Researchers have a bo 旧 new atin the dreaded disease• stop it before it starts B Y E 凵 E D 0 L G ー N

BREATHE EASY: have genetically modified cows tO be resistant to the bacterium that BRAVE M00 WOR し 0 A GENE SPLICE CAN CREATE DISEASE-RESISTANT COWS been used for all sorts of the NationalInstitute 0fAllergy FOR THE first time, researchers things, including modifying and lnfectious Diseases, says have geneticallymodified cows human embryos ⅲ thelab and having such resistant animals to be resistanttothe bacterium could help reduce the transnus- that causes bovine tuberculosis. correctingthe gene respon- sion oftuberculosis through sible for Duchenne muscular This disease is well-controlled ⅲ milk, which is a significant dystrophy ⅲ mice. mostdeveloped countries, but health problem ⅲ developing ln this case, the scienüsts used canbe 信 t forcattle ⅲ develop anewversion ofthetechnique, countries. (The widespread mg ones, and can spread tO Other whichinserts agene intO a single use ofpasteurization in the animals and evenpeople ・ snipwithin one strand 0fDNA United States and most ofthe Researchers 仕 om China's Western world has pretty much atadesired location inthe COW NorthwestA&F Universityused eliminated tuberculosis risk genome. PreviousIy, CRISPR a technique called clustered involved the use ofa molecular 仕 om milk, though the faddish regularlyinterspaced short enthusiasm for raw milk and scissors ” that cleaved bo 市 palindromic repeats (CRISPR) cheeses... has reintroduced that strands 0fDNA. The advantage tO insertagene associatedwith ofthis newtechnique isthatitis risk, ” he notes. ) tuberculosis resistance 1ntO 20 potentiallysafer, says SukSee De ChuckSattIer, thevice pres- cows, 11 ofwhichlivedpastthe Ravin, aresearcherwiththe Lab- identofgenetic programs ata age 0f3 months. These animals oratoryofHostDefenses, part cow-breedingcompanySelect were more resistantto tubercu- ofthe U. S. NationalInstitute of Sires, says the insertedgene is losis than animals that weren t alreadyfoundnaturallyinsome Allergyand lnfectious Diseases, modified, and didn't show any ca 厄 . The researchers used unintended consequences Of whowasn't involved inthe p 叩 er ・ CRISPRto make changes that He adds that "further studies to genetic modification. A study could occurwithtraditional demonstrate the safetyofthe out- descnbing these findings was breeding, butmuch more quickly come are necessary ' and notes published ⅲ thejournal G 砌 0 川 and in a more specific manner, thatthe abihtyto rarse animals 0 ル on January 31 ・ he adds. "with improved resistanceto CRISPR is an intensively Forsuchtransgemccattleto infections has the potentialto researched tO developed in be approvedinthe United States, dramaucallyreduce the overuse the past couple years, which, they'd havetobevettedbythe antibioticsinlivestock,"whic —relative tO previous technique F00d and Drug Administration ・ is a significantproblem. can quickly and cheaply insert That's cost-prohibitive atthis Harry Malech, chief ofthe genes intO specific locations in point, Sattler adds. ロ Laboratory ofHost Defenses at an organism's genome. lt has BY DOUG MAIN 当@DougIas Main NEWSWEEK 49 02 / 24 / 2017

Newsweek F E B R UAR Y 2 自 , 2 0 17 / v 0L . 16 8 / N 0 . 0 7 ー N T E R N A T ー 0 N A L 十 HANDS OFINNO- CENCE: ChiIdren in San Francisco pledge allegiance in 1942. 0 Russia Putin's Poison 20 CoIIeges ・ Zombie Boys in Black Masks' 18 」鬢ーまを - を N E W W O R L D EboIa ViraI Triage 46 05 MindYourBusiness COWS Brave M00 World 50 PharmaceuticaI Pilloried Grass Getting Bent Over Bentgrass 24 Attacking AIzheimer's Researchers have a bold new strategy for beating the dreaded disease: Stop it before it starts. 