Research Shows Links Between Gum Disease and Alzheimer’s

Don’t forget to floss: New research adds to evidence linking gum disease with Alzheimer’s disease.

The mouth is home to both harmful bacteria that promote inflammation and healthy, protective bacteria, the study authors explained.

In the new study, the researchers found that people who have more harmful than healthy gum bacteria were more likely to also have a protein marker for Alzheimer’s disease, known as amyloid beta, in their cerebrospinal fluid (CSF).

“To our knowledge, this is the first study showing an association between the imbalanced bacterial community found under the gumline and a CSF biomarker of Alzheimer’s disease in cognitively normal older adults,” said lead author Dr. Angela Kamer. She’s associate professor of periodontology and implant dentistry at New York University College of Dentistry, in New York City.

“We found that having evidence for brain amyloid was associated with increased harmful and decreased beneficial bacteria,” she said in a university news release.

About 70% of adults aged 65 and older have gum disease, which involves chronic and systemic inflammation.

Alzheimer’s is marked by two proteins in the brain: amyloid beta and tau. Amyloid beta clumps together to form plaques and is believed to be the first protein deposited in the brain as Alzheimer’s develops. Tau builds up in nerve cells and forms tangles.

According to senior study author Mony de Leon, “The mechanisms by which levels of brain amyloid accumulate and are associated with Alzheimer’s pathology are complex and only partially understood.” He is director of the Brain Health Imaging Institute at Weill Cornell Medicine in New York City.

The new study adds support to the understanding that pro-inflammatory diseases disrupt clearance of amyloid from the brain, de Leon said.

“Amyloid changes are often observed decades before tau pathology or the symptoms of Alzheimer’s disease are detected,” he added.

For the study, 48 patients aged 65 or older with normal thinking abilities had oral exams and spinal taps.

The researchers analyzed DNA in bacterial samples taken from under the participants’ gumlines. Then a lumbar puncture was done to obtain CSF to determine levels of amyloid beta and tau.

The investigators looked for lower levels of amyloid beta, which translate to higher brain amyloid levels, and higher levels of tau, which reflect higher brain tangle accumulations.

The results showed that individuals with more harmful than healthy bacteria were more likely to have reduced amyloid levels in their spinal fluid.

The researchers hypothesized that because high levels of healthy bacteria help maintain bacterial balance and decrease inflammation, they may be protective against Alzheimer’s.

Kamer said, “Our results show the importance of the overall oral microbiome — not only of the role of ‘bad’ bacteria, but also ‘good’ bacteria — in modulating amyloid levels. These findings suggest that multiple oral bacteria are involved in the expression of amyloid lesions.”

The team did not find an association between gum bacteria and tau levels in this study.

Additional research will include a long-term study and clinical trial to test if deep cleanings to remove deposits of plaque and tartar from under the gumline can modify brain amyloid and prevent Alzheimer’s, the authors said.

The findings were published in the journal Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring.

Source: HealthDay

In Pictures: Turkish Dishes

Ezogelin corba

Kısır

Yaprak dolma

Inegol kofte

Perde pilav

Testi kebab

Ekmek kadayıfı

One Year of SARS-CoV-2 Evolution

Today, researchers published an in-depth look at the SARS-CoV-2 mutations that have taken place during the past year in the Journal of General Virology. The review discusses the findings of over 180 research articles and follows the changes that have taken place in the SARS-CoV-2 genome, and the variants that have occurred as a result.

A number of SARS-CoV-2 variants have emerged from immunocompromised hosts, research has identified. It is thought that variants of concern – including B.1.1.7, a variant first identified in Kent – were a result of long-term infection in people with a weakened immune system.

Persistent infections in immunocompromised people could cause the virus to mutate more frequently because the person’s immune system cannot clear the virus as quickly as the immune system of a healthy person.

Authors Professor Wendy Barclay, Dr Thomas Peacock, Professor Julian Hiscox and Rebekah Penrice-Randal explain the importance of monitoring genetic changes in SARS-CoV-2 for future control of the virus: “As more and more variants appear, we are getting a better picture of their shared similarities and differences and can better predict what other new variants will look like. Putting all this information together will also help us design booster vaccines that protect against as many variants as possible or design targeted diagnostics” they said.

Their review discusses where mutations have occurred, what part of the virus they affect and how the resulting variants could impact vaccination efforts. According to the authors, mutations in SARS-CoV-2 are expected, as the virus is adapting to humans. “Sequencing of human seasonal coronaviruses has not been done on a scale like SARS-CoV-2, particularly when they would have initially spread into humans. SARS-CoV-2 is at the start of its journey in humans whereas other human coronaviruses have been around, in some cases, for many decades” they said.

Variants with the same or similar mutations have emerged independently in different countries: “SARS-CoV-2 is probably still finding its way in humans in terms of optimal infection and transmission. The scale of the outbreak and the massive sequencing efforts will identify concurrent mutations; basically, the virus is undergoing the same types of selection pressures wherever you are in the world, and the outbreak was all seeded by the same original virus,” explained the authors.

Mutations of particular interest include those in the spike protein. This protein allows the virus to enter host cells and is the main target of the immune system, including immunity generated by all current SARS-CoV-2 vaccines.

Mutations in the gene that codes for spike could change the shape of the protein, allowing it to no longer be recognised by the immune system. Because this protein is so important for SARS-CoV-2 entry, favourable mutations are more likely to succeed and create new, dominant variants of the virus.

