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champion speed rider valentin delluc quickly follows, videotaping for us with a camera on his helmet. the ride of a lifetime has begun. you're standing there on the top of the mountain. what goes through your mind? >> there's two mindsets, you know? there's the... there's the evel knievel, which is kind of kamikaze. and then, there's the james bond. >> cooper: which one are you? >> i'm bond. >> i'm steve kroft. >> i'm lesley stahl. >> i'm anderson cooper. >> i'm bill whitaker. >> i'm scott pelley. those stories tonight on "60 minutes."

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>> stahl: nobel-prize-winning colombian novelist gabriel garcia marquez once wrote of a mythical town in the middle of the jungle whose residents suffer from a mysterious affliction that erases their memories. today, in a region of colombia called antioquia, reality appears to be imitating fiction, in a way that may answer questions for all of us. as we first reported last fall,

antioquia is home to the largest concenio people who carry a rare genetic mutation that makes them 100% certain to develop alzheimer's disease. and as devastating as alzheimer's is anywhere, this is a particularly cruel version-- it strikes when people are in their mid-40s, and leads to death about a decade later. it is a tragic situation, but a perfect scientific laboratory. and it's now the center of a multi-million dollar, n.i.h.- backed study that's trying to find out, for the first time, whether alzheimer's disease may be preventable. these are the andes mountains and lush countryside of antioquia, colombia, whose capital city, medellin, was once famous for murder and the drug cartel of pablo escobar. today, medellin-- or medejin, as

peaceful. but for some families here, there's still a battle going on, a battle against an insidious disease. this family-- mother cecilia, her seven children, and grandchildren- lost its patriarch, alonso. >> freddie: for me, my father was-- number one. >> stahl: freddie, the oldest, remembers his dad always eager to join in and play with him and his friends. >> cecilia ( translated ): he was a very joyful person. he loved to dance. he was a really nice person, a very good father. before the disease. >> stahl: when it first started, what were you noticing that made you think he's-- he's different? >> cecilia ( translated ): he started asking, "what is the date today? do i have to go to work?" and we got concerned.

in his mid-40s, so the memory loss and confusion made no sense. his doctor suggested exercise and vitamins, but alonso just got worse, forgetting the names of his children, getting lost and disoriented. his son victor had to help him get dressed. >> victor ( translated ): i gave him his shirt, i told him "dad, come, i'll help you put your shirt on," and the first thing he did was to grab it-- and put it on through his feet. >> stahl: did he understand what was happening to him? >> victor ( translated ): there were moments of lucidity, where he would ask me and say, "son, what's happening to me? why don't i remember? i don't remember my children, or my wife. i don't know who i am."

back to see the doctor: >> julio ( translated ): when i asked the doctor, i told him, "doctor, i am not leaving here"-- sorry. --"until you tell me what is wrong with my fath." >> stahl: the doctor sent them to francisco lopera, a neurologist at the university of antioquia who knew exactly what was wrong with alonso, because he'd become the local authority on a rash of early-onset alzheimers cases in and around medellin. >> francisco lopera: they were getting disease very early in the life. >> stahl: it all began many years earlier, back in the 1980s, when lopera was a young medical resident. he had read about small numbers of people scattered around the world who had developed alzheimers in their 40s. so when a 47-year-old man came

into his medellin clinic with alzheimer's-like symptoms, he was intrigued, and decided to investigate. you met this one man, and you decided to go to where he was from? >> lopera: i decided to go to the town where he was living. >> stahl: lopera learned that the man's father and grandfather had also lost their memories in their 40s. then, a few years later, another similar patient came into the clinic, this time a 42-year-old woman from a town 40 miles away. dr. lopera's then-nurse, lucia madrigal, asked if any of her relatives also started losing their memories when they were young. >> lucia madrigal( translated ): they told us yes, that the father, the uncles, the grandfather, the great grandfather, so i started making a little family tree, on one page, and i showed it to dr. lopera. and i told him, "look what we have here. what is this?