切 / た Do / 〃 Round 'Em Up 49 52 D E P A R T M E N T S F E AT U R E S W E E K E N D 引 G S H 〇 T S 54 The PIace to Be Washington, D. C. lnterview Maarten Baas 60 Books Mario Testino, Peter Bazalgette, Yiyun Li Screening Room Big Little Lies 63 Radar Sun Kil Moon 64 Parting Shot White Rhino, Namibia 2015 Bucharest, Romania Social Democrat Unrest Washington, D. C. Unsigned Opinion GreenviIIe, South CaroIina Homels Where the Bark FareweII Spit, New Zealand The Tide That Binds 4 56 6 8 34 With President Trump calling for a border wall, a ban on Muslims, mass depoftations and black site pnsons, what better time tO visit Manzanar, where J 叩 anese-Americans were confined based solely on race. 切爿んⅣ 0 “〃 62 10 P A G EO N E 12 Trump Resistance lsn't Futile Yemen Guns and Mothers 30NV V3 工 10d00 COVER CREDIT: ILLUSTRATION BY NAEBLYS/SHUTTERSTOCK Newsweek 0SSN2052-1081 ) , is published weekly except one week in 」 anuary, 」 u ツ , August and October. Newsweek (EMEA) is published by Newsweek Ltd (part Of the 旧 T Media Group Ltd), 25 Canada Square, Canary Wharf, London E14 5LQ, UK. Printed by Quad/Graphics Europe Sp z 0.0. , Wyszkow, P01and For ArticIe Reprints. Permissions and Licensing www.旧Treprints.com/Newsweek FORMOREHEADLINES, GOTO NEWSWEEK ℃ OM 16 1 N E W S W E E K 0 2 / 2 4 / 2 017

THE ANNOUNCEMENT came the day before Thanks- giving, but there was nothing in it t0 be thankful for: An exp erime ntal Alzheimer 's drug many thought would slow the disease s steady cognitive decline had failed tO make a significant difference ⅲ a masslve trial ofpeople with early signs ofthe illness. Marty ReiSW1g took the news hard. "I was Just sad," he says. "I was really hopeful that it would be life-changing for us. ” ReiSW1g doesn't have Alzhei- mer's disease—he's a 38-year-old real estate agent in good health. But he is part 0fa large extended family that's been afficte d by Alzheimer's for generations. His Uncle Roy died 0f the disease. SO did Grandpa Ralph. EIeven gre at-aunts and gre at-uncles. D ozens ofcousins. And now, Reismg says, 。 I ve got a 64-year- 01d father who's almost dead ofAlzheimer s. His family is one ofaround 500 in the world with a genetic mutation that means its carners will develop Alzheimer's at a much younger age than those with- out the mutation, for whom the age Of onset is typi- cally about 80. For the Reisw1gs, those with the gene become sick around their 50th birthday. Other high- risk familie s c an start showlng symptoms as e arly as their 1 id -30S or, ln some cases, their late 20S. Reiswig decided not tO learn his own gene status— there's a 50 ー 50 chance he inherited his father's 信 ul 収 DNA, and he prefers livingwith the uncertainty. HOW- ever, he isn't just idly waitlng tO me et his fate. Three ye ars ago, he signed up for an innovative drug study that could alter his family's genetic destiny. Once a month, a nurse comes tO hiS home,mserts a needle in his arm and watches as a bag 血Ⅱ ofliqtud slowly drips intO his bloodstream. As with most trials designed tO te st whether an experimental drug works—even for diseases that are akin t0 de ath sentence s—Reismg might be gettmg a placebo. But there 's also a chance his monthly ⅲ血 - sions include a drug that could stop him, his family members and others like them from losing loved ones t0 Alzheimer's. Or, at the very least, delay the disease long enough t0 give them many more good years, genetics be damned. The key is early intervention, before symptoms are evident and brain damage is t00 extensive. "That's how you stop the disease, says Rudy Tanzi, director Of the Genetics and Aging Research Unit at Massa- chusetts General Hospital. “ You don't wait. P U S H B A C K T H E 0 N S し A U G H T 0 THIS AGGRESSIVE attempt tO prevent Alzheimer S rather than treating it is the most exciting new devel- opment in decades, as well as a radical departure for researchers and the pharmaceutical industry. Tradi- tionally, drug companies have tested their therapies on patients whO already have memory IOSS, trouble thinking and Other signs ofdementia. lt's been a 10S - ing tactic: More than 99 percent 0f