A century of Alzheimer’s disease

One hundred years ago a small group of psychiatrists described the abnormal protein deposits in the brain that define the most common neurodegenerative diseases. Over the past 25 years, it has become clear that the proteins forming the deposits are central to the disease process. Amyloid-b and tau make up the plaques and tangles of Alzheimer’s disease, where these normally soluble proteins assemble into amyloid-like filaments. Tau inclusions are also found in a number of related disorders. Genetic studies have shown that dysfunction of amyloid-b or tau is sufficient to cause dementia. The ongoing molecular dissection of the neurodegenerative pathways is expected to lead to a true understanding of disease pathogenesis. On3November 1906, at the 37th meetingof the Society of Southwest GermanPsychiatrists in Tübingen, Germany, Alois Alzheimer presented the clinical and neuropathological characteristics of the disease (1, 2) that Emil Kraepelin subsequently named after him (3). Alzheimer’s disease (AD) is now the most common neurodegenerative disease, with more than 20 million cases worldwide. At the time of his lecture, Alzheimer was head of th