detective hunt that lasted more than a decade. lopera and madrigal traveled all over the region, finding more and more people afflicted with early-onset alzheimers, and compiling family trees. they thought it might be genetic, so madrigal spent days at parish churches, poring over heavy ledgers where priests for generations had recorded village births, marriages, and deaths. thanks to these meticulous records, she was able to trace the disease back hundreds of years, and to make an important discovery-- the different families were actually one huge extended family, connected generations back by common ancestors who had died young, with an unusual cause of death written down by the priest: "softening of the brain."

brain" looks like in real life. fernando is 46 years old, a descendant of that second patient, years ago. he started forgetting things when he was in his late 30s, and now can no longer speak, feed himself, or do just about anything on his own. his aunt takes care of him round the clock, just as she did with his mother, when she got the disease at the same age. norelly is at an even later stage of the disease. despite her appearance, she is just 58 years old. patients were going from mild symptoms to complete dementia and then death within about a decade-- as dr. lopera showed us in these cognitive test results. >> lopera: you can see, at 38--

struggled-- as many older alzheimer's patients do-- to copy a complex drawing accurately. >> lopera: at 45. >> stahl: and things got worse from there. >> lopera: he lost more. at 50. >> stahl: ah! oh! >> lopera: at 51. >> stahl: oh! dr. lopera was convinced that what he and madrigal were discovering was scientifically important, but even as they found more patients and more related families, he couldn't get anyone outside colombia to take notice. until 1993, when a harvard professor came to give a talk about alzheimer's in bogota, several hours away. >> ken kosik: there was a person in the audience, francisco lopera, who came up after the talk and said, "you know, there's-- i have a family here that w-- has-- early-onset alzheimer's." >> stahl: ken kosik, now at u.c.

santa barbara, was that professor. a family. could've been four people. >> kosik: it could've been just four people. but he started to tell me how many it was. and as i listened to him, i became just so absorbed and taken with what he was telling me that i changed all my plans, went with him to medellín. and-- we began a collaboration that goes on to this day. >> stahl: they showed kosik what lucia madrigal showed us-- the family tree they had compiled, based on all that searching through church records, for just one of the affected families, going back all the way to the 1800s. this is one family? ( laughs ) >> madrigal: una sola! >> stahl: it just kept unfolding. and unfolding. covering these pages are small squares representing men, circles for women. the colored-in squares and circles mean the person got sick with alzheimer's at an early age. look, she had these sons and a daughter.

and then it just kept going down-- through the generations-- >> madrigal: si. >> kosik: when we looked at the family trees, about 50% of the offspring were getting the disease. that's a clear signature of a gene. >> stahl: but what gene? kosik connected dr. lopera with leading geneticists in the u.s., and they started collecting blood samples and searching. within a year, a major breakthrough-- they found a specific mutation in a gene on chromosome 14 one tiny flaw in the d.n.a. responsible for all this family's suffering. the discovery was published in 1997 in the journal of the american medical association. lopera had identified the largest concentration of early onset alzheimer's cases in the world. if a person has that mutation, do they get alzheimer's? >> kosik: yes, they do. >> stahl: if they have i t

>> kosik: right. there are some mutatiohe but this is a bad one. and if you have this mutation, you get it. >> stahl: for families like alonso's, discovering the mutation was a blessing- a crucial first step toward finding a way to fight the disease. but it was also a curse, because it meant that anyone whose parent had the mutation, has a 50/50 chance of having inherited it too. do any of you know if you have that mutation? do you know? >> victor: no. >> freddie: nobody knows. >> stahl: nobody knows. well, somebody knows. dr. lopera and his team have been testing for the mutation and compiling a database, but their policy is not to tell family members if they have the mutation or not-- and not even to reveal the results to dr. lopera, since at this point, there is nothing that can be done to help. >> cecelia ( translated ): sometimes i ask, which one will get it?

