After making the arrangements for the movie, Chen Chen went to the "Alzheimer's Disease Reversal Treatment" project team and asked for all the current research results of the project team as well as a few lab rats.
The "Alzheimer's Disease Reversal Treatment" project team did exist. The leader was another neurology professor invited by Chen Chen, Evans. He had participated in several clinical trials of Alzheimer's disease and this project could be considered as his expertise.
However, Chen Chen did not plan to conduct the experiment with Evans because Chen Chen needed NZT-48 for his own experiments.
Before his power completely transcended the mortal realm, Chen Chen would not allow anyone else to know about NZT-48.
Therefore, Chen Chen could only conduct the experiment alone.
As for the lab rats he asked for from the project team, they were genetically modified mice that carried a mutated form of human tau. These mice would begin to develop tau tangles in their brains at the age of six months and show signs of nervous system damage at the age of nine months.
These were the genetically modified mice that were similar to the Alzheimer's disease model created by humans.
Chen Chen reopened a laboratory on the fifth floor. After moving these materials in, he began to look through the research results of Professor Evans during this period.
The foreign academic community had always followed the tradition of naming the discovery after the person who made the discovery. More than a hundred years ago, a doctor named Alzheimer dissected the brain of a patient who died of dementia and discovered a shocking phenomenon.
Not only was the deceased's brain severely shrunk, but even the cerebral cortex, which was responsible for memory, thinking, and language functions, was completely destroyed. In its place were necrotic brain cells and abnormal and bizarre brain deposits...
From this day onward, mankind officially crossed swords with the disease of the century, Alzheimer's disease.
However, due to the hidden nature of Alzheimer's disease, people did not pay much attention to this disease at first. It was only in the recent twenty to thirty years when human lifespan increased and Alzheimer's patients increased, that the medical community began to pay attention to it.
However, as mankind continued to conduct deeper investigations, they found that Alzheimer's disease was far more terrifying than they had imagined...
According to the statistics of the Earth Federation Pharmaceutical Research and Development Association, from 1998 to 2017, top pharmaceutical groups including Bayer, Eli Lilly, GlaxoSmithKline, Merck, and Pfizer had invested more than 600 billion U.S. dollars in testing Alzheimer's drugs that had failed 146 times.
Including 2018 and 2019, in the past 20 years, the world's top scientists had failed 154 times in the face of Alzheimer's disease.
The most shocking news was that in January 2018, the world's largest pharmaceutical company, Pfizer, announced that it would suspend research and development of Alzheimer's and Parkinson's drugs due to a lack of technical capabilities …
In the face of this disease of the century, the world's top medical forces were at their wits' end.
Chen Chen's expression was calm as he ran his fingers through the stacks of documents. These paper documents were held in folders and each one was five centimeters thick. At this time, they were piled up like a small hill in front of Chen Chen.
However, as Chen Chen flipped through one book after another, in just a few hours, the pile of materials around him had decreased by half. This meant that the pile of materials that he had finished reading was getting taller and thicker.
If someone were to observe closely at this time, they would find that the more information Chen Chen read, the brighter his eyes became. In the end, it was as if they could shine in the dark!
After going through the latest experimental data, Chen Chen finally let out a sigh of relief. He turned on the computer again and compared it with the cutting-edge results on the Internet.
After reading these, Chen Chen closed the webpage thoughtfully.
Very good, he had a direction.
The corner of Chen Chen's lips curled into a smile. He took out a piece of chocolate the size of a finger, peeled off the tin foil, and stuffed it into his mouth.
NZT-48 allowed the brain to operate at high speed, but at the same time, it consumed a large amount of fat, carbohydrates, and protein. Chocolate could replenish these substances. At the same time, theobromine could also enhance the nervous system and help increase blood oxygen capacity.
Therefore, Chen Chen had recently developed the habit of eating a few pieces of chocolate after taking the medicine.
As the chocolate slowly melted in his mouth, Chen Chen began his own experiment.
First, he put on a sterile suit and disinfected his entire body. After that, he put on disposable rubber gloves in the laboratory. He took out an NZT-48 pill and slowly dissolved it in glucose.
At the same time, Chen Chen took out several mice with the most obvious signs of nervous system damage. He divided them into groups and filled them with an equal proportion of NZT-48 solution, then placed them into observation cages.
This was only one of the experiments.
In addition to experimenting with the effect of NZT-48 on Alzheimer's disease, Chen Chen was also conducting another experiment at the same time. However, this was different from the current experimental direction on the market. Chen Chen planned to research on inflammation.
After all, the current scientific and technological consensus was that the cause of Alzheimer's disease was "amyloid beta deposition" and "abnormal phosphorylation of tau protein". Therefore, scientists proposed the hypothesis of the etiology of Alzheimer's disease – the amyloid beta theory.
Currently, most clinical trials targeted amyloid beta in an attempt to break down or prevent the formation of amyloid beta deposition.
However, as mentioned before, all treatment experiments targeting amyloid beta around the world had failed.
Therefore, Chen Chen decided to start with the inflammation hypothesis and the brain's immune cells.
There were several hypotheses about Alzheimer's disease, one of which was the inflammation hypothesis. In 2018, a study published in the journal Neuroscience found the presence of herpes virus in the brains of Alzheimer's patients.
Subsequently, in 2019, a team published a paper in the sub-journal Science. They found Porphyromonas gingivalis in the brains of patients. Through experiments on mice, they allowed the bacteria to invade the brains of mice. After the mice died, they found dead neurons in the brains of the mice and at the same time, the level of amyloid beta increased.
At the end of 2019, in the journal PNAS, a team found that in the brains of patients, there was a sharp decrease in a protein called TOM1. TOM1 was a crucial substance in a class of inflammatory responses.
After the expression of TOM1 decreased, the beta-amyloid protein in the brains of the mice significantly increased, and at the same time, these mice also showed cognitive decline. By increasing TOM1 in the opposite direction, the mice's cognitive ability was restored.
This was the latest research result of the inflammation hypothesis. Even Professor Evans was working in this direction.
In addition to the direction of the inflammation hypothesis, Chen Chen also added the immune cell deficiency hypothesis.
This was because one of the characteristics of Alzheimer's disease was the formation of "beta deposits" and "tau tangles" in the brain. A type of immune cell known as microglia protected the brain by removing these deposits and tangles.
They surrounded these harmful substances and engulfed the deposits and tangles piece by piece.
However, the latest research found that although microglia limited the accumulation of harmful substances, it could be a double-edged sword.
This was because microglia could secrete a substance called APOE. This substance would enhance the formation of beta deposits. At the same time, in the later stages of the disease, once tau tangles formed, microglia could attack the tangles and damage nearby neurons, leading to neurodegeneration.
The research found that if there were no microglia or if the microglia were not activated, tau tangles and beta deposits would not accumulate and develop to the late stage. The nervous system would not be damaged either...
This was the direction of Chen Chen's research. With this direction, even if Chen Chen still could not cure Alzheimer's disease, at least he was confident that he could limit the deterioration of the disease and lock this disease of the century in the early stages!
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