all Alzheimer s drugs have failed tests in the clinic, and the few that have made it tO the market only ameliorate some symptoms. NOt a single medicine has been shown tO slow the relentless progression Ofthe disease. But with this new approach, even partial success— an appreciable slowing 0f brain dege neration— could have a big impact, says Dr. Reisa Sperling, a neurologist whO directs the Center for Alzheimer s Re s e arch and Tre atme nt at B 0 ston's Brigham and Women's Hospital. If a drug therapy can push back the onslaught of dementia by five or 10 years, she says, many more people would die 0f ballroom dancing instead Ofin nursing homes. lt's a strategy being te ste d in five big clinic al tri- als that collectively will cost anywhere from $ 500 million t0 a whopping $ 1 billion. But prevention More than 99 percent of all Alzheimer's Prevention, a coalition Of leading lnitiative and co-chair Of the Collaboration for utive director Of the F-Prime Biomedical Research designing better trials, says Stacie Weninger, exec- made huge progress" in learning from mistakes and because we see failure after failure, but we have while gamble. "lt sometimes doesn't feel like it, advocates are confident these studies are a worth- in the CliniC. Alzheimer's dmgs have failed tests NEWSWEEK 26 02 / 24 / 2017

EARLY DESPAIR: Some families diagnosis—and they were Often wrong. That meant prevention researchers. 1 れ ore hopeful now than carry a genetic Alzheimer's trials were filled with people wh0 had l've ever been that we can StOP thiS disease. mutation that means they Other types Of dementia and were never going tO success in one or more ofthese trials matterS not will develop benefit from the therapies. ln hindsight, it's painfully only because they may save the lives 0f the Reis- Alzheimer's clear the studies were set up tO fail. at a young wigs and for many 01der Americans; they may also age. High risk The past five years have brought two power- save our health care system. Dementia is the most families can ful diagnostic tools that help ensure Alzheimer s start showing expensive disease tO care fO ら and the Of symptoms as therapies are now being gwen only tO Alzheimer s patients with the condition is expected tO explode early as their patients. One involves a kind Of brain scan known ln the commg years. late 20S - as positron enussron tomography, or PETvwhile part ofthe problem with past efforts t0 tackle Alz- the other requires a spinal tap. B0th test for the heimer S was that therapies were tested on many presence Of the toxic amyloid protein that forms people wh0 didn't even have the disease' because the sticky brain plaques thought tO be responsible the only definitive way tO diagnose Alzheimer s was or t e lsease. 0 ーⅣ , 00 も we can through a brain autopsy. That postmortem cou match the patient population tO the anti-amyloid reveal the hallmark signs 0f the disease, but while a therapies, says James Hendrix' director 0f g10bal person is alive, doctors could make only a best-guess 、′ S ′下 K 27 02 / 24 / 2017

SC1ence mitlatives at the Alzheimer's Associat10n. of smoke—and the same could be true of when to That's what pharmaceutical company Eli Lilly deliver anti-amyloid drug the rapies ・ did in its latest trial ofsolanezumab, the drug whose trial failure before Thanksgiving had so saddened Reiswig. Lilly ha prevwus y teste SO anezuma H リ N 0 R E 0 S 0 F tWO huge studies, each involving more than 1 , 000 B ーしし一 0 N S し 0 S T presumed Alzheimer's patients. After those trials 0 THREE OF THE FIVE prevention trials are g1V1ng ended in failure, however, the company conducted drugs t0 elderly individual s wh0 are still cognitively PET scans and realized that up to one-third of its normal but have a high chance ofdeveloping Alzhei- study subjects didn't have the disease. SO Lilly tried mer's, either because Of elevated amyloid levels in again