because i don't want to think about that. i pray a lot to god that none of them gets it. i don't want to see my children with that disease. >> stahl: each one of you knows, because of your father, that you have a 50-50 chance. so what kind of a weight does that put on you, day in and day out? >> julio ( translated ): i've even prayed to god that if-- if there's one person who has to have the disease, i say to god, "let it be me." >> sara ( translated ): i thank god that i'm a nurse and that i would be able to take care of them, but i tell myself, "first i had to go through it with my dad, the experience of the disease, and i may have to go through it with one of my siblings, or with several, we don't know." >> stahl: sara told us she would

own, but given her risk ofse, ss decided against it. >> sara ( translated ): so that my children don't have to go through my same experience. >> stahl: you've been working on this 30 years. how do you cope with all this pain? >> lopera: ( crying ) >> stahl: it was not the response we had expected. it's that hard? it's that hard. but dr. lopera knew that even in the midst of all this tragedy, there might just be a glimmer of hope. because what he had discovered in these families-- hundreds of people destined to develop alzheimer's, and easily identifiable with a simple genetic test-- presented a unique scientific opportunity to test whether it's possible to

and maybe all, alzheimer's disease before it starts. that part of the story, when we come back. ♪ ♪ good is in every blue diamond almond. and once good gets going, there's no stopping it.

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>> stahl: alzheimer's disease is the sixth leading cause of death in the united states. more than five million americans have alzheimer's right now, and

given the aging baby boomer population, that number is projected to nearly triple by mid-century. yet unlike many other leading killers, there is no effective treatment. an alzheimer's diagnosis is essentially a prescription for a slow descent into oblivion-- an inexorable loss of the memories, spatial skills, and ability to think that make us who we are. early-onset alzheimer's patients, like the hundreds of family members in colombia, are a tiny fraction of the whole, but to scientists, they could be everything-- because they are offering researchers something they have never had before-- a way to test whether intervening, years before people start having symptoms, might halt the disease in its tracks. answers are still years away, but with more than 1,000 americans developing alzheimer's every day, a way to prevent it cannot come soon enough.

the scene we witnessed in dr. pierre tariot's exam room at the banner alzheimer's institute in phoenix is one that plays out in neurologist's offices every day. >> pierre tariot: so if i asked you what city we're in right now, what would you say? >> norm: ( laughs ) uh, you know, right, i don't know at this moment. >> stahl: norm, age 72, has been diagnosed with alzheimer's-- the typical, late-in-life form so many of us fear. it begins with mild memory and thinking problems, and spirals into full-on dementia. >> tariot: who is that young lady over there? >> norm: betsy. >> tariot: betsy. and is she a friend? >> norm: yes. >> tariot: how do you know betsy? >> norm: because i've been loving her for a long time. >> tariot: okay. is she your sister? >> norm: a little t

>> tariot: uh-huh. is she your wife? >> norm: i don't think so. i think you're-- somebody. i wish i was, but-- >> stahl: they've been married 51 years. unlike early-onset alzheimer's, there's been no single gene identified that causes this. >> tariot: now touch your nose. >> stahl: no way to know who among us is destined to get it. what percentage of all people are going to get alzheimer's? >> tariot: 1% of us, 60 or older, will have a dementia like alzheimer's disease. but by the time you hit 85-- >> stahl: what percent? >> tariot: --that, that percentage is approaching 40-ish percent. >> norm: that's a dogan and these are gogans. >> tariot: alzheimer's disease has been called out by the world health organization as the coming pandemic of the west. we have to do something to put it behind us. >> claudia kas

>> stahl: but dr. claudiwaa lear and clinician at the university of california-irvine, says she's frustrated that she can't offer her patients any hope. >> kawas: i have to say, i've been doing this now for a third of a century. and when i started, i just never would have believed we would still not be closer than we are now to making a real difference. it has been a little disappointing. >> stahl: it hasn't been for lack of trying. kawas gave us a quick primer on the tell-tale signs of alzheimer's in the brain after autopsy. >> kawas: every place you see a brown spot, that is a senile amyloid plaque. in contrast, you see these black things that tend to be triangular shape. those are what we call neurofibrillary tangles. >> stahl: the relationship between plaques and tangles isn't completely understood. but because it's been shth

amyloid plaques build up in the brain before tangles, and years before patients develop symptoms, pharmaceutical companies have spent hundreds of millions of dollars since the early 2000s developing drugs to remove amyloid from the brain, and hundreds of millions more to test those drugs in patients like norm. of all the trials that have been done, what percent have succeeded? >> tariot: about 1%. >> stahl: in other words, a resounding failure. so what does that say, do you think? >> kawas: well, it says either amyloid is not the right thing to go after, or it says we need to remove it earlier on in the process, before it's made all the other things cascade after it. you know, if you give a polio vaccine once somebody has polio, you can understand why it doesn't work. >> stahl: you're saying that maybe those drugs haven't worked because the person already had alzheimer's? >> kawas: exactly.

