| 1906 |
Senile plaques were first established |
| 1984 |
Amyloid β protein (Aβ) was isolated as the principal constituent found within the plaques in the brains of individuals with AD |
| 1987 |
The observation that the formation of Aβ resulted from the processing of amyloid precursor proteins |
| 1990 |
Evidence of the neurotoxic properties of Aβ aggregates was presented |
| 1992 |
The hypothesis of the amyloid cascade was put forward |
| 1995 |
AD patients exhibit a significant decrease in CSF Aβ42 levels, revealing an established connection between Aβ and inflammation |
| 1997 |
The discovery of the ability of Aβ42 to inhibit long-term potentiation |
| 1998 |
The primary instigator of neuronal damage was identified as Aβ oligomers |
| 2001 |
Evidence was provided to establish a connection between Aβ and the formation of neurofibrillary tangles |
| 2004 |
The inaugural amyloid PET tracer, Pittsburgh compound-B (PIB), was formulated |
| 2016 |
Light therapy led to a reduction in Aβ accumulation in both animal models of AD and patients |
| 2017 |
The transfer of Aβ from the periphery through the blood–brain barrier into the brain is reported |
| 2018 |
The ultrasensitive technology, Simoa, was devised for quantifying Aβ at sub-femtomolar concentrations |
| 2021 |
Aducanumab became the inaugural FDA-approved medication for diminishing Aβ plaques |
| 2023 |
FDA approval has been granted to lecanemab for the treatment of AD |