with only people who had confirmed amyloid their brains or because they inherited a risk-factor in their brains. The company also focused on only gene called APOE4. ln either case, the disease is by those with mild forms ofthe disease. Alas, the third no means a foregone conclusion for these subjects. trial was a flop t00. NOt SO in the Other tWO studies, which focus on Maybe solanezumab is a bad drug. However, those rare kin groups in which doctors know with the trials it did target amyloid as it was supposed t0, certainty, because 0f gene testing, wh0 will develop and it modestly outperformed a placebo by a range Alzheimer s in each family and at roughly what age ・ One such trial, led by the Banner Alzheimer's lnsti- "People would die of tute ⅲ phoenix, is being done in Colombia because ball r()()m danclng instead Of in it include s the world's largest known family with a mutation that triggers early Alzheimer's disease. nursing homes. The second study, run by the Dominantly lnherited Alzheimer Network TriaIs Unit (DIAN-TU) 0fWash- ington Umversity in St. Louis , include s the Reiswigs and more than 50 other families like them. ofcognitive and functional measures in clinical test- ing, even if it didn't meet the threshold needed for For us, the hope is that we re going tO stave 0 代 the damage and delay the onset of symptoms," says marketing approval. That's why Sperling and others are holding out hope for another explanation: that Reismg s second cousin Brian Whitney, whO knows he carries his family's Alzheimer s mutation. At solanezumab was simply given t00 far along in the 44 , he will soon develop Alzheimer 's if the therapy disease process, after irreparable harm has already he's recewing doesn t work. His hope for a long life occurred in the brain. If that's the case, it might hinges on DIAN-TU. prove 1 れ ore useful ifgiven sooner. 'l'm afraid that even by the stage 0f ve Ⅳ mild dementla, you've already lost 70 percent 0f the key neurons in the memory regions Of the brain," sper- ling says. "Ultimately, we need tO start treating peo- ple before there are symptoms ・ Researchers now know that amyloid starts tO accumulate in the brain at least a decade or tWO before the onset 0f cognitive problems. This stage Of the disease is referred tO by experts as pre-clin- ical Alzheimer's," although few people who qualify for this diagnostic label realize they have a problem. Dr. Jason Karlawish, a geriatrician WhO co-directs the University Of Pennsylvania's Memory Center, describes this as a real conceptual shift ” in our understanding Of the disease. Someday, you won t have to be demented to be diagnosed with Alzhei- mer's disease," he says. DIAN-TU s is a two-m-one study that s testing What's happemng in this early stage 0fAlzheimer s a pair Of different experimental therapies for their can be likene d t0 the kindling that starts a house fire. ability t0 keep Alzheimer s at bay. Participants don t Amy10id plaques slowly smolder foryears, consummg know iftheir getting a placebo or not, but they know the neuronal tinder in our brains. By the time demen- which Ofthe two drugs they are receiving otherwise. tla c s m, e e IS ragmg anditktoolatetosave ・ th hitney;i€s a Ro che drug called ganteneruma , and in Reiswig s case, it's Eli Lilly's solanezumab. house. Calling ⅲ firefighters at that point is a waste Of Both 曾 ug 、 target the amyloid protein behind time and money. You need t0 dial 911 at the first signs N ー S 駅′・ K 29 02 / 24 / 2017 LIFE BECOMES HER: A new aggress•ve attempt to prevent AIzhei- —mer's rather than treat- ing it is the most exciting development in the field in decades. INITIATIVE S 31 コ 3d7033d NOSV 「畄 08 コ OS 30N310S/SnYHVl•N vnnsun 洋」 3 コ b'N08A HEALTH ON EARTH: Ameri- can taxpayers are ponytng up tens of millions of dollars fo 「 trials as part of the U.S. :s na IOna p an tO prevent 0 「 treat AIzhei- mer's by 2025.