enough, it might work. >> stahl: but how can you test drugs on people before they develop the disease, when you don't know who among us is going to get it? dr. tariot and the executive director at the banner alzheimers institute, dr. eric reiman, realized there was a place where you could know who was going to get alzheimer's-- antioquia. >> kosik: and that's when my phone began to ring. >> stahl: by then, ken kosik had been studying the colombian extended family for 15 years. >> kosik: received a call from the people at banner. and they said, you know, "you have this family. we know when they're going to get it. we know who's going to get it. can we start treating before the disease strikes?" >> stahl: kosik connected tariot and reiman with dr. lopera, who by that time had identified hundreds of people who carried the gene mutation, guaranteeing that they would be struck with alzheimer's in the prime of their lives.

reiman and tariot traveled to medellin and met with both healthy and sick members of the extended family. is this particular family, in the world-- extraordinary? >> tariot: there's nothing else like it. the idea that there's this concentration within roughly 100 miles of each other is-- just an extraordinary-- phenomenon. >> stahl: and a perfect scientific laboratory. to lay the groundwork for a large clinical trial, banner flew a group of extended family members from medellin to phoenix for pet scans. one goal: to compare the brains of those with and without the mutation, years before any memory loss began, when they were in their 30s. dr. reiman showed us the results. >> eric reiman: this is somebody who doesn't have the gene. they have no plaques in the brain. >> stahl: but m

family with the mutation, it was a different story. >> reiman: extensive amyloid deposition in the brain. >> stahl: that's the red. >> reiman: red is more amyloid. but yellow is also amyloid. >> stahl: this brain had even more. the images showed that amyloid plaques build up in the brain more than a decade before memory loss begins. so if a drug could remove that red and yellow, maybe the disease could be prevented. banner developed a plan for a multi-million dollar drug trial, and convened a meeting with leading scientists, pharmaceutical companies, and representatives of the n.i.h. >> tariot: the end of the meeting, each scientist was allowed to say one closing thought. and francisco had the last word. >> stahl: lopera? >> tariot: and he paused a long time. and you could hear a pin drop in the room. >> lopera: i said to them, "we-- the families are waiting for you." >> stahl: "they're waiting for you."

when, you know, the goose bumpsy have to make this work. we really do." >> stahl: and they did. with a commitment of $15 million from n.i.h., another $15 million from philanthropists, and the rest from drug company genentech, the trial-- on an immunotherapy drug to remove amyloid plaque-- enrolled its first patient three years ago, and they've been enrolling more people ever since. >> freddie: they told me about the study and i said yes. i'll go right away, and anything that you need it, i am here. >> stahl: freddie and all his siblings signed up. the plan is to enroll a total of 300 members of the extended family who are healthy and have no memory loss yet; 200 who have the mutation; and another 100 who don't. that way, no one will learn their genetic status just by being accepted into the study. of the 200 with the mutation,

half will get injections of the drug; the other half will be injected with a harmless placebo. the study is double-blind: neither patients nor investigators will know who's getting what. they have to come in every two weeks, for at least five years, long enough to see whether the group taking the drug does better than the group taking placebo. final results aren't expected until 2021. is this the first time in all these years of seeing these patients that you can actually offer them-- hope? >> lopera: yes, this is the first time. because in the past we only offer them education-- better quality of life, but no hope to have a solution. and now they have hope, a big hope. >> stahl: what would be the best outcome? >> tariot: nobody who receives the immunotherapy experiences any worsening of their thinking

