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Text | Haimer
On the way to fight Alzheimer's disease (AD), the steps of the scientists are slightly heavy and slow
.
After 18 years of waiting, Bojian/Eisai’s Aduhelm was approved in the controversy, but ultimately failed to satisfy the scientific community
On July 14, the joint team of Rudolph Tanzi and Filip Swirski of Massachusetts General Hospital (MGH) of Harvard Medical School published the latest research results on AD in the top international journal Nature, which is expected to bring new treatment opportunities for neurological diseases
.
Source: Nature
Is Aβ the optimal solution for AD?
Is Aβ the optimal solution for AD?Since Dr.
Alzheimer recorded the first AD patient in 1901, researchers have not been able to reveal the exact pathogenesis of this type of disease
.
At present, a large number of drug developments are based on findings such as the deposition of beta amyloid (Aβ) in the brain of patients and the hyperphosphorylation of tau protein leading to neurofibrillary tangles
Source: NetxPharma
Aβ and neurofibrillary tangles in the brain of AD patients can cause nerve cell death, which is the root cause of cognitive decline
.
Nerve cell death will further activate neuroinflammation
Professor Rudolph Tanzi, the co-corresponding author of this new study, once made a vivid metaphor: Aβ is like a match, which can cause small local fires such as neurofibrillary tangles.
If it is not extinguished in time, it will cause raging forest fires (neuritis).
, Which ultimately leads to the decline of the patient’s cognitive function
.
Professor Tanzi mentioned that nerve cell death caused by neuroinflammation is at least 10 times higher than that caused by Aβ and neurofibrillary tangles
.
In other words, if there is no neuroinflammation, it is not enough to cause cognitive decline, which is what we usually call dementia symptoms
Discovery of "Fire Fighting" Molecules
Discovery of "Fire Fighting" MoleculesIn recent years, with the discovery of the expression of trigger receptor 2 (TREM2) by myeloid cells, microglia have become popular in the field of the central nervous system
.
In 2017, Nature Medicine published an article saying that microglia became the "Central Player" in the field of brain diseases
Microglia are immune cells in the brain and are the faithful stewards of the brain
.
When inflammation, infection or neurological disease occurs in the brain, microglia are quickly activated and gain phagocytosis
Morphological changes of microglia in different states (Source: Nature Reviews Neurology)
Under normal physiological conditions, microglia and astrocytes can remove debris from the brain and maintain the healthy operation of neurons
.
In the brains of AD patients, microglia are activated to produce inflammatory molecules and gather around plaques
Source: Nature
In this new study, Professor Tanzi and his collaborators discovered that when neuroinflammation occurs in the brain, astrocytes release the cytokine interleukin-3 (IL-3) to "extinguish the fire
.
" IL-3 can not only curb the neuroinflammation triggered by the death of nerve cells, it is also a signal molecule that cooperates with the functions of astrocytes and microglia.
IL-3 can reduce the accumulation of Aβ and slow down cognitive decline (Source: Nature)
It is worth noting that when the scientists injected IL-3 into the brains of AD mice, the accumulation of Aβ decreased and the number of microglia gathered around the plaques increased
.
At the same time, after 4 weeks of continuous treatment, the short-term memory of the mice improved
.
The IL-3 signaling pathway is related to the pathological process of AD (Source: Nature)
summary
summaryFacing the "hard bone" of central nervous system disease, every small step is undoubtedly progress and hope
.
The discovery of the role of IL-3 signaling molecules in the brain has brought new ideas for the development of AD drugs and is a key discovery with therapeutic significance
.
Reference materials:
[1] Cameron S.
McAlpine et al.
Astrocytic interleukin-3 programs microglia and limits Alzheimer's disease.
Nature(2021).
[2] A protective signal between the brain's supporting cells in Alzheimer's disease.
(Source: Nature)
