Don’t believe the hype: We haven’t cured Down Syndrome in mice

Have you heard?Scientists have discovered a drug that cures Down syndrome with a individual injection!Only they have n’t . They ’ve cured Down syndrome in mice with a individual injectant . Except … well … they have n’t really done that , either .

Science has done an awed lot for mice . Cancer , Huntington ’s disease , old age , HIV . You do n’t worry about these thing if you ’re a computer mouse , because science is on it . The tardy find : yesterday , researchers published the results of a new treatment that has since been reported far and wide asa “ cure ” foror“reversal”of Down syndrome ( in mice ) . These are , as is often the case with such claims , gross deception of the real findings .

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But this study , and its overhyped coverage , pose a unique chance for us to examine what it really imply when we “ bring around ” a disorder like Down syndrome in an animal model . It also gives us a chance to search what these research worker in reality accomplish , which is still incredibly significant .

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Here ’s the pithiest upshot of this research I can muster : researchers at Johns Hopkins University and the National Institutes of Health have identify a potent treatment for mice that exhibit hallmark symptoms of Down syndrome . A unmarried dot of a chemical substance called SAG , delivered presently after birth , seems enough to meliorate major physiologic and cognitive shortfall associated with the disorder . But it does n’t correct all of them .

The research squad , led by geneticist Roger Reeves , has put out the results of its investigation in the latest issue ofScience Translational Medicine . Over atPopular Science , where the treatment is described inaccurately as a “ cure ” in the newspaper headline , Shaunacy Ferro actually afford a groovy summary of the squad ’s determination in the context of Down syndrome ’s classical symptoms :

hoi polloi with Down syndrome usually have smaller brain volume than restraint groups , includingsignificantly smallercerebellums , a dowry of the brain regard in motor control . The research worker , led by Roger Reeves of the John Hopkins University School of Medicine , treated new-sprung mice that had been genetically engineered to have Down syndrome - like feature with a minor mote called SAG .

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After a exclusive injection of SAG on the daytime the shiner were born , their cerebellums develop usually into maturity . It improved their demeanour , too : Mice treated with SAG performed just as well as normal mice on a memory and learnedness examination .

acquire it ? in force . Let ’s take out this .

The Animal Model is a Powerful but Imperfect Tool

Here ’s what ’s crucial to call back : likeall preliminary biomedical investigation , Reeves and his colleaguesused an animal modelto assess the effectuality of their handling . In this case , they used a mouse genetically orchestrate to exhibit symptoms similar to the ones we see in humans with Down syndrome . As is typically the case , the genetic detail of the disorderliness are not selfsame between man and the good example species .

https://gizmodo.com/where-do-lab-animals-come-from-and-how-guilty-should-w-5867491

Humans with Down syndrome acquit an extra copy of their 21st chromosome . The resulting genetic instability has a significant impact on physiologic and cognitive development . It ’s an fantastically common molecular mixup – by far the most common genic abnormality in mankind . In the U.S. , one in every 691 children born carries a third copy of chromosome 21 .

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Just about every human on Earth comes genetically fit with 22 twosome of autosomal ( i.e. sexual urge - independent ) chromosomes and one pair of sex chromosome ( X and X / Y ) . But the black eye used in research ( Mus musculus ) comport just 19 pairs of autosomal chromosome and one distich of sex chromosome . In other words : your standard lab computer mouse does n’t even have a twenty-first chromosome . How can we mold Down syndrome in a species that lacks the chromosome associated with the disorderliness ?

The answer : reach of genetic information tie in with Down syndrome are found besprinkle throughout the mouse ’s genome , and in fact occur most prevalently on chromosome 16 . equip with this knowledge , investigator have genetically engineered a number of Down syndrome black eye model , each with its own special , technical - vocalise name ( Ts65Dn , Ts1Cje and Ms1Cje / Ts65Dn , to name a few ) . The black eye used in this late enquiry were Ts65Dn mice . Each one carries a small , additional chromosome gain primarily from chromosome 16 .

