In 1906, German neurologist Dr. Alois Alzheimer discovered sticky protein deposits in the brain of a patient who showed symptoms of dementia, including memory loss. This discovery led to the amyloid hypothesis, which suggests that these sticky proteins, called beta-amyloid, are the cause of dementia. While beta-amyloid exists naturally in blood, it can accumulate in the brain due to aging and other factors, forming 'fragments' or 'plaques'. These plaques produce toxins that gradually deteriorate brain function. Although physical removal of these plaques is impossible due to their integration with brain tissue, we understand the structure of beta-amyloid production and can potentially inhibit its formation. However, stopping production alone isn't effective for symptomatic patients, as their brains are already filled with existing plaques. While the exact structure of beta-amyloid was initially unknown, high-resolution structures of Aβ40 and Aβ42 fibrils were revealed in the 2010s using cryo-electron microscopy (cryo-EM) and nuclear magnetic resonance (NMR).
However, in July 2022, the amyloid hypothesis faced criticism when Science journal reported that a key paper supporting this hypothesis had been manipulated. This paper, published in Nature in 2006 by University of Minnesota researchers, was officially retracted in 2024. Nevertheless, the role of beta-amyloid in dementia is supported by over 30 years of extensive research.