Every four seconds, someone is diagnosed with Alzheimer’s disease. It’s the most common cause of dementia, affecting over 40 million people worldwide, and yet finding a cure is something that still eludes researchers today. Dr. Alois Alzheimer, a German psychiatrist, first described the symptoms in 1901 when he noticed that a particular hospital patient had some peculiar problems, including difficulty sleeping, disturbed memory, drastic mood changes, and increasing confusion. When the patient passed away, Alzheimer was able to do an autopsy and test his idea that perhaps her symptoms were caused by irregularities in the brain’s structure. What he found beneath the microscope were visible differences in brain tissue in the form of misfolded proteins called plaques, and neurofibrillary tangles. Those plaques and tangles work together to break down the brain’s structure. Plaques arise when another protein in the fatty membrane surrounding nerve cells gets sliced up by a particular enzyme, resulting in beta-amyloid proteins, which are sticky and have a tendency to clump together. That clumping is what forms the things we know as plaques. These clumps block signaling and, therefore, communication between cells, and also seem to trigger immune reactions that cause the destruction of disabled nerve cells. In Alzheimer’s disease, neurofibrillary tangles are built from a protein known as tau. The brain’s nerve cells contain a network of tubes that act like a highway for food molecules among other things. Usually, the tau protein ensures that these tubes are straight, allowing molecules to pass through freely. But in Alzheimer’s disease, the protein collapses into twisted strands or tangles, making the tubes disintegrate, obstructing nutrients from reaching the nerve cell and leading to cell death. The destructive pairing of plaques and tangles starts in a region called the hippocampus, which is responsible for forming memories. That’s why short-term memory loss is usually the first symptom of Alzheimer’s. The proteins then progressively invade other parts of the brain, creating unique changes that signal various stages of the disease. At the front of the brain, the proteins destroy the ability to process logical thoughts. Next, they shift to the region that controls emotions, resulting in erratic mood changes. At the top of the brain, they cause paranoia and hallucinations, and once they reach the brain’s rear, the plaques and tangles work together to erase the mind’s deepest memories. Eventually the control centers governing heart rate and breathing are overpowered as well resulting in death. The immensely destructive nature of this disease has inspired many researchers to look for a cure but currently they’re focused on slowing its progression. One temporary treatment helps reduce the break down of acetylcholine, an important chemical messenger in the brain which is decreased in Alzheimer’s patients due to the death of the nerve cells that make it. Another possible solution is a vaccine that trains the body’s immune system to attack beta-amyloid plaques before they can form clumps. But we still need to find an actual cure. Alzheimer’s disease was discovered more than a century ago, and yet still it is not well understood. Perhaps one day we’ll grasp the exact mechanisms at work behind this threat and a solution will be unearthed.