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There are two main proteins thought to interfere with the communication between brain cells in certain dementias – tau and amyloid.

A computerised illustration of neurones surrounded by clumps of amyloid-beta.

A labelled diagram of a neuron.

Before we explore how proteins affect brain cells’ activity, it’s important to understand their structure. Neurons are the main type of brain cell in the nervous system and are in charge of receiving and delivering messages to control the body.

Neurons have three main sections: a round cell body, a long tube called an axon, and spikes called dendrites reaching out of each end.

Neurons receive messages from other neurons via the dendrites on the cell body. These messages travel through the axon to the other end of the cell – called the axon terminal – where they are sent out from the dendrites there.

Now we understand neuronal anatomy, we can learn how tau and amyloid proteins affect their delicate structure.


Normally, tau proteins are found on the inside of neurons’ axons to maintain their correct structure. This is crucial, because if the axon is compromised, the messages it carries can leak out, meaning they don’t reach the next cell in the chain.

In some forms of dementia, including Alzheimer’s disease and frontotemporal dementia, tau proteins become damaged and detach from their axons. Now moving freely inside the neuron, the abnormal tau proteins clump together to form neurofibrillary tangles. 

This dysfunctional tau is toxic to neurons and causes them to die. When neurons in a chain die, that chain is broken, and messages can’t be delivered as effectively through the brain. This disruption of messaging is what causes the thinking difficulties that underpin dementia. 

Research is now focused on why tau is damaged in these conditions and how exactly it causes the death of neurons. One of the key tau researchers is Professor Karen Duff of the UK Dementia Research Institute, who leads the Duff Lab in studying tau. Once this is better understood, treatments could be developed that protect tau – and therefore neurons – from being damaged.

Graphic showing build-up of amyloid plaque between nerve cells in the brain.


Amyloid begins life as amyloid precursor protein (APP), which is a common, normal protein in the central nervous system. It can be processed in two different ways: one that produces a healthy soluble protein, and one that produces toxic amyloid-beta. 

Both of these processes happen normally, and in healthy brains the amyloid-beta is cleared from the brain before it can do any damage. Scientists think that people with Alzheimer’s disease overproduce amyloid-beta and/or are less able to effectively clear it from their brains. 

Amyloid-beta is dangerous because it clumps together, first forming small clusters called oligomers and eventually accumulating into bulky amyloid plaques. These clumps cause a variety of chemical reactions around neurons that damage and destroy them. One way is by activating the immune system to trigger inflammation, and another is by causing the production of abnormal tau.

New insights

Evidence is now emerging that tau and amyloid affect each other in a complicated relationship. Research suggests that amyloid-beta clusters appear first and are followed by a surge in abnormal tau once amyloid-beta has accumulated to a certain level. A positive feedback loop then occurs, triggering more production of amyloid-beta and more abnormal tau.

Dementia researchers are working hard to understand more about these two proteins in the hope they can be the target of future treatments for people with dementia.