease is caused by the Porphyromonas gingivalis bacterium, and they are already in the process of conducting clinical trials on human subjects to test the efficacy of the experimental drug.

In an interview with the New Scientist in December of 2019, one of the leading authors of the study Steve Dominy revealed that 570 people with mild to moderate Alzheimer’s from 95 health centers across the US and Europe were enrolled in the clinical trial, and we should expect the results in 2021.

A Critical View
While the gum disease study definitely uncovered one way the beta-amyloid plaques and TAU tangles characteristic of Alzheimer’s can occur, many leading scientists in the field point out that we should look at the bigger picture instead of stating that Porphyromonas gingivalis is the exclusive cause of Alzheimer’s, as any other microorganism could likewise be responsible for the formation of plaques and tangles.

Still, the research is exemplary, as it makes us reimagine what the plaques and tangles found in Alzheimer's patients' brains really are - a symptom of the disease, instead of its definitive cause. The study also managed to show how an infection considered relatively harmless managed to contribute to the development of the most widespread neurodegenerative condition - Alzheimer’s disease.

The lesson here is clear: good overall health, including dental hygiene and oral health, as well as a timely treatment of any infections, even seemingly minor one, is key in preventing serious future health issues.

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New open-source microscope may help paralysis patients

Scientists have developed a new generation of custom-built microscopes that significantly improve brain tissue imaging, an advance that could help find better treatment for patients with paralysis. The microscopes, known as mesoSPIMs - short for 'mesoscale selective plane-illumination microscopes' can image brain tissues down to the minute details of individual neurons which are five times thinner than a human hair, the study noted.

The researchers added that they can uncover the 3D anatomy of entire small organs, faster than ever before using the new microscope.

The mesoSPIM is a light-sheet microscope, which unlike traditional microscopes -- where specimens are cut in slices with a blade to view in a microscope slide -- uses a sheet of light to slice the samples into ultra-thin sections, the study noted.

According to the researchers, this helps scientists capture slivers of image in the samples without damaging it.

The images from the slices, the researchers say, are then combined to reconstruct the detailed three-dimensional image of the sample.

The problem with standard light-sheet microscopes, according to the researchers, is that the data sets they produce are huge and analysing them consumes a lot of time.

MesoSPIM, on the other hand, allows fast scanning as well as direct visualization of the captured data, the study noted.

According to the researchers, this makes the microscope suitable for screening large numbers of samples in a very short time, producing high-resolution images.

Researchers trying to restore movement in patients with paralysis, or investigating neuronal networks involved in cognition, pleasure, or drug addiction can use MesoSPIMs to get new insights into the brain and spinal cord organization, the study, published in the journal Nature Methods, noted.

The researchers said that top European neuroscientists were driving the open-source dissemination of mesoSPIMs globally by sharing their expertise and excitement as well as the images and videos they took using the new microscope.

"We created the open-source mesoSPIM Initiative to share the latest developments in microscope instrumentation and software with the imaging community," said Fabian Voigt of the Brain Research Institute at the University of Zurich in Switzerland.

Voigt added that anyone seeking high-quality anatomical data from large samples can now possess the information needed to build and operate their own mesoSPIM.

Stephane Pages from Centre Medical Universitaire in Switzerland told in an email that the only requirement for the global dissemination of mesoSPIM was to have local human resources build, maintain, and adapt the systems to the local needs.

"The technology behind the microscope is completely open-source and the overall price of a mesoSPIM is affordable enough to allow any lab interested to built its own," said Pages, a co-author of the study.

The researchers mentioned that there are currently seven mesoSPIMs in operation across Europe and several more instruments under construction.

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New skin test detects prion infection before symptoms appear

Prions can infect both humans and animals, causing Creutzfeldt-Jakob disease (CJD) in humans, mad cow disease in cattle, and chronic wasting disease in elk and deer. The infectious, misfolded protein particles often go undetected as they destroy brain tissue, causing memory loss, mobility issues, and ultimately death. Preclinical detection of prions has proven difficult, but new research suggests skin samples hold early signs of prion disease that precede neurologic symptoms. 

"Currently a definitive diagnosis of Creutzfeldt-Jakob disease is dependent on the examination of diseased brain tissue obtained at biopsy or autopsy. It has been impossible to detect at the early preclinical stage," said an associate professor of pathology.

In a ground-breaking study, an international team of researchers successfully used two methods to detect prions in skin samples collected from inoculated rodents. The study provides the first proof-of-concept evidence that readily accessible skin samples could be used to detect prion disease early—before clinical symptoms appear.

In the new study, the researchers successfully detected prions in rodent skin samples as early as two weeks post-infection. They also detected prions in the skin of uninoculated rodents that were housed alongside inoculated cage mates, demonstrating that prion transmission can occur between cohabitating rodents.

