Study: Parodontitis and Alzheimer's

ide m, Harris M, Stevens a, et al. Periodontitis and cognitive decline in Alzheimer's disease. plus one . 2016; 11 (3): E0151081.

observing cohort study

The investigators recruited 60 non -smoking adults with mild to moderate dementia from transfers to municipal memory evaluation services in the United Kingdom. All participants had at least 10 teeth and were not treated for periodontitis in the 6 months before the study. Fifty -two participants ended the study.

observation of relationships between periodontitis and the severity of dementia, the rate of cognitive decline or chronic inflammation in adults with mild to moderate Alzheimer's disease.

The cognitive status of the participants was tested both with the Alzheimer’s Disease Assessment Scale (ADAS-COG) as a primary cognitive result as well as with the standardized mini-mental state examination (SMMSE) as a secondary cognitive result. At the beginning of the study, Venous blood was tested for C-reactive protein (CRP), the inflammatory cytokin-tumor necrosis factor (TNF). a The anti-inflammatory cytokine interleukin (IL) -10 and immunoglobulin g (IGG) antibody p. gingivalis . Dental health was assessed by a dental hygienist who was blind to cognitive test results to determine the presence or non -presence of periodontitis in accordance with the established case definitions of the Centers for Disease Control and Prevention/American Academy of Periodontology (CDC/AAP). All reviews were carried out at the beginning of the course and repeated after 6 months.

The presence of periodontitis at the beginning of the study was in no context with the cognitive starting state, but was associated with a 6-fold increase in the rate of cognitive decline ( p = 0.005). There was no correlation between providers and non-supporters of Apolipoprotein E (Apoe) allels and periodontitis or cognitive decay at the start of the course. Baseline antibody mirror on p. Gingivalis were not statistically associated with cognitive results. Periodontitis at the beginning of the course was with a relative increase in the pro-inflammatory state (CRP, TNF- a ) and acceptance of the anti-inflammatory state (IL10) over the 6-month follow-up period. Regardless of the cognitive starting state, periodontitis was associated with an increase in cognitive decline in Alzheimer's disease (AD), which can be related to systemic inflammation.

First, this data indicates that an improvement in dental hygiene could slow down the rate of cognitive decline in AD. Second, this data support a new theory that AD is partly an immune response to an infection.

Several earlier studies have reported that ad patients have poorer dental health than control persons of similar age, and that dental health is the worse the worse the dementia. ^1,2 The obvious assumption was that this was due to poorer self-care while dementia has been forgotten (ie forgot their teeth, their teeth Cleaning).

This data support a new theory that AD is partly an immune response to an infection.

This study was not a clear connection between the severity of dementia and periodontitis, but this can be because patients with severe dementia were not included in the cohort. This is the first study that correlates the rates of decreasing cognitive functions with poor dental health. Knowing that periodontitis was associated with a faster cognitive decline during the 6-month follow-up period of this study suggests that we should be much more proactive in patients who show early signs of AD and insist on aggressive dental care.

While we are looking for other explanations for this connection, the most obvious is that periodontitis drives the progression of Alzheimer's disease, in view of other recent research and the newer hypothesis, which indicates that Ad is an immune response to an infection, the most sensible.

in May 2016, Science Translational Medicine published an article by the Harvard researcher Deepak Kumar and colleagues, who pointed out that the amyloid proteins that are the trademark of AD normally fulfill an antimicrobial function and protect the brain from infections. Their theory is that infections, especially light infections, in combination with an increased permeability of the blood-brain barrier (BBB) ​​cause an overreaction of the brain defense mechanism, which in its enthusiasm generates an abundance of amyloid plaques. Beta-Amyloid, the substance that forms the plaque of Alzheimer's disease, could actually have a purpose in the brain. It is a defense mechanism against infections and is now described as a "primary effectorolecules of innate immunity, antimicrobial peptides (amps), also called the tavern spept.

When a virus, fungus or bacterium slips over the BBB, the brain creates amyloid material that surrounds and captures the intruder. The amyloid wraps the intruder into a cage. Even after the intruder's death, the trap remains in place and forms permanent plaque deposits in the brain. The Harvard team has so far demonstrated this process in vitro. The currently verified study supports this theory with its preliminary finding of a connection between periodontitis and ad in humans.

There are several other examples of chronic infections related to AD. In September 2016, Shim et al. Association with cognitive impairment.

In numerous studies, a similar connection with bacterial infections was found. A meta -analysis of 25 separate studies published in August 2016 found significant relationships between the two chlamydia pneumoniae and spirochet bacteria with AD. Spirochätal infections were associated with a 10-fold increased occurrence of AD (OR: 10.61; 95 % CI: 3.38-33.29). A more than 5-way increase in the ad risk was observed in a Chlamydia infection (OR: 5.66; 95 %-KI: 1.83–17.51).

It may be less the type of infectious it is the chronicity or persistence of the infection that causes the ad-triggering reaction in the brain. Continuous antigen exposure may be necessary to trigger the amyloid reaction.

Another paper published in August 2016 expands this hypothesis and suggests that the chain of events that lead to AD begins in the intestine with intestinal microbiota, which increase the intestinal permeability and in turn increase the permeability of the BBB. This in turn presents the brain more antigenes material that triggers the Amyloid Beta-producing reaction.

In view of the many studies that have associated herpes antibody mirrors with AD, Ruth Itzhaki wrote in August 2016 in the magazine for Alzheimer's disease suggested "to be used or stop the advancement of the AD".

Therefore we could quickly enter a new era of our view of the Alzheimer's disease, in which we can understand both the underlying mechanisms and offer our patients some simple interventions, starting with the memory of brushing your teeth.

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