Changes that give the virus an advantage can quickly become dominant. For example, one mutation, named D614G, was found in 80% of SARS-CoV-2 viruses sequenced just four months after it was first detected. Now, viruses without the D614G mutation are only commonly seen in parts of Africa.

Another mutation, N501Y, is found in the SARS-CoV-2 variant B.1.1.7. This mutation is believed to be the result of infection of an immunocompromised individual and may contribute to the virus being more contagious. Infections with this variant have a higher fatality rate. In the UK, B.1.1.7 became the dominant variant within three months and is now responsible for over 90% of infections there.

Significant spike protein mutations discussed in the review include:

D614G:

In February 2020, a mutation was detected in the spike protein of SARS-CoV-2 and named D614G. This mutation was found to makes SARS-CoV-2 more infectious, however does not make the virus more harmful. This increase in infectivity led to a significant fitness advantage and within four months, 80% of SARS-CoV-2 viruses sequenced around the world were found to have the mutation. Now, only parts of Africa have circulating viruses without the D614G mutation.

Despite initial concerns, D614G does not have an effect on vaccine efficiency and in some cases, viruses with the D614G mutation are more readily cleared by antibodies against SARS-CoV-2.

Y435F:

In mid-2020, reports of mink becoming infected by humans became frequent. In mink, the spike protein of the virus commonly developed two mutations called Y435F and N501T. These mutations allow for stronger binding of the virus to human receptor cells. Viruses with these mutations were found in a cluster of human infections in Denmark, believed to have originated from mink. Concerningly, this variant was able to infect people who had previously been infected with SARS-CoV-2 and were thought to have some immunity to the virus. As a result, 17 million mink were culled.

The mutation Y435F has also been reported to have developed in an immunocompromised person, possibly as a result of chronic infection with the virus allowing it to adapt.

N501Y:

In December 2020, a highly transmissible variant of the virus was isolated in Kent, UK. This variant, named B.1.1.7, contained a mutation in the spike protein called N501Y. Not only does this mutation make the virus more contagious, but it was also found to have a higher fatality rate. In the UK, B.1.1.7 is now the dominant variant, and is responsible for over 90% of infections.

The mutation N501Y has been found to have little effect on immunity from both vaccines and previous infections.

E484K:

The spike protein mutation E484K has emerged in recent months, once in South Africa and at least twice in Brazil. Variants with the mutation of E484K are able to evade the immune system of both vaccinated and previously infected individuals.

It is thought that this mutation was driven by high levels of population immunity, which drove mutations in the spike protein to evade the immune system. In Brazil, there have been several reports of healthcare workers and other people with antibodies against SARS-CoV-2 being reinfected with variants with the E484K mutant, raising concerns about vaccine protection against this variant.

The review also examines mutations which make changes to other parts of the virus, such as ORF8, an accessory protein that is thought to supress the host immune system. Viruses with a deletion in the gene that encodes for ORF8 has been found to cause less severe clinical disease.

The authors of the review have called for increased global efforts to monitor SARS-CoV-2 mutations. Currently the United Kingdom and Denmark perform disproportionately high sequencing of the SARS-CoV-2 genome. Regular monitoring of the virus allows early identification of emerging variants and allows researchers to identify the associated mutations.

“Although the genomic surveillance in Europe and the USA is fairly strong it is becoming clear there are large areas of the world that we simply have no idea what variants are circulating. These are starting to appear in Europe as imports or community outbreaks. Better surveillance across a broader range of countries would allow us to better risk assess what the next stage of the pandemic might look like,” said the authors. “If we want to monitor the ongoing emergence, spread, and import of potential vaccine escape mutants we have to continue this effort or risk further pandemic waves and vaccine failure. Furthermore, understanding the genomic epidemiology of the virus as early as possible will allow us to rapidly develop updated vaccine boosters.”

Professor Alain Kohl, Deputy Editor-in-Chief of the Journal of General Virology said “The emergence of SARS-CoV-2 variants is one of the great challenges in the ongoing pandemic. This review article summarises our current knowledge and understanding of the evolution of the virus, as well as the consequences – for example in terms of vaccination. It is of great interest to anyone wishing to learn more about the history of this virus and what the future may hold.”

Source: Microbiology Society

Grey Mullet in Mushroom Sauce

Ingredients

1 grey mullet, about 2-1/4 1b or 2, about 1-1/4 lb each, heads removed
4 tablespoons sunflower oil

Sauce

1 large onion, peeled and thinly sliced
8 oz tomatoes, skinned and sliced
1-1/2 cups mushrooms, sliced
1/2 cup chopped walnuts
1-1/2 tablespoons chopped parsley
1 cup dry white wine
salt
freshly ground black pepper
coriander leaves or parsley, to garnish

Method

1. Cut 3 diagonal slashes in each side of the fish. Place the fish in a large oven-proof dish and broil under moderate heat for 5 minutes on each side. Cover the fish and keep warm.
2. Fry the onion for 3 minutes, then stir in the tomatoes and mushrooms, and cook for 5 minutes until softened.
3. Stir in the walnuts, parsley and wine, season with salt and pepper and bring to the boil. Simmer for 10 minutes.
4. Spoon the sauce over the fish and cook in a preheated 400°F oven for 15 minutes, until the fish is just firm.
5. Garnish with the coriander leaves or parsley.

Makes 4 servings.

Source: Cooking Naturally

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