There has been growing evidence of the importance of inflammation in Alzheimer’s disease. Briefly, there have been a number of observations that people taking anti-inflammatory medications, particularly those with rheumatoid arthritis, may have a modestly reduced risk of getting Alzheimer’s disease. Studies in animal models have shown that brain inflammation has a dual response, protective in the acute reaction and detrimental when chronic. In these animal studies, chronic neuroinflammation activates inflammatory cells in the brain called microglia, increases beta-amyloid burden, and increases the production of hyperphosphorylated tau, the toxic form of tau protein found in neurofibrillary tangles. However, trials of anti-inflammatory medications such as ibuprofen in humans have for the most part failed to show a significant reduction in the risk of getting Alzheimer’s. Recent work has suggested that this damaging effect of inflammation on Alzheimer’s risk does indeed occur in humans but is specific to those carrying the APOE-4 allele.

Recently, I came across an interesting paper from 2013 in Lancet Neurology that adds important genetic information about the case of Auguste D, the first patient diagnosed with what was later called Alzheimer’s disease. She first came under the care of Dr. Alois Alzheimer at age 51 because of rapidly progressive memory loss, hallucinations, seizures, focal neurological signs including trouble speaking, and delusions that her husband was having an affair with the next-door neighbor, fears that were apparently unfounded. She died five years later, and Dr. Alzheimer was able to examine her brain under a microscope. He was surprised to find dark blobs outside of nerve cells and smaller dark tangles within the axons of nerve cells. He reported his findings in 1906 at the 37th Conference of South-West German Psychiatrists in Tübingen, but there was little interest from the audience. Soon other pathologists started seeing these dark extracellular blobs and intraneuronal twists in the brains of demented patients, later identified as beta-amyloid plaques and tau-containing neurofibrillary tangles. Dementia associated with these characteristic pathological findings came to be called Alzheimer’s disease in his honor.