The medical black technology system of the top student

As we all know, many cells in the human body have extremely strong regenerative capabilities, such as epidermal cells, red blood cells, etc.

New cells will replace dead cells and continue to repair damage to the human body.

Without the regenerative ability of these cells, a minor scratch or a simple bleed could put a person in crisis.

New cells will replace dead cells and continuously repair damage to the human body, so that people can survive for a long time.

But not all cells in the human body, like epidermal cells and red blood cells, have such strong regenerative capabilities.

Some cells in the human body are permanent cells.

The so-called permanent cells are cells that become permanently missing when damaged.

Such cells are unable to divide and the number of cells is fixed from the moment of birth.

These cells have been functioning since a person was born, and they will not stop until the day the person dies.

Among these permanent cells are nerve cells.

This is why once the human brain is damaged, it cannot be reversed, because once nerve cells are damaged, their most basic physiological functions are lost.

Then there is no other cell that can replace it, and no technology can solve it.

Unlike cardiomyocytes, if it doesn't work, you can install an artificial heart, which will take a year or two.

After nerve cells are damaged, you can't replace the brain, right?

Alzheimer's disease is a neurodegenerative disease.

The so-called neurodegeneration means that nerve cells are slowly being damaged.

Damaged nerve cells cannot regenerate.

Therefore, as more and more nerve cells lose function over time, the entire nervous system becomes dysfunctional.

Lu Liang had to admit that even today, Alzheimer's disease still cannot be completely cured.

Lu Liang nodded and admitted, which undoubtedly extinguished the last trace of luck in Wang Wentao's heart.

Wang Wentao on the side smiled bitterly: "Senior brother, is there nothing you can do?"

Lu Liang replied: "Unless there is technology that can regenerate nerve cells, there is no way to completely cure it."

Of course, if the world can really invent technology that can regenerate permanent cells like nerve cells.

Then the entire human world is not far away from true eternal life.

Wang Wentao pursed his lips and said: "I understand, senior brother, I will adjust my condition as soon as possible and will not delay the test because of this matter."

With that said, Wang Wentao stood up and prepared to leave.

However, Wang Wentao had only taken two steps when Lu Liang's voice caught up from behind Wang Wentao: "Don't worry, I haven't finished speaking yet."

Hearing Lu Liang's voice, Wang Wentao turned around in confusion. He looked at Lu Liang and asked, "Senior brother, is there anything else?"

Lu Liang shrugged and asked, "Don't you want to solve the problem of your grandma's Alzheimer's disease?"

Wang Wentao was even more puzzled. How could he not want to solve the problem of his grandmother's Alzheimer's disease? Who would be willing to go home one day and see that the relative who loved him most did not recognize him.

"But didn't Senior Brother also say that Alzheimer's disease cannot be cured?" Wang Wentao asked feebly.

"But Alzheimer's disease can be alleviated." Lu Liang looked at Wang Wentao and said.

Wang Wentao pursed his lips: "Relieve for three to five years, and then inevitably forget everything in the end?"

Lu Liang scratched his head: "Wen Tao, I can see that you have a great prejudice against the word "relief".

"Remission does not necessarily mean delaying the disease, preventing the disease from getting worse, or improving the symptoms of Alzheimer's disease. This is also remission, do you understand what I mean!"

Wang Wentao's breathing stagnated, and he understood Lu Liang's meaning almost instantly.

"Brother, is there really a way?" Wang Wentao's tone suddenly became urgent.

Wang Wentao has already checked that the current drugs that can alleviate Alzheimer's disease can only slightly delay the progression of Alzheimer's disease, but cannot completely prevent the progression of Alzheimer's disease.

If there is a drug that can completely prevent the progression of Alzheimer's disease, it could be a treatment.

Lu Liang put his hands in his pockets and shrugged: "Maybe."

"Senior brother, don't be afraid, just give me a guarantee. You are going to kill me."

After learning that there was a way to completely prevent the deterioration of his grandma's condition, Wang Wentao's haze disappeared at this moment, and he became extremely excited.

He hurriedly approached, hoping to get a more accurate answer.

"Oh, why are you so annoyed? The test is not finished yet. Let's wait until the test is finished."

"Okay, okay, do the test. You have to tell me after the test, senior brother."

"Stop talking nonsense and wash the bottle quickly."

Lu Liang still knew something about Alzheimer's disease. In fact, the main reason was that the word "Alzheimer's" was too common. Lu Liang saw it often, so he went to look up this aspect.

In fact, Alzheimer's disease has always existed, but some research at the time was not advanced enough.

