UK doctor watched Jeremy Paxman host University Challenge and realised he had Parkinson's disease

Alzheimer's disease and other types of dementia affect more than 55 mn people worldwide.

The development of effective treatments and cures is progressing slowly because we still don't understand enough about what causes the disease and drives its progression.

In Alzheimer's disease, proteins that are normally part of healthy brain cells start sticking together in microscopic clumps. These clumps of protein, called aggregates, form in patients' brains, killing off brain cells and leading to symptoms such as memory loss.

As the number of aggregates increases, the disease worsens and eventually leads to death, often many years after the first mild symptoms.

Several processes likely contribute to the formation of aggregates, but scientists are yet to understand how aggregates form in detail.

Research often uses lab animals, such as mice. But it's not a great model because Alzheimer's takes decades to develop in humans, and lab animals can only be studied over a much shorter timescale.

Using an approach called chemical kinetics, it was revealed as to what happens at the microscopic level in the Alzheimer's brain. Chemical kinetics allows us to understand the way molecules interact with each other.

The protein aggregates in brains of Alzheimer's patients multiply exponentially, meaning one aggregate produces two aggregates after a certain period of time, which then, after the same amount of time produce four aggregates, and so on.

In Alzheimer's disease, patients experience no symptoms or mild symptoms while aggregates initially build up, followed by much more rapid progression and worsening of symptoms.