or memory ability. doesn't change at all. doesn't decline. that would be fabulous. that's a stretch goal. >> stahl: and that would be just the beginning. >> kawas: if it makes a difference for them, i think there's a reasonable chance it could make a difference for all the rest of the people who get alzheimer's disease. >> stahl: and that of course is the ultimate goal: to help prevent the late-in-life form of alzheimer's that we're all susceptible to. the hope is that one day, every one of us could be screened and when necessary, treated, before problems begin. >> kawas: it might be the case that, just like when you go to your doctor to get your cholesterol checked in your blood to see if you need drugs to lower your cholesterol, you would go, and get an amyloid pet scan, and it would be part of-- >> stahl: routine. >> kawas: --routine prevention. >> stahl: what if the drug removes the amyloid, and they still get the disease? >> kawas: i think that'll mean that there are otherng

amyloid. >> stahl: but will you say that the drug test was successful? >> kawas: hard as this is to say, yes. i think that we need to know the answer. >> stahl: the answer to whether the field's focus on amyloid plaque removal for the last 15 years has been a failure. if this test doesn't work, they will at least know they need to go in a different direction. you know, victor, all the other drug trials that have gone on for years have all failed. >> victor ( translated ): yes. >> stahl: you know that. >> victor ( translated ): but this is going to be the exception. this is the exception! ( laughs ) >> stahl: if it does work, this saves this community. >> kosik: wouldn't that be amazing? >> stahl: that would be amazing. >> kosik: to me, i am always impressed that these families that come from such a remote area of the world, have the

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network. get this amazing offer: 150 meg internet with equal upload and download speeds, tv and phone for just $79.99 per month for the first year. cable can't offer internet speeds this fast at a price this good, only fios can. >> anderson cooper: the eiger in the swiss alps is one of the most forbidding mountains in the world. locals call it "the ogre." and for more than a century, this monster of a mountain has attracted thrill-seekers eager to risk their lives on its nearly vertical slopes. more than 60 climbers have frozen or fallen to their deaths. as we first reported in 2015, a new breed of daredevil is taking on the eiger-- not by climbing up the mountain, but by plunging down it.

of planning, a new kind of descent was about to be attempted, we went to switzerland to see firsthand something no one had ever tried before. at 13,000 feet, the icy summit of the eiger is too steep and rocky to simply ski down... >> j.t. holmes: you ready? >> cooper: ...so j.t. holmes is training in three extreme sports, to rocket down more of the eiger than anyone ever has. right now, he is practicing one of those sports, speed riding, on a nearby mountain slope, with his friend and cameraman, valentin delluc. to speed ride, j.t. is using skis, but he's also attached to a glider-like parachute called a speed wing. it allows him to soar over rocks and ledges impossible to ski. >> holmes: you're capable of transitioning in and out of flight at will. >> cooper: so you'ot

flying... and then you're skiing a little bit more. >> holmes: exactly. >> cooper: but speed riding will only take j.t. so far down the eiger. he'll also ski off a cliff, and then free-fall the rest of the way, all in one long, non-stop, breathtaking ride. >> holmes: three sports, one run. and they're my three favorite sports, so... >> cooper: these are the three things you love? >> holmes: yeah. these are three of the things that i love. >> cooper: j.t. needs perfect conditions for this dangerous descent, and so far, he hasn't been lucky. weather on the eiger is unpredictable. fierce winds whip the slopes and change direction dramatically. j.t. checks the eiger every day to see if he can finally head to the summit. the past two years, he's had to cancel plans because wind blew the snow off the top of the mountain. today, the conditions are not right? >> holmes: well, yeah, today you can't even see the top of the eiger.

so, first of all, you couldn't lonhave youopter up there. been planning this? >> holmes: you know, the first kind of thoughts of it were upwards of six years ago, but really focused on it for three. >> cooper: why has it taken so long? >> holmes: you'd be putting your life, you know, in unnecessary risk. so i need the right day. >> cooper: j.t. is well aware of the risk. he started out as a professional skier-- the steeper the slope, the better. >> j.t. holmes: ready, set, go! >> cooper: now, at 36, he makes a living through endorsements and filming his remarkable feats. when we first met him seven years ago in norway, he and his daredevil friends were pioneering the use of wingsuits, jumping off mountains and flying at more than 100 miles an hour. but in the last several years, a number of j.t.'s friends and acquaintances have died in wingsuit accidents. eiliv ruud, who was flying with j.t. in norway, was killed in 2012 when he struck a cliff and fell 1,000 feet.