It ’s not a perfect analog for human Down syndrome ( Ts65Dn mice exhibit a dose imbalance for roughly half the gene found in a person with an spare 21st chromosome ) , but the effect on development is unmistakably similar : like humans with Down syndrome , Ts65Dn mouse demo several of the upset ’s physiologic and behavioural symptoms . Two heavy ace :

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Asmaller cerebellum(a neighborhood of the wit closely tied to motor control)with fewer neuron .

Impairments to learning and remembering , associated withphysiological change to the hippocampus .

So what did the researchers actually do?

Reeves and his colleagues were concerned in studying the physiologic and behavioral effects of a chemical called SAG on Ts65Dn shiner . SAG is know to activate the Sonic hedgehog pathway , a molecular communicating mesh so - mention because fruit flies ( another ubiquitous good example being ) that lack the protein by the same name develop spine - like jut resonant of one video - game protagonist ’s .

Both the Sonic - the - hedgehog protein and Sonic - the - hedgehog pathway have been designate to act polar roles in the establishment and proliferation of neurons in the developing brain . Crucially , Reeves and his squad were concerned in seeing what long - full term effect an SAG loony toons administered shortly after nascency would have on a Ts65Dn mouse as it get along into adulthood .

The research worker demonstrate that a single dose of SAG administered to Ts65Dn mouse right on after birth make their cerebellum to develop like those of normal mouse , growing to a comparable size and containing a similar number of nerve cell . This is a fantastic result !

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But there ’s a caution , because the researchers also show that something called recollective - term Great Depression remains an issue in the cerebellar circle of Ts65Dn mice that are treat with SAG . In neurophysiology,“long - term depression”is used to describe not an emotional body politic of being , but a signaling problem watch over in the brain circuitry of hoi polloi with Down syndrome . The consequence : SAG may help preserve the growth and structure of the cerebellum , but its effects on the cerebellum ’s use rest ambiguous , at well .

A couple more promising watching : Ts65Dn mice treated with SAG were shown to execute better on undertaking that rely on learning and retentiveness than mice that went untreated . Both of these faculty are closely associated with the hippocampus , a region of the brainpower that has been love to develop abnormally in humanity with Down syndrome . When Reeves and his team examined the hippocampi of SAG - treated Ts65Dn mouse , they found them to be more full develop than the hippocampi of the untreated mice . In these model organisms , at least , SAG appear to have a normalizing outcome on hippocampal development , and a positive outcome on learning and memory . The researchers note , however , that Ts65Dn mice find out no welfare from SAG on task that rely on the normal function of the prefrontal cortex – a region of the brain associated with cognitive functions like provision , moderating social doings , and determination - making .

The condensed version of the researcher ’ finding is that , in mice , SAG appear to have a normalizing effect on some of Down syndrome ’s hallmark symptom , and no observable effect on others . The results are anticipate , but , as is vulgar in bailiwick like this , a mixed bag . It is clearly a far cry from a remedy . Even if it was exact to say that mice can tolerate from Down syndrome as we recognize it in humans , to say that they were “ cured ” of the upset , when the mouse intelligibly exhibit behavioral and physiological deficit , would be wholly and utterly incorrect .

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We ’re taught to be skeptical of how well research translates from animals to humans . Asthis JAMA articleputs it : “ patient and medico should remain cautious about extrapolating the findings of prominent animal inquiry to the care of human disease … even eminent - quality animate being study will replicate poorly in human clinical research . ”

What we ’re reminded of less often is that even the “ high - quality ” animal studies seldom warrant the use of a word as charge with underlying substance as “ cure . ” As Reeves himself noted in a statement : “ Down syndrome is very complex , and nobody think there ’s going to be a silver bullet that normalizes cognition … Multiple approaches will be needed . ”

In medicine , the true cures tend to issue forth few and far between . Even if you ’re a mouse .

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