cell death

Why gum disease increases dementia risk

  • A very large Korean study found older adults with chronic periodontitis had a 6% higher risk for dementia.
  • Two animal studies found that the bacteria involved in gum disease increases amyloid-beta, brain inflammation, and neuron death.

Periodontitis raises dementia risk

A 10-year South Korean study using data from 262,349 older adults (50+) has found that those with chronic periodontitis had a 6% higher risk for dementia than did people without periodontitis. This connection was true despite behaviors such as smoking, consuming alcohol, and remaining physically active.

https://www.eurekalert.org/pub_releases/2019-03/ags-pmr031519.php

Gum disease link to Alzheimer's explained

Gum disease has been linked to Alzheimer's as a risk factor, and now an animal study provides evidence that Porphyromonas gingivalis (Pg), the bacterium associated with chronic gum disease, colonizes the brain and increases production of amyloid beta.

Moreover, the bacterium's toxic enzymes (gingipains) have been found in the neurons of patients with Alzheimer’s. Gingipain levels were associated with two markers: tau, and ubiquitin (a protein tag that marks damaged proteins).

When molecule therapies targeting Pg gingipains were applied, there was reduced bacterial load of an established Pg brain infection, blocked amyloid-beta production, reduced neuroinflammation and protected neurons in the hippocampus.

Around half the population are said to have this bacteria in some form, and around 10% of those with the bacteria will develop serious gum disease, loose teeth, and have an increased risk of developing Alzheimer´s disease.

https://www.eurekalert.org/pub_releases/2019-01/uol-nsd012319.php

https://www.eurekalert.org/pub_releases/2019-06/tuob-byt060319.php

Mouse study links periodontal disease bacteria to greater amyloid plaques, brain inflammation, neuron death

A mouse study found that long-term exposure to periodontal disease bacteria resulted in significantly higher amounts of amyloid beta plaque, more brain inflammation and fewer intact neurons. It’s important to note that the mice used in the study were not genetically engineered to develop Alzheimer's.

https://www.eurekalert.org/pub_releases/2018-10/uoia-pdb100318.php

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Neuron death a natural protective mechanism

  • Fruitflies genetically engineered to express amyloid-beta show that neuron loss is not always bad, but reflects the removal of defective neurons.

A fruitfly study suggests that losing neurons is not necessarily a bad thing. The study used fruitflies genetically engineered to express human amyloid-beta proteins in their brains. When neuronal death was blocked, the flies developed even worse memory problems, worse motor coordination problems, died earlier and their brain degenerated faster. However, when the normal process of cell competition was enhanced, the flies showed an impressive recovery.

Cell competition is a cell quality control mechanism, by which fitter cells trigger the suicide of less fit ones. Research has shown that cell competition is a normal, powerful anti-aging mechanism.

The findings suggest that neuron loss reflects the brain protecting itself from defective neurons, not something that should be prevented. (What we want, of course, is for the neurons not to be damaged.)

https://www.eurekalert.org/pub_releases/2018-12/ccft-lnc122018.php

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Tracking preclinical Alzheimer's progression

New research supports the classification system for preclinical Alzheimer’s proposed two years ago. The classification system divides preclinical Alzheimer's into three stages:

Stage 1: Levels of amyloid beta begin to decrease in the spinal fluid. This indicates that the substance is beginning to form plaques in the brain.

Stage 2: Levels of tau protein start to increase in the spinal fluid, indicating that brain cells are beginning to die. Amyloid beta levels are still abnormal and may continue to fall.

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Blood test predicts Alzheimer’s risk early

A five-year study involving 525 older adults (70+) found 46 had Alzheimer’s or aMCI and a further 28 went on to develop the conditions. The blood levels of 10 specific lipids predicted with more than 90% accuracy whether an individual would go on to develop either Alzheimer’s or aMCI within 2-3 years. The researchers speculate that the lower lipid levels could be an early indication that brain cells are beginning to lose their integrity and break down.

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