When amyloid precursor proteins are broken down in the brain, they become beta-amyloid proteins. These proteins come in various forms that collect between neurons. One of these protein forms, beta-amyloid 42, is considered more damaging than others. For people with Alzheimer’s, excess amounts of this protein gather in the brain forming plaques and disconnecting the communication between and function of cells (National Institute on Aging, 2017). Researchers that focus on Alzheimer’s are still unclear of how these plaque formations specifically affect various stages of Alzheimers.
Another process that occurs in the Alzheimer’s brain is the entanglement of ‘tau’ proteins that are abnormally shaped in comparison to the healthy brain. The entanglement of tau proteins creates a blockage of the transport system inside neurons. This blockage restricts the neuron’s ability to synaptically communicate.
Figure 8. Neuron comparison. Adapted from "Alzheimer's diease," by Alzheimer's Clinics, 2021.
Alzheimer’s brains also typically exhibit chronic inflammation. One theory behind this inflammation is the failure of microglial cells to consume and dispose of various types of brain build up, including the build-up of beta-amyloid protein plaques. As mentioned above, these protein plaques cause significant disruption and death to neurons. Inflammation can also be worsened by the common occurrence of vascular comorbidities that results in the deterioration of the blood-brain barrier. The blood-brain barrier prevents the entry of toxicities into the brain while permitting the entry of essential glucose. Between a defective blood-brain barrier and the failure of microglial cells, the brain is unable to reduce and prevent the amount of detrimental toxins allowed to neurologically accumulate.