In addition, most old people will suffer from symptoms such as poor memory and forgetfulness, so people don't pay much attention to it and just think that the old man is dying.

Therefore, after 1901, Alois Alzheimer, a doctor in Frankfurt, discovered that this was actually a disease, and the disease was named after the doctor.

In the general public's mind, Alzheimer's disease is a disease that only the elderly can get.

But it's not.

Alzheimer's disease is divided into two types, one is early-onset and the other is late-onset.

According to statistics from the World Health Organization, nearly 47.5 million people worldwide suffer from dementia, of which Alzheimer's disease accounts for 60% to 80%.

Alzheimer's disease that develops before the age of 65 is called early-onset Alzheimer's disease, which is mainly related to autosomal dominant inheritance. Patients will develop the disease when they are 40 to 50 years old, or even earlier.

In January, Xuanwu Hospital reported a case of Alzheimer's disease. The patient was only 19 years old when he developed the disease.

Suffering from Alzheimer's disease at the age of 19 sounds like a fantasy, but the reality is so outrageous.

Alzheimer's disease that develops after the age of 65 is called late-onset Alzheimer's disease.

The main factors causing the disease include hypertension, atherosclerosis, diabetes, smoking and metabolic syndrome, etc.

Lu Liang continued to search for the documents he had saved before. There was a folder on his computer dedicated to storing documents.

The documents he had read before were all classified and saved in folders by Lu Liang, so as to avoid the situation where he suddenly remembered a certain document that day and wanted to take a closer look, but couldn't find it.

Lu Liang quickly found the document he was looking for.

That was a review published in the journal Alzheimer's disease.

You can tell from the name of the journal "Alzheimer's disease".

This is a journal dedicated to Alzheimer's disease research.

It can be said that anyone who studies Alzheimer's disease cannot avoid this journal.

The review Lu Liang found was a review on late-onset Alzheimer's disease, and Lu Liang continued to browse the literature.

It has to be said that even today, Alzheimer's disease is still one of the most difficult diseases to treat in the world.

Some important issues related to basic research on Alzheimer's disease, such as the cause, pathogenesis, early diagnostic markers and treatment directions, are still in the exploratory stage and have not yet been finalized.

When it comes to the pathogenesis of Alzheimer's disease, it can be described as complicated.

Amyloid plaque formation, NFTs, neurotransmitter deficiencies, oxidative stress, inflammation, genetic mutations, excitotoxic neurotoxins, and more.

However, there are currently two medically recognized pathogenesis mechanisms of Alzheimer's disease.

One is the "beta-amyloid abnormal deposition hypothesis."

The other is the "Tau protein hypothesis."

The so-called "beta amyloid abnormal deposition hypothesis."

It is the abnormal processing of amyloid precursor protein by β-secretase and γ-secretase that results in the production of two monomers, Aβ40 and Aβ42.

These monomers further oligomerize and aggregate to form plaques.

And the culprit is these plaques.

These plaques block ion channels and disrupt calcium homeostasis, leading to increased mitochondrial oxidative stress and weakened energy metabolism.

Eventually, these plaques cause the neurons to deteriorate and eventually lead to nerve cell death.

And the "Tau protein hypothesis".

It refers to the hyperphosphorylation of Tau protein.

Tau protein is found in neurons and one of its main functions is to regulate the stability of axonal microtubules.

When Tau protein is hyperphosphorylated, it forms insoluble aggregates called neurofibrillary tangles, which can lead to neuronal loss of function.

Lu Liang rubbed his brow. He just felt a headache now.

The complexity of the nervous system really exceeded Lu Liang's imagination.

This thing is just as unpredictable as intestinal flora.

The key is that there are also studies showing that the cause of Alzheimer's disease is related to intestinal flora.

This is simply extremely difficult.

Lu Liang shook his head, and then he opened another document. This document came from "Nature Medicine", an important sub-journal of Nature.

This article is also a review.

The article summarizes the target mechanisms of Alzheimer's disease so far, and also makes a statistics on the research and development of Alzheimer's disease.

Over the years, a large number of pharmaceutical companies around the world have invested huge amounts of money in the research and development of Alzheimer's disease drugs.

The research and development of most pharmaceutical companies is almost carried out around the two generally recognized theories of "β-amyloid hypothesis" and "Tau protein hypothesis".

Most drug candidates target different forms of beta-amyloid in the hope of clearing plaques or abnormal accumulations of amyloid in tissues.

However, according to statistics, since the beginning of the 21st century, more than 320 clinical trials have failed.

There are some pharmaceutical giants among them.

Looking at this data, Lu Liang couldn't help but fall into deep thought.