LivingActivate immune cells for Alzheimer's progression

Activate immune cells for Alzheimer's progression

Among other things, Alzheimer’s disease is characterized by neurological damage that is believed to be caused by plaques of a “sticky” protein called beta-amyloid. This is normally found in the membrane that surrounds nerve cells, but when it clusters into small lumps or plaques between neurons, it can prevent them from communicating with each other and impair brain function.

For years, researchers have tried to understand exactly how the production of beta-amyloid triggers the symptoms of Alzheimer’s disease.

Now, a team of researchers led by Huaxi Xu – director of the Neuroscience Initiative at the Sanford Burnham Prebys Medical Research Institute in La Jolla, California (USA) offers a new potential strategy to eradicate excessive accumulation of this protein.

They studied the behavior of a trigger receptor (TREM2) found on a type of cell called microglia, or immune cells of the central nervous system, in two experiments with mice.

Researchers have known that mutations in TREM2 significantly increase the risk of Alzheimer’s , indicating a critical role for this particular receptor in protecting the brain,” Xu explains.

But what the new research reveals are “specific details about how TREM2 works.” Specifically, the first study shows that the amyloid beta protein binds to the receptor, initiating a chain reaction that can culminate in slowing the progression of Alzheimer’s.

Once bound to beta amyloid, the trigger receptor TREM2 “tells” immune cells to begin to break down and remove beta amyloid, “possibly delaying the pathogenesis of Alzheimer’s disease,” he continues. Xu.

Furthermore, the study showed that the removal of TREM2 in mice completely interfered with the electrical currents that normally activate microglia.

TREM2 can stop the progression of Alzheimer’s

The second study strengthened the findings of the first , showing that increasing TREM2 levels made the microglia more receptive and reduced the symptoms of Alzheimer’s disease.

More specifically, the researchers added TREM2 to mice that had been genetically engineered to develop an aggressive form of Alzheimer’s. Increased TREM2 signaling prevented the disease from progressing and even reversed some of the cognitive decline, the authors of the study published in the journal Neuron reported.

A new therapeutic path

“Following the microglia, rather than the generation of beta amyloid, may be a new avenue of research for Alzheimer’s disease. We could use immune cells in the brain to solve what is becoming a public health crisis,” says Xu. .

However, it also warns against potential risks , as it activates the microglia excessively or produces an overactivation, which can damage healthy synaptic junctions as a side effect.

Reference: TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function. Yingjun Zhao, Xilin Wu, Xiaoguang Li, Lu-Lin Jiang, Xun Gui, Yan Liu, Yu Sun, Bing Zhu, Juan C. Piña-Crespo, Muxian Zhang, Ningyan Zhang, Xiaochun Chen, Guojun Bu, Zhiqiang An, Timothy Y Huang, Huaxi Xu. Neuron 2018. DOI: https://doi.org/10.1016/j.neuron.2018.01.031

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