Name: 6 Reasons We Have to Say a Study Was "In Mice"
Uploaded: 2020-03-30T02:53:35.000Z
Duration: 9 min 39 s
Description: Thousands of YouTube videos with English-Chinese subtitles! Now you can learn to understand native speakers, expand your vocabulary, and improve your pronunciation...

and more suitable for experiments than actual human people.

We're sorry you had to find out this way.

And neither are rats, guinea pigs, rabbits,

or other animals used to study stuff that happens with humans.

Although mice are pretty much our favorite model organism for medical research,

and they don't always respond to drugs the same way we do.

Researchers can design mouse models that are really close to certain human diseases,

and use that to make incredible progress in medical research.

Here are six times the science only worked in rodents --

In the brain of an Alzheimer's patient, a protein known as beta-amyloid clumps together

These clumps form plaques that settle between neurons, disrupting cell function.

Unfortunately, scientists have had a hard time making mouse models for Alzheimer's.

In 1995, researchers thought they'd made a breakthrough.

There's a rare, inherited form of Alzheimer's disease in humans,

in which people develop symptoms as early as their forties.

The researchers genetically engineered a mouse model

to have a single gene variant associated with that form of the disease.

This mouse, and similar models that followed in the next decade,

accumulated plaques in ways that provided researchers with important insight into Alzheimer's.

A drug called Aducanumab showed promise in targeting the beta-amyloid protein plaques.

Some even called it a holy grail because of how well it targeted the plaques in mice.

Unfortunately, the drug failed to work in humans during clinical trials.

but one reason could be because beyond the cellular level, our brains are pretty different.

Changes in rodent brains don't necessarily affect their behavior

the same way comparable changes affect behavior in humans.

It's a similar case with multiple sclerosis, or MS,

it's thought that the immune system attacks

the protective myelin sheath surrounding nerve fibers.

This interferes with the communication signals

between the brain and the rest of the body, resulting in a wide variety of symptoms

including problems with mobility, vision, sensation, cognition, and speech.

Since it's most likely an auto-immune disease,

it makes sense to study treatments that interfere with the out-of-whack immune response in the

That's why scientists in the 80s were interested in IFN-γ.

which are proteins involved in activating the immune system's defenses.

so much so that it made it into clinical trials for humans.

But, it turns out that our immune systems differ in some important ways from mice immune

and the drug ended up worsening patients' MS.

Scientists later realized that the mouse model of MS does resemble human MS in terms of symptoms.

But the way it actually works in our cells is very different.

Similar to other mouse models used to study diseases,

scientists can't always get mice to have the exact same disease that happens with human

Usually, the best they can do is something that looks and acts similar enough to study.

In the case of MS, what the mice actually have

is something called experimental autoimmune encephalomyelitis, or EAE.

Even though EAE mice have provided a lot of insight into MS,

there are certain phases of MS that don't happen in an EAE mouse.

To date, that same mouse model from the 80s remains the most widely used

to study immune disease mechanisms and potential treatments for MS.

But one avenue of inquiry is understanding

how human MS is different from the mouse model.

Our mouse models for infectious disease can be tricky as well.

a viral infection of the liver that can become chronic,

It can cause serious complications, including cirrhosis and liver cancer.

The drug Fialuridine showed a lot of promise not only in mouse models for hepatitis B,

The drug incorporates itself into viral DNA,

blocking the viruses' ability to multiply.

scientists did know that fialuridine's mechanism isn't unique to viral DNA.

It can also affect the DNA of mitochondria,

the organelles that cells use to produce energy.

But this didn't cause problems in any of the four mammalian models they studied.

So clinical trials in humans moved ahead in 1993.

seven out of fifteen people enrolled in the trial developed liver failure,

It turns out that human liver cells have a unique protein

that actually helps drugs like fialuridine get into the mitochondria.

Making it toxic to humans, even when other mammals aren't bothered.

scientists figured that since fialuridine couldn't get into the animal models' mitochondria,

Realizing that this unique protein affects how drugs like fialuridine work

including creating a woodchuck disease model for hepatitis B.

a potentially severe infection of the lungs caused

by a bacterium called Mycobacterium tuberculosis.

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6 Reasons We Have to Say a Study Was "In Mice"

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