When inflammation occurs in combination with plaque and tangles, there is acceleration in the decline of cognition, and, eventually, other physical functions.
The human brain has a natural cleaning system that goes to work during periods of sleep. Glial cells, called microglia, scavenge through the brain and remove unwanted particles—including some proteins. In patients with Alzheimer’s disease, however, there is buildup of Abeta protein over time into plaque bundles.
The changing chemistry of the tau of some neurons results in what is called a tangle. Tangles trap some of the plaque bundles, and may also create blockages of normal neurotransmitters—signals in the brain that inform memory and other cognitive ability.
Finally, there is inflammation in the brain. When this occurs in combination with plaque and tangles, there is acceleration in the decline of cognition, and, eventually, other physical functions.
Genetic and environmental factors can trigger Abeta protein accumulation, tau tangle formation, and inflammation. It is thought that once one element of the pathology is in place, it may act as a trigger for the others. For example, Abeta accumulation can lead to increased inflammation, and vice versa. These vicious cycles continue over time, causing increasing damage and ultimately nerve cell death. When the damage becomes severe enough, the patient begins to experience loss in cognitive function: The first external symptom of the disease.