Interleukin 3: The most promising drug to treat Alzheimer’s disease
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Interleukin 3: The most promising drug to treat Alzheimer’s disease
Interleukin 3: The most promising drug to treat Alzheimer’s disease
In 1901, German doctor Alois Alzheimer admitted to a 51-year-old woman. She suffers from severe memory impairment, difficulty speaking and understanding other people’s words, and has no idea of time and place.
Dr. Alzheimer realized that this was a previously unknown disease. After the patient’s death, Dr. Alzheimer performed an autopsy and was surprised to find that there were many amyloid plaques and neurofibrillary tangles in the patient’s brain.
This is Alzheimer’s disease (AD), commonly known as Alzheimer’s disease.
The two most important pathological features of AD: amyloid plaques formed by the deposition of misfolded β-amyloid (Aβ) in the brain and neurofibrillary tangles caused by the hyperphosphorylation of Tau protein.
A century later, scientists finally confirmed the high-definition structure of these two AD biomarkers.
On July 5 this year, researchers from the MRC Laboratory of Molecular Biology revealed the high-resolution protein structure of Tau protein through cryo-electron microscopy (cryo-EM) on Nature.
Two months later, a group of researchers in Germany and the Netherlands also used cryo-electron microscopy to determine the high-definition structure of another AD-related protein, Aβ. This discovery once again brings new hope for the development of AD drugs.
Recently, “Nature” published a blockbuster study by a research team led by Filip K. Swirski and Rudolph E. Tanzi of Massachusetts General Hospital and Harvard Medical School: Proving the possibility of using IL-3 to treat AD.
They found that during the onset of AD, astrocytes and microglia interact with interleukin 3 (IL-3) and its receptors to achieve the immune response of phagocytosis and clearance of beta amyloid. More importantly, after they injected exogenous IL-3 into AD mouse models, they could reduce the content of β-amyloid plaques in the brain tissues of the mice and improve the memory of the mice.
This study revealed a new pathophysiological mechanism of AD and also proved the possibility of using IL-3 to treat AD.
(source:internet, reference only)
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