Chapter 120: Found an Approach

After laying the groundwork for the film, Chen Chen went to the team in charge of the “Alzheimer’s Disease Reversal Treatment” to receive the latest research report and also to get several mice.

The “Alzheimer’s Disease Reversal Treatment” project was a real thing. It was led by Evans, another neurology professor invited by Chen Chen. He had participated in countless clinical trials of Alzheimer’s disease in the past. This was a subject he was all too familiar with.

However, Chen Chen did not plan to work in collaboration with Evans since Chen Chen needed the NZT-48 for the experiment.

Unless he had reached the absolute extent of his capabilities, Chen Chen was not going to let any outsider find out about NZT-48.

On that account, Chen Chen could only conduct the experiments by himself.

As for the mice he needed from the research team, they were a batch of genetically modified mice carrying a mutant form of human tau. These mice began to develop tau tangles in the brain at 6 months old and began showing signs of nervous system damage at 9 months old.

These were the genetically modified mice that humans had created as an Alzheimer’s disease symptom model.

Chen Chen reopened a laboratory on the fifth floor. After bringing in the relevant information, he began to look through the research results of Professor Evans throughout this period.

The foreign academic circles had always upheld the tradition of the naming convention based on the person who had made the discovery. More than a hundred years ago, a man named Alzheimer was the one who dissected the brain of a deceased man who suffered from dementia and discovered the shocking phenomenon.

Not only did the brain of the deceased had gone through severe atrophy, even the cerebral cortex which governed memory, thought, and speech functionalities was destroyed. What took its place was necrotic brain cells and strange, abnormal brain deposits...

From that fateful day onward, humanity began mounting its effort against Alzheimer’s, a disease persisting across the century.

Due to the concealed nature of Alzheimer’s disease, humans never really took the disease seriously. It was not until recent decades when the average life expectancy went up which led to more and more people suffering from Alzheimer’s which caused the academic world to begin addressing the issue.

As humanity began to devote its efforts to further inspecting the disease, they began to realize that Alzheimer’s was far more threatening than they initially thought...

According to the findings of the Earth Federation Laboratory Research and Development Association, top pharmaceutical groups the likes of Bayer, Eli Lilly, GlaxoSmithKline, Merck, and Pfizer had invested more than US$600 billion from 1988 to 2017. A total of 146 Alzheimer’s drugs failed.

Including 2018 and 2019, top scientists all over the world had failed to come up with a solution against Alzheimer’s more than 154 times over the last two decades.

One of the most shocking events was in January 2018 when the pharmaceutical company Pfizer issued a statement: Due to the technical challenges, the research and development of Alzheimer’s and Parkinson’s drugs will be suspended...

The world’s pioneering medical factions were rendered completely useless before the disease of the century.

Chen Chen kept a calm expression as his fingers glided across stacks of folders containing data charts. Each one of these folders was five centimeters thick, piling themselves into the size of a miniature mountain.

As Chen Chen scanned through them one after the other, the pile was cut in half within a few hours. As time went on, the stack of folders that he had already gone through began piling up higher and higher.

If someone was there to witness it, they may notice that as Chen Chen went through the folders, the spark in his eyes grew ever brighter to a point where it could illuminate the darkness by itself!

Chen Chen finally heaved a breath after finishing the latest experimental data. He booted up the computer again to compare his findings with the latest extracted data on the Internet.

After completing this final process, Chen Chen thoughtfully closed the webpages.

Excellent, the approach had been determined.

The corner of Chen Chen’s lips crooked up with a hint of a smile. Then, he took out a finger-sized piece of chocolate, peeled off the tin foil, and tossed it into his mouth.

NZT-48 enabled the brain to function at accelerated efficiency, but it also greatly exhausted substances such as fat, carbohydrate, and protein. Chocolate was able to make up for these substances as its theobromine was also able to provide a boost for the nervous system and help increase blood oxygen capacity.

On that account, Chen Chen had begun to develop a habit of eating several chocolates after taking the drug.

As the chocolate slowly melted in Chen Chen’s mouth, he began to conduct his experiment as well.

He first put on sterile clothes and went through a full disinfection process. Then, he entered the laboratory and put on a disposable glove. After that, he took an NZT-48 and dissolved it in glucose.

At the same time, Chen Chen selected several mice which displayed the most evident signs of nervous system damage. He grouped them accordingly and poured a fitting amount of NZT-48 solution for each of them before settling them in separate observation cages.

This was only one of the experiments.

While researching the NZT-48’s effects on Alzheimer’s disease, Chen Chen was conducting a separate experiment simultaneously. Unlike the conventional experimental method used, Chen Chen intended to research it from an inflammatory angle.

In the current day and age, the general scientific consensus was that the cause of Alzheimer’s disease was “β amyloid deposition” and “abnormal phosphorylation of tau protein”. As a result, scientists raised a hypothesis of the etiology of Alzheimer’s disease – Amyloid β-Protein Theory.

Presently, most clinical trials had assumed Amyloid β-Protein as the target subject and attempted to break down or prevent the formation of Amyloid β-Protein.

As mentioned before, all of the experimental treatment which based Amyloid β-Protein as the target element had resulted in failures.

This was why Chen Chen had decided to take an approach revolving around inflammatory theory and brain immunity cells.

There were several established hypotheses around Alzheimer’s disease, with one being the inflammatory theory. In 2018, Nerve magazine published a research article concerning the discovery of herpes virus in the brain of an Alzheimer’s patient.

In the following year in 2019, another team published a thesis in Science detailing their discovery of Porphyromonas Gingivalis in a patient’s brain. They then experimented on mice and injected these viruses into their brains. After the mice were deceased, they discovered dead neurons in the mice’s brains and also noted an increase in Amyloid β-Protein level.

Nearing the end of 2019 in the journal PNAS, a team noticed a sharp decrease of a protein known as TOM1 in the brain of Alzheimer’s patients. TOM1 was a vital element in a form of inflammatory response.

Following the decrease of TOM1 readings, the mice’s brains displayed an increase in Amyloid β-Protein. These mice also subsequently experienced cognitive decline. The cognitive abilities of the mice were able to be restored by reversely increasing the concentration of TOM1.

This was the latest findings of the inflammatory theory. Even Professor Evans himself took a similar approach in his experiments.

In addition to the inflammatory approach, Chen Chen further supplemented the immune cell deficiency theory.

One of the unique traits of Alzheimer’s disease was the formation of “β deposit” and “Tau tangle” in the brain. A class of immune cells known as microglia was able to protect the brain by eliminating these deposits and tangles.

However, the latest findings revealed that despite microglia’s potency in limiting the accumulation of harmful substances, it was a double-edged sword.

This was because microglia were able to secrete a substance known as ApoE. This substance was able to enhance the formation of β deposits. Also, in the later stages of the disease, once the tau tangle was formed, microglia may harm nearby neurons while eliminating the tangles which may lead to neurodegenerative diseases.

Research showed that if microglia was not involved in the process or simply was not simulated, the tau tangle and β deposit would not be accumulated into the later stages of the disease. Similarly, the nervous system would not be harmed as well...

This was Chen Chen’s research approach. With these approaches, even if Chen Chen was not able to wholly cure Alzheimer’s disease, he was confident he was at least able to limit the severity of the disease, in turn locking the disease of the century in the early stages of its formation!