Do Microbes Trigger Alzheimer’s Disease?
Excerpted from The Scentist : (09/01/2017)
In late 2011, Drexel University dermatology professor Herbert Allen was astounded to read a new research paper documenting the presence of long, corkscrew-shape bacteria called spirochetes in postmortem brains of patients with Alzheimer’s disease.1 Combing data from published reports, the International Alzheimer Research Center’s Judith Miklossy and colleagues had found evidence of spirochetes in 451 of 495 Alzheimer’s brains. In 25 percent of cases, researchers had identified the spirochete as Borrelia burgdorferi, a causative agent of Lyme disease. Control brains did not contain the spirochetes.
The study made Allen think back to 40 years earlier, when he was an intern at Johns Hopkins University and had treated a patient diagnosed with neurosyphilis, a neurological syndrome that included dementia and resulted from the invasion of the syphilis spirochete into the brain. “The parallel between Lyme disease and syphilis had me intrigued,” he says.
Allen had recently proposed a novel role for biofilms—colonies of bacteria that adhere to surfaces and are largely resistant to immune attack or antibiotics—in eczema. He suggested that because biofilms block skin ducts and trigger innate immune responses, they may cause the stubborn skin condition. Allen knew of recent work showing that Lyme spirochetes form biofilms,2which led him to wonder if biofilms might also play a role in Alzheimer’s disease. When Allen stained for biofilms in brains from deceased Alzheimer’s patients, he found them in the same hippocampal locations as amyloid plaques.3 Toll-like receptor 2 (TLR2), a key player in innate immunity, was also present in the same region of the Alzheimer’s brains but not in the controls. He hypothesizes that TLR2 is activated by the presence of bacteria, but is locked out by the biofilm and damages the surrounding tissue instead.
Spirochetes, common members of the oral microbiome, belong to a small set of microbes that cross the blood-brain barrier when they’re circulating in the blood, as they are during active Lyme infections or after oral surgery. However, the bacteria are so slow to divide that it can take decades to grow a biofilm. This time line is consistent with Alzheimer’s being a disease of old age, Allen reasons, and is corroborated by syphilis cases in which the neuroinvasive effects of spirochetes might appear as long as 50 years after primary infection.
Allen’s work contributes to the revival of a long-standing hypothesis concerning the development of Alzheimer’s. For 30 years, a handful of researchers have been pursuing the idea that pathogenic microbes may serve as triggers for the disease’s neuropathology. Most came across the connection serendipitously, as Allen did, and some have made it their life’s work, in spite of scathing criticism and related challenges in attracting funding and publishing results.
Lyme Handbook 