In Alzheimer's patients, the protein tau gets out of control. Deposits form in the nerve cells, blocking the exchange of information and gradually spreading to all regions of the brain.
The network of nerve cells in the brain can be imagined like a highway network; it ensures the rapid flow of information. In this picture, the microtubules of the nerve cells are the roadways: The tube-like components enable the cellular exchange of molecules and thus of information. They are stabilized by tau proteins. In Alzheimer's patients, however, the regulation of tau becomes unbalanced. The tau proteins detach from the microtubules and form fibrous structures, which eventually blocks transport within the nerve cells*. The exchange of information comes to a standstill - and gradually the affected nerve cells die.
When the physician Alois Alzheimer first described the dementia that would later be named after him at the beginning of the 20th century, he found that deposits of neurofibrils had formed in his patient's brain. These are bundles of fibers, insolubly clumped together - the very bundles that the protein tau forms when it is misdirected. It was later shown that the amount of tau deposits was related to the clinical symptoms of Alzheimer's disease: The more deposits, the greater the loss of neurons and the more pronounced the cognitive and memory problems*. And: step by step, the tau pathology affects more and more areas of the brain. The altered tau apparently has the ability to influence even those neighboring tau proteins that are actually inconspicuous. In the meantime, research has been able to demonstrate that the tau aggregates actually spread throughout the brain in a kind of chain reaction in which new aggregates are constantly being formed*.
The first tau deposits form in the brain areas responsible for memory and spatial memory*. It is apparently related to this that forgetfulness and disorientation are also the first symptoms that Alzheimer's patients usually complain about. From these brain areas, tau pathology then progressively encompasses broader areas.
Tau is often mentioned in connection with another protein, amyloid-beta. Amyloid is also found in all humans; in Alzheimer's patients, it forms clumps that are deposited in the brain. The difference with tau is that amyloid is deposited in the spaces between cells, whereas tau fibrils are found inside neurons. How exactly the two proteins interact, how (and whether) they affect each other - that is the subject of research. For a long time, there were two conflicting theories in science - the amyloid hypothesis and the tau hypothesis. The proponents each considered one of these proteins to be the trigger of Alzheimer's dementia. In the meantime, however, the opposition between the hypotheses has been largely resolved; it has been shown that both pathologies develop in parallel and that they are both, in interaction with other mechanisms, a part in the highly complex machinery of the disease.