Aisen and Sperling recently launched a huge pre- everyone above a certain age—say, 50—would get vention trial, called EARLY, which is administering screened regularly for mole cular and ge netic risk that same beta-secretase-targeted drug tO people factors for Alzheimer's. If they test positive, they who, as in A4, are healthy but have elevated amy- could start taking a preve ntlve me dicine , much as those W1th highcholesterolto ay can pop a al y s a- loid in their brains. Dr. Roy Twyman, head ofAlzheimer's drug devel- tin t0 ward 0 圧 a heart disease. 'We will eventually opment at Janssen, a division Of Johnson & Johnson think about tre ating a much broader population, and the manufacturer Of the beta-secretase inhibitor says Sperling. But statins cost pennies a pill. Any new Alzhei- mer's drug would likely cost tens of thousands of dollars per year. lnsurance companies may balk at 'l'm more hopeful now paymg that for seemingly healthy individuals, espe- than l've ever been that we can cially because not everyone with elevated amyloid or stop this disease. APOE4 will develop dementia. Howard Fillit, chief science offcer of the AIzhei- mer s Drug Discovery Foundation, thinks researchers should focus on treatmg people with symptoms but in the EARLY and DIAN-TU tnals, points t0 a study halting the disease at the pre-dementla stage when 仕 om lceland as evidence that the strategy should only mild cognitive imp alrment is evident. Problems work. Five years ago, researchers there discovered with memory, thinking and judgment at that point are the first known gene mutation that protects individ- 1 れ ore pronounced than for those WhO expenence nor- uals against Alzheimer 's. lt's extremely rare, found mal, age-related "senior moments. ” But most people ⅲ less than one ⅲ 200 people 仕 om Nordic countries. with MCI are not so far gone that they reqture con- Yet those whO carry the mutafion are about five times stant care. They can keep living independently. more likely t0 re ach their 85th birthday dementia-free. MCI is the sweet spot in terms ofthe cost oftrials, the cost ofdrugs and quality of ⅱ for patients, ” Fil- And what does that mutation d0?It impairs the abil- lit says. That's still prevention because you re pre- ity ofbeta-secretase tO dO its 怛 b. Nature has already taught us a lesson in humans, says Twyman—and it's venting dementia. Anyone whO's ever had a spouse get lOSt coming one that J&J hopes to take to the pharmacy shelf. Another beta-secretase inhibitor, from Novartis, home from the grocery store or a parent unable tO is one Of tWO drugs included in a prevention study, write a check might disagree. And SO many research- the Generation trial, run by Dr. Eric Reiman and ers continue tO dream Of a time when they can pre- his colleagues at the Banner Alzheimer's lnstitute. vent all cognitive impairment. TO that end, they That study, like A4 and EARLY, is being done with plan tO start testing drugs even earlier in the disease cognitively normal older adults at risk 0f develop - process, before any amyloid has started t0 damage ing Alzheimer's. But rather than looking for signs 0f the brain. For example, Aisen and Sperling will soon amyloid accumulation, the Generation trial involves launch a placebo-controlled trial involving peo- ple wh0 weren't eligible for the A4 or EARLY trials volunteers wh0 inherited two copie s 0fAPO E4. That increases their odds 0fdevelopingAlzheimer's about because their amyloid levels didn't reach the thresh- fifteenfold, compared with the general population. 01d for inclusion. And Dr. Eric McDade, a neurolo- An estimated 2 percent Of the population has gist involve d with DIAN-TU, plans t0 start tre ating two copies 0f APOE4, but few in that select group people with the sure-thing, genetic form 0f Alzhe i- know it. lt hasn't been worth getting tested for this mer's—families like the Reiswigs and others—even sooner than the current trials allow. "GOing as early gene because there was little you could d0 with the results. "Really, for the first time, what t0 d0 about as possible is really the goal," McDade says. Developing drugs tO prevent Alzheimer's disease it is different, says Dr. Pierre TariOt, the Banner Alzheimer's lnstitute's director. You can choose to could be a discovery 0f N0bel proportions. There particip ate in a trial. IS no guarantee the current tnals will succeed, but researchers believe they are getting close tO solving what had, until recently, seemed t0 be one of medi- al research's toughest challenges. W H AT 0 0 YO U M ミ A N lt's an exciting time for us, says the Banner ド M N 0 T C 0 E R E 0 ? Alzheimer's lnstitute's Reiman. "The hope is that 0 IF THE DRUGS prove tO be effective at preventing Alz- we already have a treatment that can substantially re ducetheriskofAIzhe imer'saButthere'sonIyon heimer S, elr success lmme late y ralse ano er way to find out, and that's through these trials that urgent question: Wh0's gomg t0 pay for them? chart new territory. ”ロ prevention proponents envision a day in WhiCh 1 コ S8 コ N を′ S 1 を K 33 02 / 24 / 2017