Prions were detected in skin samples from the inoculated rodents before they showed any clinical signs of prion disease. The researchers first inoculated the brains of hamsters and humanized transgenic mice with rodent or human prion samples, respectively. Then, they collected skin and brain samples at different time points, and used two different methods to detect disease-associated prion proteins in the tissues. In both hamsters and mice, the researchers detected prions in skin before they could be detected in brain tissue. The researchers concluded that skin prions could serve as a useful biomarker for preclinical diagnosis of prion diseases.

The study compared two highly-sensitive prion detection methods: RT-QuIC (real-time quaking-induced conversion) and sPMCA (serial protein misfolding cyclic amplification). "Both assays were able to efficiently amplify trace amounts of disease-associated prion protein found in the skin tissues of infected animals," said the study's first author. The tests use prions in tissue samples as a template and either normal brain tissue or synthetic prion protein as "building blocks" to dramatically amplify minute amounts of prions to detectable levels.

One of the methods, RT-QuIC, has been used to detect prion particles in symptomatic CJD patients. However, it normally requires invasive cerebrospinal fluid (CSF) sampling that may be contraindicated for certain patients. Additionally, "The CSF-based prion test results could be uncertain in some cases and not all CSF specimens from patients with prion disease are RT-QuIC positive," said an associate professor of pathology. "Although skin samples may not replace CSF in routine RT-QuIC-based prion disease diagnosis, they may be helpful when prion disease is suspected but CSF is either unavailable or RT-QuIC-negative."

The study results build upon previous work by the researchers showing that autopsy skin samples from human prion disease patients exhibit prion seeding and infectivity. The next step will be to develop and validate the skin prion tests for clinical use.

Said the researcher, "Since the skin is readily accessible and skin biopsy is minimally invasive, detection of skin prions will be very useful for monitoring disease progression and assessing therapeutic efficacy during clinical trials or treatments when prion therapy becomes available in the future."

 The researchers were recently awarded a $2.9 million grant to validate the test methods using human skin samples. They will determine if skin prions could serve as a diagnostic biomarker for CJD or a source of prion transmission.

The researchers believe the methods may also be adapted for diagnosis of other diseases involving misfolded proteins. "Sensitive, minimally invasive detection of various misfolded proteins in skin, such as tau in Alzheimer's disease and alpha-synuclein in Parkinson's disease, could be highly valuable for disease diagnosis and monitoring of disease progression and efficacy of treatments," the researcher said. "It's possible that the skin will ultimately serve as a mirror for us to monitor these misfolded proteins that accumulate and damage the brain in patients with these conditions." 
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Brain Aneurysms & How to Spot Them

Brain aneurysms kill people suddenly every year, yet few of us know what the warning signs of this deadly attack are. Recent estimates suggest that 90% of Americans are not sure what a brain aneurysm really is. And because anything from between 6% to 9% of people actually have an aneurysm, this lack of knowledge is tragic. This necessary guide will give you important information about brain aneurysms, telling you everything you need to know, and explaining what you can do to spot the signs before the worst happens.

Lisa Colagrossi's story

Some of you may know the story of Emmy Award-nominated US news anchor, Lisa Colagrossi, who died in 2015 from a brain aneurysm, aged only 49. Lisa was a hard-working woman who began to feel excruciating head pain. After discussing it with her husband, she decided to let it pass and get on with her work. Sadly, she was taken ill and died only two weeks after the initial headache passed. 

Following this awful turn of events, Lisa’s husband established the Lisa Colagrossi Foundation (LCF) to raise public awareness about the silent killer that had taken her away from him and their two poor children. Her husband understood that it was only a lack of knowledge that prevented Lisa from going to the doctor before it was too late.

This story dramatically illustrates the need for more widely-spread knowledge about brain aneurysms. 

What is a brain aneurysm?

Neurosurgeon  describes a brain aneurysm as a weakness of the wall in one of the brain’s blood vessels. The weakness lets the wall form a bulge, due to the pressure of the blood running through the vessels. When this bulge becomes over-inflated it can rupture and seep blood into the brain tissue.

This bulge, or aneurysm, is something that anywhere from 6% to 9% of us are walking around with, unaware that it could rupture. They can even be seen on an MRI scan. Yet if the aneurysm is of a tolerably small size, doctors will not recommend invasive and dangerous surgery. 

When you suffer a rupture...

The frightening description above may give you the idea of blood squirting all over the place, but the truth is not quite so dramatic. There may be a little dribble for a few moments, but generally a platelet plug naturally forms, according to a Dr. However, even this little trickle can be fatal. Between 30% to 50% of sufferers die immediately after a rupture occurs.

The small blood leak irritates the brain tissues it comes into contact with, and this drastically increases pressure within the head. Furthermore, the loss of blood is catastrophic for the brain regions which have lost out. These areas need a constant supply of blood to function as they should.

Pressure and a lack of blood combine to induce either death or unconsciousness.

