Recent research published in the journal Communications Medicine and highlighted by the Fondation Alzheimer investigates how the Bacillus Calmette-Guérin (BCG) vaccine modifies immune responses linked to Alzheimer’s disease. While observational studies have historically suggested a lower incidence of Alzheimer’s among bladder cancer patients treated with the immunotherapy, the new trial demonstrates that BCG induces measurable, long-term changes in central nervous system immune cells.
BCG Vaccine Alters Central Nervous System Immune Cells
From Tuberculosis Prevention to Trained Immunity Mechanisms
Originally developed as a tuberculosis vaccine, the BCG vaccine has been administered for decades as a targeted immunotherapy for specific types of bladder cancer. According to the Fondation Alzheimer, its relevance to neurodegenerative research stems from a biological mechanism known as “trained immunity.” When immune cells encounter BCG, they undergo a functional reprogramming that alters their response to subsequent stimulations.
As humans age, the immune system undergoes gradual shifts that often foster a state of low-grade, persistent systemic inflammation, a phenomenon frequently termed “inflammaging.” Researchers investigating neurodegenerative disorders monitor this process closely because neuroinflammation could participate in the mechanisms of Alzheimer’s disease. Consequently, scientists are exploring whether peripheral immune stimulation via agents like BCG can induce effects within the central nervous system.
Tracking Biomarkers and Cerebrospinal Fluid in Adult Participants
To evaluate these immunological effects in humans, investigators tracked 23 adult participants aged 55 years and older over the course of one year. Each participant received two separate BCG injections administered one month apart. Following the treatment protocol, researchers collected and analyzed both blood samples and cerebrospinal fluid—the protective fluid surrounding the brain and spinal cord.
According to the study results, analysts identified lasting alterations within specific immune defense cells residing in the cerebrospinal fluid. These findings suggest that a form of trained immunity could also develop within the central nervous system. Furthermore, among trial participants who lacked biological markers associated with Alzheimer’s disease, researchers observed changes involving beta-amyloid, a protein studied in the condition.
Despite these immunological shifts, the research does not establish BCG as a preventative measure or treatment for Alzheimer’s disease. As noted by the Fondation Alzheimer, the investigation remains strictly preliminary, is limited by a small cohort of 23 participants, and lacks a control group for comparative analysis.
Larger, controlled clinical trials are required to determine whether these preliminary biological observations are confirmed. At this stage, the primary value of the research lies in its contribution to understanding the complex physiological intersections between immune system aging, inflammation, and Alzheimer’s disease.
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