U.S. NATIONAL INSTITUTES OF HEALTH
N I A Logo
LEADING THE FEDERAL EFFORT ON AGING RESEARCH

Then and Now: The Fast Pace of Developments in AD Research


Then and Now: The Fast Pace of Developments in AD Research

As shown in this timeline, we have learned a lot since Dr. Alzheimer presented the case of his patient, Auguste D. The pace of research continues to accelerate as new findings open more and more doors to discovery.

1906

  • Dr. Alois Alzheimer, a German neurologist and psychiatrist, describes the case of a 51-year-old woman, Auguste D., who had been admitted to a hospital 5 years earlier with a cluster of unusual symptoms, including problems with comprehension and memory, an inability to speak, disorientation, behavioral problems, and hallucinations. After her death, Dr. Alzheimer examined her brain tissue and described two of the hallmarks of AD—numerous globs of sticky proteins in the spaces between neurons (beta-amyloid plaques) and a tangled bundle of fibrils within neurons (neurofibrillary tangles).

1910s – 1940s

  • Belief persists that “senile dementia” is a normal part of aging.

1950s

  • Scientists study the biological structure of plaques and tangles.

1960s

  • Scientists discover a link between dementia and the number of plaques present in the brain. AD is recognized as a distinct disease, not a normal part of aging.

1970s

  • Scientists find that levels of acetylcholine, a neurotransmitter important in memory formation, falls sharply in people with AD. This discovery is one of the first to link AD with biochemical changes in the brain.
  • “Alzheimer’s disease” becomes a common term as recognition of AD as a major public health problem grows.
  • NIA is established.

1980s

  • Diagnostic criteria for AD are established.
  • Genetic links to early-onset AD begin to surface.
  • Congress mandates NIA as lead Federal agency for AD research.
  • Scientists start to unravel the biological pathways that lead to the development of beta amyloid plaques in the brain.
  • Abnormal tau protein in tangles is identified.

1990s

  • The U.S. Food and Drug Administration (FDA) approves tacrine (Cognex®), the first drug used to treat AD. This drug has since been replaced by other medications.
  • Genetic mutations linked to early-onset and late-onset AD are discovered.
  • The first transgenic mouse model of AD is created.
  • Additional diagnostic criteria are developed for AD.
  • Characteristics of mild cognitive impairment are described and defined.
  • NIA launches the Alzheimer’s Disease Education and Referral Center, AD Cooperative Study, and other initiatives to conduct and support AD treatment and prevention clinical trials.

2000s

  • The FDA approves other AD drugs, including rivastigmine (Exelon®), galantamine (Razadyne®), donepezil (Aricept®), and memantine (Namenda®) to treat symptoms of AD.
  • Early work on an AD vaccine begins.
  • Many new AD clinical trials, initiatives, and studies are launched, looking at a broad array of translational, treatment, and prevention issues.
  • New transgenic mouse models, including one that develops both plaques and tangles, are developed.
  • Pittsburgh Compound B (PiB) is developed, allowing researchers to “see” beta-amyloid plaques in the brains of living people.
  • The growing sophistication of neuroimaging techniques, genetics, memory and cognitive tests, structured interviews, and other technologies improve our ability to identify people at high risk of AD.

<< Back | Next >>




Page last updated Nov 25, 2008

Phone Table of Contents