Instructor

Monica E. Embers, PhD
Associate Professor in the Division of Immunology
Director of Vector-borne Disease Research
Tulane National Primate Research Center

Description

This module describes the features of dementia and microbes which have been implicated in the development of this type of neurological disease. The gaps in knowledge regarding the development of dementia are highlighted. Finally, a case report from a patient who developed Lewy body dementia following a Lyme disease diagnosis is discussed.

Learning objectives

  1. To review the prevalence and different types of dementia
  2. To describe the clinical and pathological features of dementia
  3. To consider the possible mechanisms of neurological damage (that are consistent with dementia pathology) induced by microbes
  4. To define the gaps in knowledge regarding the etiology of Alzheimer’s and Lewy body dementia• To provide evidence for the probable role of the Lyme disease spirochete in dementia etiology several years after unsuccessful treatment for Lyme disease (case report).


Accreditation Statement

This session, Chronic infection and the etiology of dementia, is approved for 0.5 enduring AAFP Prescribed credits.

The AAFP has reviewed One Health Medical Education for a Changing Climate, and deemed it acceptable for AAFP credit. Term of approval is from 01/01/2025 to 12/31/2025. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

AAFP Prescribed credit is accepted by the American Medical Association as equivalent to AMA PRA Category 1 credit(s)™ toward the AMA Physician’s Recognition Award. When applying for the AMA PRA, Prescribed credit earned must be reported as Prescribed, not as Category 1.


Evidence-based bibliography for further study

  • Embers ME, Hasenkampf NR, Jacobs MB, Tardo AC, Doyle-Meyers LA, Philipp MT, Hodzic E: Variable manifestations, diverse seroreactivity and post-treatment persistence in non-human primates exposed to Borrelia burgdorferi by tick feeding. PLoS ONE 2017, 12(12):e0189071.
  • Crossland NA, Alvarez X, Embers ME: Late Disseminated Lyme Disease: Associated Pathology and Spirochete Persistence Posttreatment in Rhesus Macaques. The American Journal of Pathology 2018, 188(3):672-682
  • A.B. MacDonald: Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete. Med Hypotheses, 67 (2006), pp. 592-600
  • Serrano-Pozo A, Frosch MP, Masliah E, Hyman BT. Neuropathological alterations in alzheimer disease. Cold Spring Harbor perspectives in medicine. 2011;1(1):a006189. https://www.ncbi.nlm.nih.gov/pubmed/22229116. doi: 10.1101/cshperspect.a006189.
  • Qiu C, Kivipelto M, von Strauss E. Epidemiology of alzheimer’s disease: Occurrence, determinants, and strategies toward intervention.
    Dialogues in clinical neuroscience. 2009;11(2):111-128. https://www.ncbi.nlm.nih.gov/pubmed/19585947.
  • Raber J, Huang Y, Ashford JW. ApoE genotype accounts for the vast majority of AD risk and AD pathology. Neurobiology of Aging. 2004;25(5):641-650. https://www.sciencedirect.com/science/article/pii/S0197458004001009. doi: 10.1016/j.neurobiolaging.2003.12.023
  • Itzhaki RF, Lin W, Shang D, Wilcock GK, Faragher B, Jamieson GA. Herpes simplex virus type 1 in brain and risk of alzheimer’s disease. The Lancet. 1997;349(9047):241-244. https://www.sciencedirect.com/science/article/pii/S0140673696101495. doi: 10.1016/S0140- 6736(96)10149-5.
  • Itzhaki RF. Herpes simplex virus type 1 and alzheimer’s disease: Increasing evidence for a major role of the virus. Frontiers in aging neuroscience. 2014;6:202. https://www.ncbi.nlm.nih.gov/pubmed/25157230. doi: 10.3389/fnagi.2014.00202.
  • Itzhaki RF. Herpes simplex virus type 1 and Alzheimer’s disease: Possible mechanisms and signposts. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2017;31(8):3216. https://www.ncbi.nlm.nih.gov/pubmed/28765170.
  • Mawanda F, Wallace R: Can Infections Cause Alzheimer’s Disease? Epidemiologic Reviews 2013, 35(1):161-180.
  • Soscia SJ, Kirby JE, Washicosky KJ, Tucker SM, Ingelsson M, Hyman B, Burton MA, Goldstein LE, Duong S, Tanzi RE et al: The Alzheimer’s disease-associated amyloid beta-protein is an antimicrobial peptide. PLoS ONE 2010, 5(3):0009505.
  • Miklossy J: Bacterial Amyloid and DNA are Important Constituents of Senile Plaques: Further Evidence of the Spirochetal and Biofilm Nature of Senile Plaques. J Alzheimers Dis 2016,  53(4):1459-1473.
  • Gadila, S. K. G., Rosoklija, G., Dwork, A. J., Fallon, B. A., & Embers, M. E. (2021). Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens. Front Neurol, 12, 628045. https://doi.org/10.3389/fneur.2021.628045
  • Balin BJ, Hammond CJ, Little CS, et al. Chlamydia pneumoniae: An Etiologic Agent for Late-Onset Dementia. Front Aging Neurosci. 2018;10:302. Published 2018 Oct 9. doi:10.3389/fnagi.2018.0030216. Gérard HC, Dreses-Werringloer U, Wildt KS, Deka S, Oszust C, Balin BJ, Frey WH 2nd, Bordayo EZ, Whittum-Hudson JA, Hudson AP. Chlamydophila (Chlamydia) pneumoniae in the Alzheimer’s brain. FEMS Immunol Med Microbiol. 2006):355-66. doi: 10.1111/j.1574-695X.2006.00154.x. Epub 2006 Oct 18. PMID: 17052268.

Monica E. Embers, PhD

About the Instructor

Monica Embers, PhD

Director of Vector-borne Disease Research, Tulane National Primate Research Center

Dr. Embers is currently an Associate Professor in the Division of Immunology and the Director of Vector-borne Disease Research at the Tulane National Primate Research Center. Her research program regarding Lyme disease and its infectious cause Borrelia burgdorferi specializes in animal models. The research is centered around three major efforts: (1) identifying treatments that can eradicate B. burgdorferi infection; (2) detection of persistent Lyme disease spirochetes in human (autopsy) tissues; and (3) immunodiagnosis for B. burgdorferi infection and cure. By transmitting Lyme disease to mice and nonhuman primates by tick, and studying the natural course of infection, her group aims to attain a better understanding of the clinical quandaries of human Lyme disease, including effective diagnosis and treatment. Due to the many similarities between Bartonellosis and Lyme disease, her team has begun to develop research models for Bartonella infection. The goals of Bartonella research involve developing improved treatment strategies, understanding the pathophysiology of co-infection, and interrogating tick vector transmission of these pathogens.