Author Interviews, Dental Research, Mental Health Research, NYU / 15.04.2021
Periodontal Bacteria Linked to Alzheimer’s Amyloid
MedicalResearch.com Interview with:
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Dr. Kamer[/caption]
ANGELA R. KAMER, DMD, MS, PhD
Associate Professor
Periodontology and Implant Dentistry
NYU Dentistry
MedicalResearch.com: What is the background for this study?
Response: The accumulation of amyloid β plaques and neurofibrillary pathology in the brain are pathognomonic to Alzheimer's disease (AD). Brain amyloid deposition begins decades before cognitive dysfunction and is thought to be the first AD pathological feature followed by tau tangle accumulations and other pathologies.
The mechanisms by which brain amyloid develops are incompletely understood although inflammation and bacterial imbalances (known as dysbiosis) of the gut and oral cavity may be involved. Periodontal disease affecting more than 50% of elderly is an inflammatory, chronic condition characterized by periodontal tissue destruction and bacterial imbalances. Using PET studies, we showed previously that measures of periodontal destruction were associated with brain amyloid retention in the brain [1]. In this study, we sought to investigate whether subgingival (under the gum line) bacteria associated with Alzheimer’s disease specific pathology, namely amyloidosis and tauopathy.
Dr. Kamer[/caption]
ANGELA R. KAMER, DMD, MS, PhD
Associate Professor
Periodontology and Implant Dentistry
NYU Dentistry
MedicalResearch.com: What is the background for this study?
Response: The accumulation of amyloid β plaques and neurofibrillary pathology in the brain are pathognomonic to Alzheimer's disease (AD). Brain amyloid deposition begins decades before cognitive dysfunction and is thought to be the first AD pathological feature followed by tau tangle accumulations and other pathologies.
The mechanisms by which brain amyloid develops are incompletely understood although inflammation and bacterial imbalances (known as dysbiosis) of the gut and oral cavity may be involved. Periodontal disease affecting more than 50% of elderly is an inflammatory, chronic condition characterized by periodontal tissue destruction and bacterial imbalances. Using PET studies, we showed previously that measures of periodontal destruction were associated with brain amyloid retention in the brain [1]. In this study, we sought to investigate whether subgingival (under the gum line) bacteria associated with Alzheimer’s disease specific pathology, namely amyloidosis and tauopathy.
Dr. Spampinato[/caption]
Maria Vittoria Spampinato, MD
Neuroradiology Division Director
Department of Radiology and Radiological Science
Medical University of South Carolina
Charleston, SC 29425-3230
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Alzheimer’s disease (AD) represents a major public health crisis worldwide. More than 5 million people currently have AD in the United States. AD is a slowly progressing neurodegenerative brain disorder with a long preclinical phase. Many people with AD first suffer from mild cognitive impairment (MCI), a decline in cognitive abilities like memory and thinking skills that is greater than that associated with normal aging. A person with MCI is at an increased risk of developing AD or another dementia, although some individuals with MCI remain cognitively stable or improve.
Anxiety is frequently observed in individuals with MCI. The reported prevalence of anxiety in MCI patients varies between 10 and 50%. In this study we evaluated a cohort of 339 individuals with MCI participating in the Alzheimer’s Disease Neuroimaging Initiative study (ADNI2). During the five years of study participation, 72 patients experienced cognitive decline and were diagnosed with AD. We did not find difference in age, gender and education among patients with and without AD conversion. Patients who progressed had greater atrophy of the hippocampi and entorhinal cortex on their MRI scan, as expected (hippocampal atrophy is often used as a marker of neurodegeneration in AD), as well as greater prevalence of APOE4 is the strongest known genetic risk factor for AD. Patients who progressed to Alzheimer’s disease also had greater severity of anxiety during the study, as measured using the Neuropsychiatric Inventory-Questionnaire. Next we determined the effect of the MRI findings (hippocampal and entorhinal cortex atrophy), of the genetic risk factor (APOE4) and of the severity of anxiety on the time to progression to AD. We found that higher levels of anxiety were associated with faster progression from MCI to AD, independently of whether they had a genetic risk factor for Alzheimer’s disease or brain volume loss. We still need to understand better the association between anxiety disorders and cognitive decline. We do not know whether increased levels of anxiety are a consequence of cognitive decline or if anxiety exacerbates to cognitive decline. If we were able to find in the future that anxiety is actually contributing to cognitive decline, then we should more aggressively screen for anxiety disorders in the elderly population.


Dr. Mikkola[/caption]
Tomi Mikkola MD
Associate Professor
Helsinki University Hospital
Department of Obstetrics and Gynecology
Helsinki, Finland
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: In Finland we have perhaps the most comprehensive and reliable medical registers in the world. Thus, with my research group I have conducted various large studies evaluating association of postmenopausal hormone therapy use and various major diseases (see e.g. the references in the B;MJ paper). There has been various smaller studies indicating that hormone therapy might be protective for all kinds of dementias, also Alzheimer’s disease.
However, we have quite recently shown that hormone therapy seems to lower the mortality risk of vascular dementia but not Alzheimer’s disease (Mikkola TS et al. J Clin Endocrinol Metab 2017;102:870-7). Now in this upcoming BMJ-paper we report in a very large case-control study (83 688 women with Alzheimer’s disease and same number of control women without the disease) that systemic hormone therapy was associated with a 9-17% increased risk of Alzheimer’s disease.
Furthermore, this risk increase is particularly in women using hormone therapy long, for more than 10 years. This was somewhat surprising finding, but it underlines the fact that mechanisms behind Alzheimer’s disease are likely quite different than in vascular dementia, where the risk factors are similar as in cardiovascular disease. We have also shown how hormone therapy protects against cardiovascular disease, particularly in women who initiate hormone therapy soon after menopause.

