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In addition to neurons, there is another type of cell: glial cells. There are three main types of glial cells in the brain: astrocytes that provide support for mutual communication between neurons, oligodendrocytes that surround an axon to form an insulating myelin sheath structure, and microglial cells. Microglia are specialized macrophages, which are immune cells in the brain, phagocytosis in the central nervous system, clearance of pathogens or damaged neurons.

In the 1980s, researchers found at autopsy that the amyloid plaques in the brain of patients with Alzheimer’s disease were usually surrounded by microglia. At that time, people did not know what this phenomenon meant. In 2001, with the development of neuroimaging, we could finally see the activation state of microglia in the living brain: If the activation state of microglia in healthy human brains is only stars, Alzheimer’s disease Inside the patient’s brain is a lit Christmas tree in the dark.

In fact, this may be the normal process of immune cells clearing the amyloid protein: perhaps we can use the power of microglia to clear the amyloid protein. But the next discovery made our hopes shatter. In vitro experiments found that if the activation state of microglia is not controlled, then microglia will not only produce no protective effect on neurons, but will directly kill neurons.

Perhaps the accumulation of abnormal amylin and Tau protein can trigger the activation of the immune system, mobilize immune cells to cause inflammation in the brain, and excessively activated microglia can become extremely dangerous and begin to kill neurons, leading to nerves. The irreversible mass death of Yuan.

However, reducing the immune response will not be beneficial to patients? Approximately 20 epidemiological studies in the last century have found that long-term use of COX1 inhibitors (indolent anti-inflammatory drugs, such as indomethacin and ibuprofen) can reduce the risk of Alzheimer’s disease.

From the mechanism of action, if non-steroidal anti-inflammatory drugs can really reduce the risk of disease, the more likely mechanism of action is to reduce the inflammatory state of the brain, rather than inhibit the formation of plaque or nerve fiber tangles. Since then, a number of clinical trials have been conducted to study the effects of non-steroidal anti-inflammatory drugs. But so far there is no evidence to support the feasibility of using non-steroidal anti-inflammatory drugs for the treatment of Alzheimer’s disease.

Neither is it easy to reduce the level of inflammation in the brain or directly target microglia. The physiological state of microglia and the physiological processes involved are much more complicated than we thought. Even if we can successfully induce the transformation of microglia activation state, the safety is difficult to guarantee. Even if the function of microglia is really able to stop the disease process, finding a safe and effective microglia is not easy.

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