Borrelia Invasion of Brain Pyramidal Neurons and Biofilm Borrelia Plaques in  Neuroborreliosis Dementia with Alzheimer’s Phenotype 

Alan B. MacDonald* 

Received 29 Janaury 2021; Accepted: 25 February 2021


Dementia in Lyme borreliosis complex has been reported, mainly in post-mortem studies without available  antemortem evidence of active borrelia infection. Blanc in 2014 studied living patients with Lyme neuroborreliosis dementia and several dementia phenotype illnesses including an Alzheimer’s Phenotype. Herein we report an additional case study of a longitudinal evolution of European neuroborreliosis over eight years from tick bite to mild cognitive disease, to advanced dementia to death with a brain Alzheimer’s disease phenotype and concurrent borrelia deposits in brain Alzheimer’s disease sites at autopsy. 

Intrathecal borrelia specific antibodies were detected by commercial diagnostic laboratories (antemortem).  Molecular autopsy tissue imaging was completed with borrelia specific DNA probes and an immunomicroscopic  detection histopathology method. 

Results: Autopsy showed intact spirochetes, fragmented spirochetes, deposits of borrelia-specific proteins inside  plaque lesions and inside of neurons, and borrelia DNA deposits in plaque and neuronal sites. Pure Alzheimer’s  disease (without Lewy bodies) was a routine neuropathological finding. 

CSF evidence for a brain compartment immune response is established here. Intrathecal antibodies to infection  presented as oligoclonal total CSF IgG bands (n=twelve increase to n=13 bands) and separate borrelia IgG  western blot band analysis in cerebrospinal fluids (seven diagnostic borrelia CSF antibody bands). Blood western  blot disclosed triple borrelia species infection; burgdorferi European type (eighteen bands), garinii (twelve bands)  and afzelii (eighteen bands). Total borrelia IgG antibodies in blood during life were two hundred-fold higher  than normal range. Western blot of cerebrospinal fluid prior to death disclosed 7 protein bands which were not  represented in simultaneous blood western blot studies, further validating the intrathecal fingerprint of a separate  brain compartment immune response to neuroborreliosis infection. 

Conclusion: Borrelia protein antigenic stimulation of intrathecal borrelia antibodies was caused by resident  deposits of spirochetal protein deposits in plaques, in diseased neurons, and in neuropil brain sites, and in intact brain spirochetes. Deposits of borrelia proteins inside neurons and brain phagocytes and in neuropil sites (invasosomes) confirm remnants of chronic brain infection. 

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