One ⅲ every five Medicare Alzheimer's but dO SO in different ways: Roche's gan- tenerumab breaks up the amyloid plaques that can dollars iS IÄ()W S ent ()IÄ P00P10 、 ith 0i0 、 0 パ 00d spur neuron death; Eli Lilly's solanezumab leaves plaques alone but can mop up free-floating protein tO prevent further plaque formation. other dementias. ln 2 ( ) 5 ( ) , れ will Solanezumab thus operates like an outreach coun- be one ⅲ every three dollars. selor wh0 helps take crime-prone youth 0 代 the stre ets of a grafflti-filled neighborhood. If the kids aren t left to form gangs, they won t vandalize the are a any further. The drug, by eliminating scattered amyloid, With Alzheimer S reqture around-the-clock care— stops the deuant proteins 仕 om clumping together and more than one-third Of all dementia caregivers and forming additional brain- destroying plaques ・ develop clinical depresslon. That's the idea, but researchers don't yet know As Gregory Petsk0, director of the Appel Alzhei- mer's Disease Research lnstitute at Weill Cornell whether a drug that has failed time and again as a treatment for Alzheimer S can prevent it. Some Medicine in New York City, says, Pretty much experts remain skeptical. They argue that further studies on anti-amyloid drugs are a waste when what is really needed are new therapeutic strategies—and that anyone whO still sees prom- 1Se solanezumab because it beat a placebo by some tiny amount is guilty 0f spin and wishful thinking ・ We re treating asymptomatic people with a drug that has no evidence whatsoever ofeffcacy, says Peter DaVles, a neurosclen- tist whO dire cts the Litwin-Zucker Research Center for the Study of Alzheimer's Disease at the Feinstein lnstitute for Medical Research. "You might as well give them asprin. But the federal government cle arly thinks the trials are worth- while. ln addition to funding from drug compames and philan- thropies, taxpayers are ponymg MIND CRAFT: up tens of millions 0f dollars for drug therapy these trials as part 0f the country's national plan to every family is going t0 have a relative affected by can push back the onslaught effectively prevent or treat AIzheimer's by 2025. Alzheimer s, and that's going to change the way of Alzheimer's The consequences offailure could be dire. Approx- we live, the way we think, the way we plan for our by five tO 10 years, many imately 5.4 million Americans suffer from Alzhei- future—everything. more people mer s, and if no disease-delaying therapies are could avoid such an ago- found soon, that number is expected to nearly triple nizing end. by 2050 , at which point the cost Of treating and car- CA N ' T F 0 R G E T ing for all those people could top $ 2 trillion per year, YO U R FA C E ' after adjusting for inflation. That's up from $ 236 bil- 0 lion tOday. One in every five Medicare dollars is now DR. RANDALL BATEMAN had no warning the latest spent on people with Alzheimer's and other demen- solanezumab trial was going tO be a failure. He was tias. ln 2050 , it will be one 1n every three dollars. And racing around the house dOing chores in anticipa- those figures don't even include the hundreds of tion 0f a big family dinner last Thanksgiving when billions more in lost wages for family members wh0 he received an early-morning phone call on Novem- ber 23 from executives at Eli Lilly. was extremely take time away from their jObs tO care for loved ones. disappointed," says Bateman, who leads DIAN-TU. lt's not a question Ofa day 0 伍 now and again. People NEWSWEEK 30 02 / 24 / 2017

NEWSWEEK (FEB24 # 8 ) FEB24 # 8 Newsweek oscow MurdersLLawyers-ys..Trump THE AR ON ・・ . ZHEIMER'S 2 4 . 0 2 . 2 0 1 7 徳 ー N T E R N AT ー 0 N A L 160987481 市立文 STOPPIN BEFO HE DISEASE STARTS 本体 雑誌 28224 ー 02 04 / 08 / 17 しン " ー u 0 u 4910282240 ~ 77 01300 アメリカ合衆国 CYPRUS C6.50 CZECH REP CZK180 DENMARK DKR50 0 リ BA ー DH35 EGYPT E 見 60.00 FINLAND €7.60 FRANCE €6.50 GERMANY €6.50 GIBRALTAR 6.05 GREECE C6.25 HOLLAND ℃ 6.50 HONG KONG $ 80.00 HUNGARY FTI. 800 DONE 引 A 2R175.00 IRELAND ℃ 6.25 ISRAEL NlS35 A Ⅳ C6.50 JORDAN 」 D5.95 KUWAIT KD3.00 LATVIA も 6.50 LEBANON LLIO , 000 LITHUANIA も 8.99 LUXEMBOURG 06.25 MALTA も 6.50 MONTENEGRO ℃ 8.30 MDH70 NEW ZEALAND $ 14.00 NIGERIA $ 3.40C NORWAY NKR85 OMAN OR 3.250 POLAND PLN28 PORTUGAL €6.50 QATAR 0R65 MALAYSIA RM29.50 ROMANIA LEI 42.00 SAUDI ARABIA SR35.00 SERBIA RSD1035 S LEONE SLL30 , 000 SINGAPORE $ 11.95 SLOVAKIA を 6.50 SLOVENIA も 8.50 SOUTH AFRICA R55.00 SPAIN を 6.50 SWEDEN SKR60 SWITZERLAND CHF8.50 TURKEY TL17 UK を 4.95 リ 5 $ 799 ZIMBABWE ZWD4.00