Signs and symptoms of a rupture:

Here are several symptoms that have been reported by those who have suffered a rupture:

•    An excruciating headache
•    Neck stiffness
•    Tingling face
•    Light sensitivity
•    Seizures
•    Weak limbs
•    Blurry or double vision
•    Extreme tiredness
Most of these symptoms are secondary, however, to the headache. Colagrossi’s husband describes this as “W-H-O-L” or ‘the worst headache of your life’. This could be felt anywhere and at any time, though it may be felt more strongly behind the eyes. It is hard to describe this pain, some compare it to being hit by a bolt of lightning, others have said it felt like hearing a gun shot.

What to do:

Dr.’s advice is that if you or someone close to you experiences any of these symptoms, make an emergency call for an ambulance or go to the hospital directly. Doctors have several things they can do to get rid of the pressure that results from the rupture, but that doesn’t mean that everything will be well.

Of those who receive treatment a third die, a third suffer permanent impairment, and a further third go back to normal. The goal of the Lisa Colagrossi Foundation is to help increase the number of people who can go back to normal. He says:

"If someone had been doing the work we're doing now to raise public awareness, Lisa and millions of others would still be alive".

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International scientists have found autism's cause

Five clear, replicable, and related discoveries explaining how autism is triggered have formed an undeniably clear picture of autism’s causation, and possibly ways to alleviate the symptoms, too. Most of the research that has created this understanding has been published in the last 36 months, and largely from international scientists in the United Kingdom, Canada, France, Israel, and China. 

In early December 2017, the team published a paper that for the first time looked at the brain tissue of subjects with autism to determine the level of aluminum (note: they spell “aluminum” as “aluminium” in the United Kingdom) found within their brain tissue. For anyone trying to convince the world that “the science is settled and vaccines don’t cause autism,” the study’s findings are deeply contradictory to that statement. In a post written by the Professor on the day his study was published, he explained the groundbreaking results:

“…while the aluminium content of each of the 5 brains [of people with autism] was shockingly high it was the location of the aluminium in the brain tissue which served as the standout observation…The new evidence strongly suggests that aluminium is entering the brain in ASD [autism spectrum disorders] via pro-inflammatory cells which have become loaded up with aluminium in the blood and/or lymph, much as has been demonstrated for monocytes at injection sites for vaccines including aluminium adjuvants.”

Dr.’s quote includes a reference to “monocytes at injection sites” and the fact that the interaction between these monocytes and aluminum has been demonstrated in previous published science. I know, that sounds pretty technical, but bear with me. A “monocyte” is a type of white blood cell, of which one form of monocyte is a “macrophage.” A macrophage can be thought of as the garbage man of the immune system, eating up foreign substances, cell debris, etc. As you will see in a moment, macrophages appear to be playing a critical and devastating role in triggering autism, serving to escort aluminum injected from a vaccine directly into the brain, where it can disrupt brain development and trigger autism.

Dr.’s study — “Aluminium in brain tissue and autism” — is the final piece of a puzzle that first started to come together in 2004, and picked up steam since 2010, that has dramatically furthered the scientific understanding of exactly how a vaccine can trigger autism. This timeline is critical to recognize, because the Vaccine Court in the United States dismissed the vaccine-autism hypothesis in 2009, long before most of what I’m about to explain even existed. Science is a continuum, an emergence of truth through many different studies that often have to be pieced together before the picture becomes clear. And, scientific progress can sometimes move slowly until that moment when an emerging truth presents itself in such a way that it can no longer be denied. In my opinion, Dr.’s study provided the only data missing from an airtight explanation of what happened to my son and so many other children.

Why is aluminum in vaccines at all?
Aluminum is a critical component of most vaccines given to children. It serves as an “adjuvant” meaning the aluminum serves to “wake up” the immune system, provoking the immune system to recognize the “antigen” within the vaccine for whatever disease the vaccine serves to protect against. The amount of aluminum in vaccines given to children skyrocketed beginning in the early 1990s for two reasons: 1), more vaccines were added to the children’s vaccine schedule and, 2), the vaccination rate for all vaccines given to children rose (from 50–60% of children vaccinated in the mid-1980s to over 90% today). A child in the mid-1980s would have received 1,250 micrograms of aluminum from their vaccines by their 18-month birthday if they were fully vaccinated. Today, that number is 4,925 micrograms, a near-quadrupling of total aluminum. 


 Mystifyingly, aluminum has never experienced biological testing to consider its safety for being injected into babies, having been “grandfathered” into our modern safety standards. Canadian scientists addressed this omission in a critical study they published in 2011 titled, “Aluminum Vaccine Adjuvants: Are they Safe?” They wrote:

“Aluminum is an experimentally demonstrated neurotoxin and the most commonly used vaccine adjuvant. Despite almost 90 years of widespread use of aluminum adjuvants, medical science’s understanding about their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds. In spite of this, the notion that aluminum in vaccines is safe appears to be widely accepted. Experimental research, however, clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans. In particular, aluminum in adjuvant form carries a risk for autoimmunity, long-term brain inflammation and associated neurological complications and may thus have profound and widespread adverse health consequences.”

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