Judith Miklossy, Ph.D, MD, DSc will speak at the NorVect conference about the link between Borrelia and Dementia, such as Alzheimer disease.
Lecture: "Chronic Lyme disease and Lyme dementia"
Whether the spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was also the subject of long debate in the history of syphilis, and today, the same question is in the center of debate with respect to Lyme disease. Detection of Treponemapallidum in the brains of patients suffering from general paresis established a direct link between persisting infection and tertiary manifestations of neurosyphilis. As pathological changes characteristic of tertiary neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi was detected in tertiary brain lesions clearly indicate that in a similar way to Treponema pallidum, Borrelia burgdorferi is also responsible for the neuropsychiatric manifestations of late or chronic Lyme neuroborreliosis. Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and define tertiary Lyme disease. The use of chronic Lyme disease as a different entity is inaccurate and confusing. It is well established that chronic spirochetal infection can cause slowly progressive dementia, cortical atrophy and amyloid deposition in the atrophic form of general paresis in syphilis. Various types of spirochetes, including periodontal pathogen spirochetes and Borrelia burgdorferi may well behave as Treponema pallidum, and cause dementia, vascular infarcts and other tertiary manifestations of chronic neurospirochetosis.
Recent observations show that Borrelia burgdorferi and several periodontal pathogen Treponemes (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) can persist in the brain and cause dementia and beta amyloid deposition. A statistically significant association following Hill’s criteria is in favor of a causal relationship. As the host pathogen interactions in chronic spirochetal infections are similar to those occurring in AD indicates that escaping host immune reactions, spirochetes can sustain chronic infection and inflammation, cause dementia. Confirmation and reproduction of these data by historic and recent observations made by others is highlighted.
If various types of spirochetes are implicated in the pathogenesis of AD, similarly to syphilitic dementia, Alzheimer’s dementia might be prevented. The impact would be inestimable.
For Prof Miklossy's biography, read more here:http://norvect.no/conference-2014/speakers/#judith_miklossy
Whether the spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was also the subject of long debate in the history of syphilis, and today, the same question is in the center of debate with respect to Lyme disease. Detection of Treponemapallidum in the brains of patients suffering from general paresis established a direct link between persisting infection and tertiary manifestations of neurosyphilis. As pathological changes characteristic of tertiary neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi was detected in tertiary brain lesions clearly indicate that in a similar way to Treponema pallidum, Borrelia burgdorferi is also responsible for the neuropsychiatric manifestations of late or chronic Lyme neuroborreliosis. Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and define tertiary Lyme disease. The use of chronic Lyme disease as a different entity is inaccurate and confusing. It is well established that chronic spirochetal infection can cause slowly progressive dementia, cortical atrophy and amyloid deposition in the atrophic form of general paresis in syphilis. Various types of spirochetes, including periodontal pathogen spirochetes and Borrelia burgdorferi may well behave as Treponema pallidum, and cause dementia, vascular infarcts and other tertiary manifestations of chronic neurospirochetosis.
Recent observations show that Borrelia burgdorferi and several periodontal pathogen Treponemes (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) can persist in the brain and cause dementia and beta amyloid deposition. A statistically significant association following Hill’s criteria is in favor of a causal relationship. As the host pathogen interactions in chronic spirochetal infections are similar to those occurring in AD indicates that escaping host immune reactions, spirochetes can sustain chronic infection and inflammation, cause dementia. Confirmation and reproduction of these data by historic and recent observations made by others is highlighted.
If various types of spirochetes are implicated in the pathogenesis of AD, similarly to syphilitic dementia, Alzheimer’s dementia might be prevented. The impact would be inestimable.
For Prof Miklossy's biography, read more here:http://norvect.no/conference-2014/speakers/#judith_miklossy