j.t. won't be wingsuit-flying off the eiger. the most dangerous part of his descent will be after he finishes speed riding, when he tries to jettison his skis and free-fall down the rest of the mountain. to practice, he makes base jumps without skis off a tiny, slippery piece of rock he calls "the mushroom." >> holmes: i stepped off the helicopter onto the mushroom, and that was fine. i had a good grip. but then i took another step and there was this really thin ice layer. yeah, it feels a little more uneven than i remember it. >> cooper: he's off. he falls for about 20 seconds, accelerating to 110 miles an hour before opening his parachute. he's starting right toward us. parachute is open. it's a white parachute-- he's red. that was amazing.

>> holmes: ( laughs ) scary. >> cooper: when j.t. jumps off the cliff on the eiger, he'll have his skis on. properly releasing them is critical. what's the danger if you can't get the skis off? >> holmes: you're at risk of an unstable parachute deployment or a snag. >> cooper: so, the biggest danger is that the ski is going to get tangled up in the parachute? >> holmes: that's the risk. >> cooper: that risk is foremost in his mind because of what happened to his best friend, shane mcconkey. in 2007, j.t. and shane started skiing off mountains, dropping their skis, and then flying away in wingsuits. it was a dangerous combination they found thrilling. >> shane mcconkey: oh, yeah, another wingsuit ski base. here we go. >> cooper: but on this jump in italy in 2009, shane mcconkey's ski release mechanism jammed. he couldn't get his skis to come off. he crashed into the ground at high speed, and was killed instantly. that's how he died, his skis didn't come off? >> holmes: he couldn't get his skis off, strule

wingsuit, and... and crashed. >> cooper: when j.t. is training at the eiger, he wears a t-shirt with a funny picture of shane on it. >> holmes: this eiger descent... >> cooper: without his old friend there to help him, he has turned to new friends. martin schurmann is an experienced swiss mountain guide. >> martin schurmann: it can change very quickly from good conditions to really nasty. >> cooper: it can turn bad very quickly? >> schurmann: oh, yeah. and then, you're in trouble. >> cooper: one wrong step, and you can plunge off... >> schurmann: you're... you're gone. >> cooper: martin and j.t. are cautious and methodical, making numerous trips up the eiger to plan, in advance, every part of the complex descent, particularly this spot where j.t. will jump, jettison his skis, and begin to free-fall. you're standing there on the top of the mountain, what goes through your mind? >> holmes: there's two mindsets, you know? there's the... there's the evel knievel, which is kind of kamikaze, and "who knows how it's going to work out?" and "will you hit the landing ramp or not?" and then, there's the james bond.

and bond is composed and dialedf gear which he developed with "q" to, you know, outwit hisopnentsf tremendous things, and... >> cooper: which one are you? >> holmes: i'm bond. ( laughs ) >> cooper: after days of waiting, and years of false starts and cancelled attempts, on this visit in april, the weather on the mountain suddenly clears. j.t. decides the time is right. he and his team take a chopper to the eiger summit. >> holmes: i'm checking for landmarks on the way up and kind of confirming my line, my path of descent. >> cooper: so you already have a path of descent in your mind? >> holmes: it's something that's been memorized. >> cooper: the eiger may be a monster of a mountain, but up close, the summit is shockingly small. here, there is no room for error, no room for the helicopter. it's not big enough for the helicopter to land? >> holmes: no, it... it does what we call a tow-in, where it just puts its nose into the

and it just hovers there. >> cooper: how big is the... the area that you're standing on at the top? >> holmes: the... the top of the eiger is pretty small. it's... there is no flat spot. you know, workable space is... three ping-pong tables. >> cooper: three ping-pong tables? >> holmes: yeah. >> cooper: that's it? >> holmes: something like that, yeah. >> cooper: a mistake here, one wrong step at 13,000 feet could cost them their lives. j.t. and his team work for almost an hour. wearing crampons on their ski boots, they dig trenches with ice axes so they won't fall down the nearly vertical slope. the surface is jagged ice, not powdery snow, and it can easily rip the speed wings. >> holmes: i don't like how those things grab the lines. >> cooper: they file down the sharp pieces of ice so they won't snag the speed wing lines. but the wind kicks up and they have to quickly reposition them. j.t. decides it's now or never. >> holmes: okay, you're good? >> valentin delluc: yeah.

