Amyloid beta proteins are ordinarily thought to have several roles including anti-infective activity, repairing injuries and leaks in the blood brain barrier, and being involved in synapse regulation. Meanwhile, tau proteins hep to stabilise the internal microtube skeleton of neurons allowing the movement of nutrients and other substances within the neuron.^13,26

In Alzheimer’s, amyloid beta plaques (containing misfolded amyloid beta proteins plus debris from cell breakdown) form between the nerve cells. In addition, tau protein structure is changed into tangled pairs of helix-shaped filaments (tau protein neurofibrillary tangles) preventing the microtubes from function, causing neurons to die.^22,26

There is some debate as to whether the amyloid beat plaques are the cause of Alzheimer’s, if they are harmful or are instead a side effect of the Alzheimer’s disease process.²⁶

Evidence questioning the theory about plaques causing dementia includes many older people having plaques in the brain but not having neurological symptoms such as memory loss. Another factor to consider is that medicines designed to reduce plaque build do not necessarily restore cognitive function, but just delay the decline.²⁷