Today at the Global Dementia Legacy Event in London, the UK prime minister David Cameron announced a global push to defeat dementia by 2025, saying: “Dementia now stands alongside cancer as one of the greatest enemies of humanity.” These are the most promising ways to achieve that goal.

1. Open up the brain

The biggest hurdle to producing an effective treatment for dementia is getting drugs into the brain in sufficient quantities. “You can be as clever as you like working out how to develop a drug but if you can’t get it to the body part its useless,” says Matthew Wood, a neuroscientist at the University of Oxford. “It’s as much about getting them there as developing them.”

The problem is that our blood-brain barrier (BBB) – a tightly packed layer of cells that wrap around every blood vessel throughout the brain – blocks 98 per cent of our drugs arsenal from penetrating the brain. Next month, though, a team at Sunnybrook Research Institute in Toronto, Canada, will open up the BBB for the first time in humans by injecting microbubbles into the bloodstream and making them vibrate using ultrasound waves. This should mechanically force open the BBB for a few vital hours, allowing drugs to sneak into the brain.

The team hopes to start testing the technique with Alzheimer’s drugs within a year. “We have Alzheimer’s drugs that work in a dish – we just need to get them to the brain in high enough quantities,” says Kullervo Hynynen at Sunnybrook Hospital, who is conducting the trial.


2. Test drugs early

Another major hurdle for combating dementia is that the symptoms of the disease occur decades after the damage to the brain begins. Many researchers believe that drug trials have failed because the drugs are taken too late into the disease.

A small population in Yarumal, Colombia, might be able to help. Here, thousands of people suffer from what locals call La Bobera – “the foolishness”. Once believed to be a curse put on the village by an angry priest, La Bobera makes the townspeople confused before robbing them of their memories. We know now that it is a form of early onset Alzheimer’s, caused by a rare mutation in a gene called PSEN1. About 5000 people in this community have the mutation, and they will be diagnosed with Alzheimer’s by the age of 45.

This gives researchers the unique opportunity to test Alzheimer’s drugs on the inhabitants – with the added knowledge of who will definitely get the disease and who won’t. The trial will begin later this year.

The world’s first blood test to predict Alzheimer’s disease before symptoms occur might lend a helping hand in recruiting volunteers elsewhere in the world. The test, which was developed in March, identifies 10 chemicals in the blood associated with Alzheimer’s two to three years before symptoms start. If a pre-clinical population could be identified with this blood test, it could be game changing. The latest guidance from the US Food and Drug Administration also supports earlier treatment.

3. Link with diabetes

Some researchers think type 2 diabetes can set you on a path to Alzheimer’s. If so, there’s a way to fight back – take regular exercise and eat sensibly.

Type 2 diabetes is a risk factor for Alzheimer’s but there is growing evidence that the link between the two diseases could be stronger. Rats fed so that they develop diabetes have brains littered with amyloid plaques – one of the calling cards of Alzheimer’s. Other research suggests that the memory problems that often accompany type 2 diabetes could be a sign that someone is already in the early clutches of dementia.

If the connection holds up, it may be good news, as type 2 diabetes is essentially a lifestyle disease. “The real answer is that people should go to the gym and that would fix it,” says Ewan MacNay at the State University of New York. “Exercise reverses insulin sensitivity, cures type 2 diabetes, increases blood flow to the brain and spurs the growth of new neurons”.

4. Beat inflammation

The speed at which Alzheimer’s develops has been linked to whether patients suffer frequently from infections, such as cold and flu, or chronic inflammatory diseases including diabetes, coronary heart disease and obesity. This year, researchers announced that they have pieced together how this happens.

When parts of the body outside the brain are infected or chronically inflamed, the immune system becomes overactive, and this eventually spills over into the brain, damaging its ability to dispose of the beta-amyloid plaques that clog the brain and are thought to play a major role in Alzheimer’s. A trial is under way in the UK to see if an anti-inflammatory arthritis drug called etanercept helps people with Alzheimer’s .

5. Antibody attack

Several pharmaceutical companies are developing monoclonal antibodies, which target amyloid plaques. However, trials of these drugs in people with mild-to-moderate Alzheimer’s have failed. It may be that clearing plaques is not enough – one antibody trial cleared the plaques but volunteers showed no clinical improvement. Recent studies suggest that tiny amyloid clumps called oligomers, which appear before larger plaques, might be key to fighting the disease. A new antibody developed by Roche called gantenerumab attacks both plaques and oligomers – results from clinical trials are expected in 2016.

Such antibodies might be boosted by another technology from Roche – a molecular shuttle, which hijacks a natural transport mechanism used to transfer proteins from the blood into the brain. In animal studies, attaching the antibody to this “taxi service” increased by 50-fold the concentration of antibodies in the brains of mice.