Can Prozac help treat autism?

Study finds im­proved func­tion in mice, but hu­man tri­als would pose eth­i­cal is­sues.

Los Angeles Times - - CAL­I­FOR­NIA - MELISSA HEALY melissa.healy@la­ Twit­ter: @LATMelis­saHealy

Af­ter drink­ing mother’s milk spiked with the an­tide­pres­sant Prozac for 19 days, in­fant mice bred to mimic the dis­tinc­tive be­hav­iors and brain ab­nor­mal­i­ties seen in autism ex­pe­ri­enced dra­matic im­prove­ments in their so­cial in­ter­ac­tions, com­mu­ni­ca­tion pat­terns and a wide range of neu­ro­chem­i­cal pe­cu­liar­i­ties that are a hall­mark of the dis­or­der, ac­cord­ing to a new study.

And when new­born mice got a daily in­jec­tion of Prozac in their first six days of life, the treat­ment ap­peared to re­store nor­mal vo­cal­iza­tion pat­terns and re­duce anx­i­ety-like be­hav­iors well into adult­hood, the new re­search showed.

The an­tide­pres­sant Prozac, a se­lec­tive sero­tonin re­up­take in­hibitor (or SSRI), is one of the world’s most widely used med­i­ca­tions. It is thought to el­e­vate mood and quell anx­i­ety by in­creas­ing the avail­abil­ity of the neu­ro­trans­mit­ter sero­tonin in the spa­ces be­tween cer­tain types of brain cells.

Re­search on hu­mans sug­gests that, dur­ing early brain devel­op­ment, those who even­tu­ally de­velop autism have un­usu­ally low lev­els of sero­tonin in cru­cial ar­eas of the brain.

The new study, pub­lished last week in the jour­nal Sci­ence Ad­vances, of­fers strong ev­i­dence that a sero­tonin short­age and faulty sero­tonin sig­nal­ing play key roles in the neu­rode­vel­op­men­tal dis­or­der, in which so­cial skills and ver­bal com­mu­ni­ca­tion are im­paired, be­hav­ior is of­ten in­flex­i­ble and sen­sory over­load is com­mon.

The study’s au­thors, from Hiroshima Univer­sity and the RIKEN Brain Sci­ence In­sti­tute in Saitama, Ja­pan, ad­min­is­tered Prozac (also known by its generic name, flu­ox­e­tine) to the mice dur­ing the first three weeks of their lives. In a hu­man child, the treat­ment pe­riod was roughly the equiv­a­lent of the span from 6 months of age to about 2½ years.

At UC Davis’ MIND In­sti­tute, the pos­si­bil­i­ties of SSRIs as an autism treat­ment are al­ready un­der in­ves­ti­ga­tion in hu­mans.

“This study sup­ports what we see clin­i­cally,” said Dr. Randi J. Hager­man, med­i­cal di­rec­tor of the MIND In­sti­tute, which treats peo­ple with a range of neu­rode­vel­op­men­tal dis­or­ders and con­ducts re­search on their causes and treat­ment.

In chil­dren 2 to 6 years old with Frag­ile X, a ge­netic dis­or­der that fre­quently causes autism, Hager­man and her col­leagues have found that six months of treat­ment with the SSRI an­tide­pres­sant ser­tra­line (com­mer­cially mar­keted as Zoloft) im­proved the use of ex­pres­sive lan­guage and other mea­sures of cog­ni­tive func­tion.

Hager­man said the SSRI treat­ment ap­pears to boost the creation of neu­ral con­nec­tions through­out the brain, and to stim­u­late the growth of new neu­rons in chil­dren with Frag­ile X and autism. In a field where be­hav­ior-based treat­ments dom­i­nate, med­i­ca­tions that can im­prove brain func­tion hold the promise of mak­ing those be­hav­ioral in­ter­ven­tions more ef­fec­tive, she said.

“I think it’s mak­ing a dif­fer­ence,” said Hager­man.

The au­thors of the Prozac study ac­knowl­edged that it would be “dif­fi­cult to sim­ply ap­ply the strat­egy used in this study to hu­mans.” Giv­ing SSRIs to ba­bies too young to be di­ag­nosed with autism — much less putting it in their mother’s milk — would be eth­i­cally prob­lem­atic with­out far more re­search, they wrote.

Fur­ther com­pli­cat­ing mat­ters is the fact that some stud­ies have linked SSRIs in gen­eral — and Prozac in par­tic­u­lar — to higher rates of autism in ba­bies who were ex­posed to the an­tide­pres­sants in utero. Those re­search re­sults, how­ever, have been in­con­sis­tent. And they have not ruled out the pos­si­bil­ity that the ge­netic un­der­pin­nings of parental de­pres­sion — in­clud­ing sero­tonin in­ad­e­quacy — may be passed on, man­i­fest­ing as autism in a child.

But in mice at least, the Ja­panese re­searchers sug­gested that Prozac could “re­store” the struc­ture and per­for­mance of the brain’s so­cial, sen­sory and com­mu­ni­ca­tions cir­cuitry when a ge­netic tran­scrip­tion er­ror has set their devel­op­ment on an er­rant course.

In the mice bred to de­velop autism, the early ad­min­is­tra­tion of Prozac in­creased the avail­abil­ity of sero­tonin in a struc­ture in the mid­brain called the dor­sal raphe nu­cleus, a switch­ing sta­tion that plays a key role in learn­ing, mem­ory and emo­tions. It re­stored an im­bal­ance of ac­tiv­ity in cells there that turn some neu­rons “up” and other cells that tamp down elec­tri­cal fir­ing in the brain.

Com­pared with peers that didn’t get Prozac, the treated mice chose to spend more time in the com­pany of un­fa­mil­iar mice. They also showed less anx­i­ety while ex­plor­ing a maze. And as young pups, their vo­cal­iza­tions re­flected less stress and fear.

“Restora­tion of nor­mal sero­tonin lev­els” in the mice bred to de­velop autism “re­vealed the re­versibil­ity … in the adult” of some of autism’s most trou­bling symp­toms, the study au­thors con­cluded.

PROZAC, the pop­u­lar an­tide­pres­sant, im­proved so­cial in­ter­ac­tion among in­fant mice, a study found.

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