Harvard Medical School researchers have made a groundbreaking discovery detailing the mechanisms through which bacteria can penetrate the brain’s protective layers, leading to potentially fatal conditions like meningitis. Published in Nature on March 1, the study, conducted on mice, reveals how bacteria exploit the interaction between nerve and immune cells to breach the meninges and infect the brain.
In a separate context, the role of inflammation in brain health is under investigation. Notably, Dr. Eric Larson, during his internship at Beth Israel Hospital in the mid-1970s, observed that cognitive decline in older individuals was often attributed to senile dementia or arterial hardening. However, recent insights from Harvard Medicine Magazine suggest that inflammation, traditionally considered a defense mechanism against brain injury and infection, might also contribute to cognitive decline.
A brain abscess, as explained by Harvard Health and the Children’s Hospital of Philadelphia, is a pus-filled swelling in the brain tissue, usually a result of bacterial or fungal infection. This condition can arise from various sources, including nearby infections, bloodstream infections, or direct entry through head wounds, especially in individuals with compromised immune systems.
Further research from Harvard Medical School, published on March 8 in Nature, investigates how the brain detects flu infections. Studying mice, scientists identified a group of neurons in the airway that alerts the brain about the infection, suggesting the existence of a pathway from the lungs to the brain that activates later in the infection process.
Adding to this complex picture, researchers at Massachusetts General Hospital discovered channels in the skull that allow cerebrospinal fluid to flow into the bone marrow, aiding in the detection of brain infections and injuries. This finding, detailed in the Harvard Gazette, highlights an intricate system of brain-immune interaction.
Acute disseminated encephalomyelitis (ADEM), a rare disorder following viral or bacterial infections, involves an intense immune attack on the brain, spinal cord, and optic nerves. The Children’s Hospital of Philadelphia notes that identifying a specific preceding infection is uncommon in ADEM cases.
Lastly, the long-term cognitive effects of COVID-19, as discussed in a Harvard Health blog, include brain damage from direct infection, strokes, or oxygen deprivation, and are particularly evident in patients who have experienced severe illness requiring intensive care.
