Alzheimer's disease begins in one region of the brain and rapidly spreads to other brain cells just like an infection, American scientists have discovered.

Researchers from Columbia University Medical Center (CUMC) in New York found viruses and bacteria aren't cause this infection-like spread, but an abnormal protein in the brain called 'tau' that propagates along linked brain circuits - by 'jumping' from neuron to neuron.

Researchers tested on mice which were genetically grown to accumulate human tau in the key memory centre of the brain, otherwise known as the entorhinal cortex (where Alzheimer's usually starts to develop).

The progression of tau was monitored over 22 months, where researchers discovered that it had managed to spread across linked pathways from the entorhinal cortex to the hippocampus and neocortex (the brain areas that control the formation and storage of memories).

The tau cells were able to move from brain cell to brain cell using synapses, the connection points that allow nerve cells to communicate with each other. Since other cells were unable to make human tau in the lab mice, the only way these cells could spread is by cell-to-cell transmission.

"Everyone talks about Alzheimer's 'spreading', but there really has not been a standard theory," says Dr Karen Duff and Dr Scott Small from the study.

"In the past, we have asked many of our colleagues in the field of Alzheimer's research what they mean when they say 'spread'. Most think that the disease just pops up in different areas of the brain over time, not that the disease actively jumps from one area to the next.

"Our findings show for the first time that the latter might be true."

It's long been known that tau-filled cells play a huge role in the development of Alzheimer's, as they first appear in small areas of the brain where memories are made and stored.

However, these findings open up greater understanding of how the disease develops and supports the idea that Alzheimer's disease doesn’t just 'pop up' spontaneously in different areas of the brain and can be transmitted from brain cell-to-cell.

Scientists also hope these findings could help them bring a patient’s Alzheimer's disease to an abrupt halt during the early stages by preventing the faulty protein jumping from one brain cell to another, using treatment that blocks tau.

"The implication of our study is that if it were possible to 'treat' Alzheimer's when it was first detected in the entorhinal cortex, this would prevent spread," Dr. Duff added.

The study results were published in PloS One Journal.

Dr Marie Janson, Director of Development at Alzheimer’s Research UK, the UK’s leading dementia research charity, told The Huffington Post:

“The protein studied here, tau, is one of two hallmark proteins involved in Alzheimer’s disease – together with another protein, amyloid. Understanding how Alzheimer’s progresses is vital for developing effective treatments, and Alzheimer’s Research UK is funding similar work to investigate whether the disease may spread from one part of the brain to another.

"If Alzheimer’s does in fact develop in this way, this would suggest that any new drugs would need to be given as early as possible to stop the disease in its tracks – this means the ability to diagnose people at an earlier stage will be crucial."

In the UK alone there are 820,000 people living with a type of dementia, a number forecast to rise as the population ages. According to Alzheimer's Research UK, one in three people aged over 65 will die with a form of dementia with there being 163,000 new cases of dementia in the UK recorded every year - that's one diagnosis every 3.2 minutes.