>> holmes: okay, three, two, one. go! >> cooper: j.t. launches off the summit. champion speed rider valentin delluc quickly follows, videotaping for us with a camera on his helmet. the ride of a lifetime has begun. >> holmes: that's when you turn your skis downhill. now, doing that, that's very committing. because, you know, you point your skis down the eiger, you're probably not going to stop till the bottom. >> cooper: one way or the other. >> holmes: one way or the other. >> cooper: j.t. uses the speed wing for much of the descent, flying over outcroppings of rock and icy slopes too steep to ski. he reaches an open slope on the eiger's western flank and lands. he cuts loose his speed wing so it won't slow him down. now, he relies solely on his skis and skill. >> holmes: it's black diamond skiing. you're in a really cool place where few pele

really, what you're going to try to do is just gather as much speed as possible and just propel yourself off the cliff. >> cooper: the cliff he'll ski off is coming up fast. this is the most dangerous part of j.t.'s descent. there is no stopping. he completes a double-back flip to stabilize himself, releases his skis, then free-falls. his nylon suit is aerodynamically designed, propelling him forward, so he doesn't crash into any rock ledges. he falls nearly 2,000 feet, finally opening his parachute... >> holmes: whoo-hoo! yeah! yeah, buddy! whoo-hoo! whoa! >> cooper: he drifts safely to the ground, landing more than a mile below the eiger summit. >> holmes: whoa, dude! whoa! oh, my god, that was pretty intense, man.

nailed it. >> cooper: nailed it? >> holmes: nailed it. i don't have words to describe how it felt to go and pull that off after so much time. and, you know, it's kind of a twisted style of having fun, but it was really fun. if you're too fast, it's a little just kind of scary. >> cooper: we assumed j.t. would call it a day after making it down the eiger in one piece. but after catching his breath and repacking his equipment, he decides to head back to the summit and do the whole run down the mountain once again. >> holmes: three, two, one, go! >> cooper: his speed ride off the summit goes perfectly. he flies over trouble spots, and builds up speed as he approaches the cliff edge. but when he tries to release his skis, one of them won't come off. this is whil

j.iend, shane mcconkey. agonizing seconds, then finally manages to drop the ski. it's a close call, but it doesn't seem to stop him from enjoying the rest of the ride. could you give it up? >> holmes: i believe that i could. because i don't feel that i'm-- you know, addicted to this sort of... type of thing, this adrenaline, or this sort of high-risk activity. >> cooper: you're not an adrenaline junkie, you don't think? >> holmes: absolutely not. i... i prefer "adrenaline enthusiast." ( laughter ) i truly believe that i don't have to do this. and i truly believe that i enjoy doing this and... >> cooper: that's pretty clear. >> holmes: the day will come when i tone it down significantly. >> cooper: but that day is not here yet? >> holmes: it's not today. >> how'd they get those

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>> stahl: now, an update on a story we called "water." as we first reported at the height of the california drought, the deep aquifers of fresh groundwater in the state's central valley are depleting faster than they can be replenished. as the groundwater deep below the agricultural valley is pumped out, the ground sinks. it's called subsidence, and can wreak havoc on roads, bridges and aqueducts.

talking about groundwater. >> stahl: back in 2014, we asked university of california-irvine professor jay famiglietti about reversing the process. now, when they take water out, and it rains-- >> famiglietti: yes. >> stahl: --doesn't the water go back down there? >> famiglietti: these aquifers near the surface, they can sometimes be replenished very quickly. if we're talking about a deeper aquifer, that could take tens or hundreds of years to recharge. >> stahl: in spite of months of rain this winter, the groundwater crisis is far from over. a new nasa report says the central valley is continuing to sink. in some places, the ground has dropped as much as 20 inches since may, 2015. i'm lesley stahl. we'll be back next week with a brand new edition of "60 minutes." before i had the shooting, burning, pins and needles of diabetic nerve pain these feet... jumped into city life as a kid...

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