The basics of Alzheimer’s disease

Scientists are conducting studies to learn more about plaques, tangles, and other biological features of Alzheimer’s disease. Advances in brain imaging techniques allow researchers to see the development and spread of abnormal amyloid and tau proteins in the living brain, as well as changes in brain structure and function. Scientists are also exploring the very earliest steps in the disease process by studying changes in the brain and body fluids that can be detected years before Alzheimer’s symptoms appear.

One of the great mysteries of Alzheimer’s disease is why it largely affects older adults. Research on normal brain aging is exploring this question. For example, scientists are learning how age-related changes in the brain may harm neurons and affect other types of brain cells to contribute to Alzheimer’s damage. These age-related changes include atrophy (shrinking) of certain parts of the brain, inflammation, blood vessel damage, production of unstable molecules called free radicals, and mitochondrial dysfunction (a breakdown of energy production within a cell).

Most people with Alzheimer’s have the late-onset form of the disease in which symptoms become apparent in their mid-60s or later. Researchers have not found a specific gene that directly causes late-onset Alzheimer’s, but having a form of the apolipoprotein E (APOE) gene increases a person’s risk. This gene has several forms, and one of those, APOE ε4, increases a person’s risk of developing Alzheimer’s and is also associated with an earlier age of disease onset. However, carrying the APOE ε4 form of the gene does not mean that a person will definitely develop the disease, and some people with no APOE ε4 may also develop Alzheimer’s.

This content is provided by the NIH National Institute on Aging (NIA). NIA scientists and other experts review this content to ensure it is accurate and up to date.