I Have A Super USB Drive

Chapter 120: Find direction

   Layout of the filming plan, Chen Chen came to the "Alzheimer's disease reversal treatment" project team, and asked for all the current research results of the project team, and a few white mice.

The "Alzheimer's disease reversal treatment" project team does exist. The leader is another neurology professor Evans invited by Chen Chen. He has participated in several clinical trials of Alzheimer's disease. This project also Be regarded as his old line.

   But Chen Chen does not plan to experiment with Evans, because Chen Chen needs to use NZT-48 for experiments.

   Chen Chen will not tolerate NZT-48 being known to any outsider until his power has completely surpassed the ordinary.

   Therefore, Chen Chen can only conduct experiments alone.

As for the mice required by the project team, they are genetically modified mice carrying human tau mutations. These mice will begin to develop tau tangles in the brain when they are 6 months old. It showed signs of nervous system damage at month.

   This is a genetically modified mouse that is similar to the Alzheimer's symptom model created by humans.

   Chen Chen reopened a laboratory on the 5th floor. After moving all these materials in, he began to watch Professor Evans’ research results one by one during this period.

Foreign academic circles have always followed the tradition of who discovered and named after. More than 100 years ago, a doctor named Alzheimer dissected the brain of a patient who died of Alzheimer’s and found shocking phenomenon.

   The deceased’s brain was not only severely atrophied, but even the cerebral cortex, which controls memory, thinking, and language, was completely scrapped, replaced by necrotic brain cells and abnormal and strange brain deposits...

  From this day, human beings formally crossfire with Alzheimer’s disease, a disease of the century.

However, because of the hidden nature of Alzheimer’s disease, people did not pay much attention to this disease at the beginning. It was not until the last two to thirty years that human life expectancy was getting longer and more and more patients with Alzheimer’s disease. The medical community has taken it seriously.

   However, as human beings have more and more in-depth investigation, it is found that Alzheimer's disease is far more terrifying than human imagination...

According to statistics from the Earth United Laboratories Research and Development Association, from 1998 to 2017, top pharmaceutical groups including Bayer, Eli Lilly, GlaxoSmithKline, Merck, and Pfizer invested more than US$600 billion to test Alzheimer’s disease that failed. A total of 146 times of medication.

   Including 2018 and 2019, the world’s top scientists have failed 154 times in the face of Alzheimer’s disease in the past 20 years.

  The most shocking thing is that in January 2018, Pfizer, the world's largest pharmaceutical company, issued a statement: Due to insufficient technical capabilities, it will suspend the development of Alzheimer's and Parkinson's drugs...

  In the face of this century's disease, the world's top medical forces are unable to do anything.

   Chen Chen looked calm, and ran his fingers across the stacks of materials. These paper materials were all held in folders, and each of them was five centimeters thick. At this time, they were piled as high as a hill in front of Chen Chen.

   However, as Chen Chen turned over the pages one by one, within a few hours, the data next to him was reduced by half, and the pile of data representing the reading became higher and thicker.

   If someone gets closer and observes at this time, they will find that the more information they flip through, the brighter Chen Chen's eyes become, and it seems that they can flash in the dark in the end!

   Until after reading the latest experimental materials, Chen Chen finally took a breath, turned on the computer again, and compared it with the most cutting-edge results on the Internet.

   After reading these, Chen Chen thoughtfully closed the web page.

   Very good, the direction is already there.

   Chen Chen raised a smile at the corner of his mouth, then took out a finger-sized piece of chocolate, peeled off the tin foil, and stuffed it into his mouth.

  NZT-48 can make the brain run at high speed, but it also consumes a lot of fat, carbohydrates, and protein. Chocolate can make up for these substances. At the same time, theobromine can also increase the nervous system and help increase blood oxygen.

   Therefore, Chen Chen has recently developed the habit of eating a few pieces of chocolate after taking medicine.

   As the chocolate slowly melted in his mouth, Chen Chen also began his own experiments.

  He first put on sterile clothes and disinfected his whole body. Then he put on disposable rubber gloves in the laboratory, took out a NZT-48, and slowly dissolved it in glucose.

   At the same time, Chen Chen took out the mice with the most obvious signs of nervous system damage, and poured them into equal proportions of NZT-48 solution according to the grouping method, and then put them into each observation cage.

   This is just one of the experiments.

   In addition to experimenting with the efficacy of NZT-48 on Alzheimer’s disease, Chen Chen is also conducting another experiment at the same time. However, unlike the experimental directions on the market today, Chen Chen intends to start research on inflammation.

You know, nowadays, science and technology generally believe that the cause of Alzheimer’s disease is "beta amyloid deposition" and "abnormal phosphorylation of Tau protein", and thus scientists put forward the hypothesis of the cause of Alzheimer's disease-amyloid beta theory.

   Most of the current clinical trials are targeting β amyloid, trying to break down or prevent the formation of β amyloid deposits.

   But as I said before, all global treatment experiments targeting amyloid beta have failed.

   So Chen Chen decided to start with the inflammation hypothesis and brain immune cells.

   There are several hypotheses about Alzheimer's disease. Among them is this inflammation hypothesis. A study in the journal Neurology in 2018 found that the herpes virus is present in the brains of Alzheimer's disease patients.

Then in 2019, a team published a paper in a sub-Journal of "Science". They found Porphyromonas gingivalis in the brains of patients, and through mouse experiments, the bacteria invaded the brains of mice. After the mice died , They found dead neurons in the brains of mice, and β amyloid levels also increased.

At the end of 19 years, in the journal PNAS, a team found that a protein called TOM1 in the brain of the patient had a sharp decrease, and TOM1 is a vital substance in a type of inflammatory response~www.mtlnovel. com~ After the expression of TOM1 decreased, the β-amyloid protein in the brain of mice increased significantly. At the same time, these mice also experienced cognitive decline. By increasing TOM1 in the opposite direction, the cognitive ability of mice was again Has been restored.

   This is the recent research result of the inflammation hypothesis, and even Professor Evans is studying in this direction.

   In addition to the direction of the inflammation hypothesis, Chen Chen also added the immune cell deficiency hypothesis.

   Because a characteristic of Alzheimer's disease is the formation of "beta deposits" and "Tau tangles" in the brain, and a type of immune cell called microglia can protect the brain by removing these deposits and tangles.

   They surround these harmful substances, engulfing deposits and entanglements piece by piece.

   However, the latest research has found that although microglia limit the accumulation of harmful substances, it may be a double-edged sword.

Because microglia can secrete a substance called ApoE, which in turn enhances the formation of beta deposits. At the same time, in the later stages of the disease, once tau tangles are formed, microglia attacks the tangles and may damage nearby Neurons, leading to neurodegeneration.

  Research found that if there are no microglia or microglia are not activated, tau tangles and β deposition will not accumulate and develop to the late stage, and the nervous system will not be damaged...

   This is the research direction of Chen Chen. With these directions, even if Chen Chen still cannot cure Alzheimer's disease, he is at least sure to limit the deterioration of the disease and lock this century's disease in the early stage!