An Alzheimer patient can be significantly recognized by detecting the presence of tangled tau protein in their brain. The tau protein is basically contained in nerve cells’ axons. When tau gets tangled, it becomes prone to microglia—immune brain cells—attacks. According to the recent experimental studies carried out on mice, during the attacks, the neurons are wrongly damaged in actual, which cause a severe damage—may also result in brain damage—leading to degenerative diseases.
The latest researches by Washington University, if microglia can be overpowered with proper medications, the risk of memory-robbing ailment onsets can be easily reduced or totally vanished. Though the research is claimed as too preliminary, Prof. David Holtzman— a neurologist and lead author—the experiment is worthy if microglia can be deactivated at the early stage of neurodegenration, with the help of specific drugs.
Microglia is found in spinal cord and brain and is one of the immune defense forms in central nervous system. Previously, the presence of microglia helped in delaying increasing rate of dementia as it attacks tau tangles, which plays a destructive role causing the dementia. However, tau protein presence is considered common in healthy people. Additionally, the protein contributes in making neurons function properly.
According to the research by Prof. Holtzman and team, the microglia attacks on tau with such aggressiveness that it ends up damaging neuron cells unintentionally. The team experimented on mice by modifying them with APOE4—An Alzheimer related protein—and some of them were fed PLX3397—a preventive compound—to deplete microglia. The ones with APOE4 and microglia were found with shrunken brains. On the contrary, the mice with APOE4 and PLX3397 showed healthy brains.
Although, PLX3397may have several side-effects on humans such as fatigue, diarrhea, vomiting, nausea and changes in hair color. The detailed study was published in Journal of Experimental Medicine.