People with Alzheimer’s develop plaques of misfolded proteins in their cortex, as well as some subcortical regions of the brain. These plaques are made of a protein called amyloid beta (Aβ), formed from the breakdown of a larger protein, called amyloid precursor protein. In the Alzheimer’s brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function. Research is ongoing to better understand how, and at what stage of the disease, the various forms of beta-amyloid influence Alzheimer’s.
Neurofibrillary tangles are misfolded “tau” proteins that collect inside neurons. Healthy neurons have support systems called microtubules, which help guide nutrients and molecules from the cell body to outer parts of the neuron, such as the axon and dendrites. In healthy neurons, tau normally binds to and stabilizes microtubules. In Alzheimer’s disease, abnormal chemical changes cause tau to detach from microtubules and stick to other tau molecules, forming tangles inside neurons. These tangles block the microtubules from transporting molecules along the neuron, which harms the communication between neurons.