Alzheimer’s disease is a devastating brain illness that affects an estimated 47 million people worldwide. It is the most common cause of dementia in the Western world.
Despite this, there are currently no treatments that are effective in curing Alzheimer’s disease or preventing its relentless progression.
Alzheimer’s disease is caused by the build-up of two abnormal proteins, beta-amyloid and tau. Tau is particularly important because it causes neurons and their connections to die, preventing brain regions from communicating with each other normally.
In the majority of cases, tau pathology first appears in the memory centres of the brain, known as the entorhinal cortex and hippocampal formation. This has been shown to occur many years before patients have any symptoms of disease.
Over time, tau begins to appear in increasing quantities throughout the brain.
This causes the characteristic progression of symptoms in Alzheimer’s diseases, where initial memory loss is followed by more widespread changes in thinking and behaviour that lead to a loss of independence. How this occurs has been controversial.
In our study, published in Brain, we provide the first evidence from humans that tau spreads between connected neurons.
This is an important step, because stopping this spread at an early stage might prevent or freeze the symptoms of Alzheimer’s disease.
This idea, called “transneuronal spread”, has been proposed before and is supported by studies in mice. If abnormal tau is injected into a healthy mouse brain, it quickly spreads and causes the mice to manifest dementia symptoms.