The most common form of dementia. Between 1995 and 2021 private money spent on Alzheimer's research came to $42.5bn, but more than 140 trials failed to yield a single drug capable of slowing the disease. Women are twice as likely to develop Alzheimer's as men, a difference that cannot be explained solely by their longer lifespans. At any given stage of the disease, tau proteins spread farther in women's brains than in men's.
For decades the dominant theory has been that the primary cause of Alzheimer's is the accumulation of plaques of beta-amyloid proteins in the brain, leading to neuronal dysfunction, brain-cell death and neuroinflammation. The hypothesis was supported by genetic evidence linking mutations in certain genes to early onset of the disease. James Rowe, a professor of cognitive neurology at the University of Cambridge, argues that although amyloid accumulation is a critical "early trigger", by the time patients present clinically, other processes are accelerating the illness: accumulation of misshapen tau protein, increased metabolic stress on brain cells, neuroinflammation and degeneration of the brain's blood supply.
There were 182 clinical trials for Alzheimer's treatments under way in 2025—an 11% increase on the year before—testing 138 different drugs.
Approved drugs. The first two drugs capable of slowing Alzheimer's arrived on the market in quick succession: lecanemab in 2023 and donanemab in 2024. Both help clear amyloid from the brain and slow disease progression by about one-third, meaning patients can retain their quality of life for longer. They offer modest benefits to a subset of patients for whom they are thought to be safe and useful.
Repurposed drugs. Fully one-third of the drugs in the 2025 pipeline are repurposed from other conditions, which allows faster approval and cheaper development because safety profiles are already known. Examples include:
Novel approaches. Particular attention is being paid to microglia, brain cells that play an important role in the immune response. They have been described as acting as the brain's fire service, police and binmen. A number of drugs are trying to target the protein TREM2 on the surface of microglia to boost their activity. Combination therapies—such as pairing the cancer drug dasatinib with quercetin, a plant-derived molecule, to clear ageing cells—are also being tested, following the model of combination treatments that transformed outcomes in cancer and HIV.
Synthetic proteins. The Institute for Protein Design at the University of Washington, led by David Baker, is using AI-designed proteins that bind to the molecular precursors of the neuronal plaques and tangles found in the brains of those afflicted.
The problem with any unwritten law is that you don't know where to go to erase it.