But I wouldn't say it was surprising. ” He'd been expected t0 have Alzheimer's long before death, and saymg prevention has a better shOt Of success than I haven t yet, says Blackerby, 82 , a retired technical writer whose mother died from the disease, as did treatment for years. Another leading prevention proponent is Dr. Paul her three siblings. "lf l'm going to have it, I want to AISen , a neurologistvvho¯difeets-th€Älzheimer's e lnvolved ⅲー the study to try to keepothers,e The rapeutic Re se arch lnstitute at the Unive rsity Of cially my descendants, from having to go through the hell l've seen family members go through ・ Southern California. ln 2014 , Aisen teamed up with Sperling for a 1,150-person trial called A4. Short for Last December, Blackerby drove more than 100 miles from his home in southern Oklahoma to the Anti Amyloid Treatment in Asymptomatic Alzhei- mer's, A4 tests solanezumab for prevention. The University Of Texas Southwestern Medical Center drug iS given tO semors WhO have no signs ofdemen- in Dallas to receive his first infusion. He will make this same four-hour round-trip trek every month for tia but d0 have elevated amyloid levels, as measured by a PET scan ofthe brain. lt is looking for changes the next three years. over a 39-month periOd in cognitive function, self- For Don, a retired insurance agent, the motiva- c are abilitie s, brain tissue he alth and Othe r indic ators tion tO participate in A4 was his partner, Fran. He first noticed her Alzheimer's four years ago when he arrived at her house expectmg a dinner ofmeat stew, only t0 find a ne ar- empty pot. "She had remembered the onions, ” he recalls. "But she had forgotten everything else ・ Don (who asked that his last name not be used because he didn't want tO come across as self-promotional) tried to enroll Fran in A4, but her disease was t00 far advanced. Only he was eligible—a PET scan showed he had the hallmark amyloid logjam in his brain. He started gettlng infusions last fall at Brigham and Women s Hospital in BOSton. On a rainy day in late Novem- ber, Don, with a plaid-blue shirt sleeve rolled up past the elbow and an IV catheter in his right arm, remmisced about meeting Fran mne ye ars ago at a single S dance at Vincent's Nightclub EXPENSIVE in the suburbs south Of Boston. FAILURE: He's mild-mannered and surprisingly youthful for of Alzheimer's. "we still need to find out what the About 5.4 million Amer- benefits and risks are ' in patients not yet showing a 76-year-01d, gray-haired grandfather who raised icans suffer symptoms, Aisen says. SiX children on hiS own after hiS Wife died in a car from AIzhei- ー第 e 「 ' S. け no The trial asks a lot of its participants. A4 subjects crash 33 years ago. He beams when he talks about therapies are must be willing tO come tO a hospital once a month Fran retaining her sense Of humor and ability tO found soon, that number for more than three years tO recelve infusions con- play tennis, but he turns solemn when he describes is expected tO an unproven medicine for a disease they hOW it tOOk four tries tO explain tO her why he was triple by 2050 , don't have and might not get. There's no guarantee going t0 the hospital today. "She knows," he says at which point the cost of 0f benefit or even safety. And the trial is not partic- "but she forgets ・ care could top larly remunerative. Some participants can receive while .he's talking, a nurse comes tO deliver the $ 2 trillio up t0 $ 2 , 480 ifthey complete all the study protocols, saline flush that always follows Don s infusion. She including tW0 PET scans, four MRI scans, tW0 spinal introduces herself, although Don recognizes her from a prevlous visit. I can't forget your face, ” he taps and 42 infusion visits. But many dO not get any t01d you, You 100k just like mycousin ・ ' compensatlon, un ess you coun par lng validation. The amyloid in Don's brain has clearly not None of that dissuaded Jerry BIackerby from taking part in A4. "With my family history, I have impaired his memory, but it's there. And perhaps S01 0 (Z) dV 乙 0 コ > NVAA NEWSWEEK 31 02 / 24 / 2017