Spirochete bacteria have been identified in the brains of patients with Alzheimer's disease. Infectious organisms have been thought to be a cause or trigger of Alzheimer's disease, and Borrelia has been implicated along with other spirochete bacteria.
September 21 is World Alzheimer's Day, a date chosen by the World Health Organization and the International Alzheimer's Federation. The purpose of this commemoration is to raise awareness about the disease and disseminate information about it, requesting the support and solidarity of the general public, institutions, and official bodies.
As almost everyone knows, Alzheimer's disease is a progressive, degenerative, and irreversible disorder of the brain that causes weakness, disorientation, and eventual intellectual death.
Chronic Lyme disease, sometimes caused by a tick bite, is known as "the great imitator" because of its ability to mimic the symptoms of multiple diseases, from organic and neurological to musculoskeletal.
Recent research shows a possible link between Lyme disease and Alzheimer's disease.
Research presented at the 2005 annual conference of the American Association of Nurse Practitioners (AANP) showed that in 10 post-mortem Alzheimer's patients, 7 had DNA fusion from Bb flagellin with human DNA from chromosome 11, producing a transfection product. Samples were taken from neurofibrillary tangles in the hippocampus and analyzed using PCR and DNA sequencing.
For several years, it has been known that spirochete bacteria have been identified in the brains of patients with Alzheimer's disease and that inflammation plays an important role. It has been thought that infectious organisms may be a cause or trigger of Alzheimer's disease, and Borrelia has been implicated along with other spirochete bacteria.
It was also long debated whether spirochetes persist in host tissues and cause ultimately chronic manifestations of neurosyphilis. The detection of Treponema pallidum in the brains of patients with general paralysis established a direct link between persistent infection and tertiary manifestations of neurosyphilis.
Today, the same question is at the center of debate regarding Lyme disease. The aim of this review was to compare the established pathological features of neurosyphilis with those available for Lyme neuroborreliosis. If the main tertiary forms of neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi can be detected in brain lesions, this would indicate that the spirochete is responsible for the neuropsychiatric manifestations of chronic Lyme neuroborreliosis.
The substantial amounts of data available show that the main forms of chronic Lyme neuroborreliosis (meningovascular and meningoencephalitis) are clinically and pathologically confirmed.
Borrelia burgdorferi was detected in association with tertiary brain lesions and cultured from the affected brain or cerebrospinal fluid.
The accumulated data also indicate that Borrelia burgdorferi is capable of evading destruction by the host tissue's immune responses, persisting in the host tissues and maintaining chronic infection and inflammation.
These observations provide evidence that Borrelia burgdorferi, in a manner analogous to Treponema pallidum, is responsible for the chronic end stages of Lyme neuroborreliosis. The use of chronic and end-stage Lyme neuroborreliosis as separate entities is inaccurate and may be confusing. It is clear that pathological research and the detection of spirochetes in tissues and body fluids are needed.
Dr. Mariano Bueno is one of the Spanish specialists who has trained in the specialization programs of the ILADS (International Lyme And Associated Diseases Society) in the United States for the treatment of Lyme disease.
