According to recent study from NYU College of Dentistry and Weill Cornell Medicine, older people with more harmful than good bacteria in their gums are more likely to have signs of amyloid beta — a crucial biomarker for Alzheimer’s disease — in their cerebrospinal fluid (CSF). A other Alzheimer’s biomarker known as tau, however, was not linked to an imbalance in oral flora. Periodontal disease (also known as gum disease) has long been suspected to be a risk factor for Alzheimer’s disease, and now a new research suggests it may be linked to it. Chronic and systemic inflammation characterizes periodontal disease, which, according to the CDC, affects 70% of people 65 and older. The pockets between the teeth and gums enlarge and become breeding grounds for bacteria.
A CSF biomarker of Alzheimer’s disease has been discovered in cognitively normal older people in this research, according to main author Angela Kamer, DDS, PhD, an associate professor of periodontology and implant dentistry at New York University College of Dentistry. “Inflammatory bacteria thrive in the mouth, but so do beneficial, defensive microorganisms. We discovered that having amyloid deposits in the brain was linked to higher levels of dangerous bacteria as well as lower levels of good bacteria.” Both amyloid beta (the first protein to accumulate in the brain as Alzheimer’s progresses) and tau (which builds up in nerve cells and creates tangles) are characteristic of Alzheimer’s disease in the form of hallmark proteins in the brain.
“Brain amyloid accumulation and its connection to Alzheimer’s disease are complicated processes that are only partly understood. According to the results of this study, which can be estimated from CSF levels, proinflammatory diseases disrupt amyloid clearance from the brain “Professor of neuroscience in radiology and director of Weill Cornell Medicine’s Brain Health Imaging Institute, Mony J. de Leon, EdD, was the study’s senior author. There are frequently decades before tau pathology or Alzheimer’s disease symptoms are diagnosed in which amyloid alterations are seen.” To find out whether older people were at risk for dementia, the researchers looked at 48 cognitively normal seniors. A lumbar puncture was utilized to acquire CSF in order to measure amyloid beta and tau levels in the participants’ saliva, and oral exams were performed to collect microorganisms from under the gumline. Researchers used CSF levels of amyloid beta and tau to assess brain expression of Alzheimer’s proteins. Greater levels of amyloid beta indicate higher brain amyloid levels, while higher levels of tau indicate increased brain tangle accumulations.
Following Deepak Saxena’s direction at NYU College of Dentistry, researchers analyzed the bacterial DNA of samples obtained from beneath the gumline and quantified microorganisms known to damage oral health (e.g. Prevotella, Porphyromonas, Fretibacterium) as well as pro-oral health bacteria (e.g. Corynebacterium, Actinomyces, Capnocytophaga). Patients with a bacterial imbalance, preferring harmful bacteria over good bacteria, had a higher risk of developing Alzheimer’s disease, as shown by lower amounts of amyloid in their cerebrospinal fluid (CSF). High numbers of good bacteria, say the researchers, may help prevent Alzheimer’s disease because they keep the body’s bacterial balance in check and reduce inflammation. He said, “Our findings demonstrate how important the entire oral microbiome is in regulating amyloid levels — not only of the role played by the bad but also the beneficial” bacteria in the mouth. Multiple oral bacteria are implicated in the development of amyloid lesions, according to these results.
Reference : Angela R. Kamer, Smruti Pushalkar, Deepthi Gulivindala, Tracy Butler, Yi Li, Kumar Raghava Chowdary Annam, Lidia Glodzik, Karla V. Ballman, Patricia M. Corby, Kaj Blennow, Henrik Zetterberg, Deepak Saxena, Mony J. Leon. Periodontal dysbiosis associates with reduced CSF Aβ42 in cognitively normal elderly. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, 2021; 13 (1) DOI: 10.1002/dad2.12172