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Boston Globe
29-06-2025
- Health
- Boston Globe
Max Fink, champion of electroconvulsive therapy, dies at 102
'Many severely depressed patients are maintained for weeks, for months and even years on antidepressant drugs,' he told a conference on depression in Philadelphia in 1988. 'Are we not unfair when we do this to our patients when ECT remains an active and excellent treatment?' He first witnessed the use of ECT in 1952, on his first day as a neurology and psychiatry resident at Hillside Hospital (now Zucker Hillside Hospital, a part of Northwell) in the New York City borough of Queens. One by one, he watched as five patients — under restraints, with rubber bite-blocks in their mouths and electrodes applied to their temples — received enough electrical current to induce a grand mal seizure. Get Starting Point A guide through the most important stories of the morning, delivered Monday through Friday. Enter Email Sign Up 'Observing a full grand mal seizure in each patient jarred me,' he wrote in 2017 in an unpublished memoir for Stony Brook University in New York, where he worked for many years. But over the next few months, he said, 'I had learned that ECT effectively reduced suicide thoughts, relieved negativism, aggression, depressed and manic moods. Of the hospital populations, the patients treated with electroshock improved the most.' Advertisement Although Dr. Fink was convinced of ECT's positive effects, others in the psychiatric profession weren't. Advertisement 'Max was trained in an era when the main theme of psychiatry was orthodox Freudian psychoanalysis,' said Dr. Charles Nemeroff, chair of the department of psychiatry and behavioral sciences at Dell Medical School at the University of Texas at Austin, who collaborated with Dr. Fink on a paper about ECT. 'But he was part of a small group of academic psychiatrists who recognized that severe depression and schizophrenia were brain diseases.' Dr. Fink, author of many scientific articles about ECT and founding editor of the quarterly Convulsive Therapy (now The Journal of ECT), faced opposition from other doctors, Scientologists and protesters at conferences. 'We had a problem getting this accepted by the public, and I was protested at meetings across the United States and Europe,' he said in 2019, when he received an award for lifetime achievement from the Institute of Living, a psychiatric center in Hartford, Connecticut. Some opponents of ECT said it was ineffective or left people with memory loss and trauma. Others described it as a brutal practice, an enduring view reinforced by the 1975 film 'One Flew Over the Cuckoo's Nest,' in which a patient at a psychiatric hospital, played by Jack Nicholson, undergoes ECT without anesthesia as a punishment for his rebelliousness. In his book 'Electroshock: Healing Mental Illness' (1999), Dr. Fink wrote that 'the picture of a pleading patient being dragged to a treatment room, where he is forcibly administered electric currents, as his jaw clenches, his back arches, his body shakes, all the while he is held down by burly attendants, may be dramatic but it is wholly false. Patients aren't coerced into treatment.' Advertisement Critics of Dr. Fink's passionate support of ECT said he downplayed the risks, including memory loss and cognitive impairment. 'One of Fink's books describes going to get ECT as no more significant than going to the dentist, which I thought was pretty glib,' said Jonathan Sadowsky, author of 'Electroconvulsive Therapy in America: The Anatomy of a Medical Controversy' (2017). 'And there are a lot of scientific studies about memory loss from ECT.' Dr. Fink insisted that antidepressants and antipsychotics could cause more damage, including memory loss, than ECT did. Nemeroff — who described Dr. Fink as 'an irascible, dominant figure' as well as 'the world's leader in electroconvulsive therapy' — said Dr. Fink's focus was firmly on the effectiveness of the treatment. 'He was a zealot, no question about it,' Nemeroff said. 'He thought ECT was a panacea.' ECT's effectiveness in treating serious mental illness has been recognized by, among others, the American Psychiatric Association, the American Medical Association and the National Institute of Mental Health. But although it is useful for treating serious mental illness, it does not prevent recurrence. Consequently, most people treated with ECT need to continue the procedure or use another type of maintenance treatment. Maximilian Fink was born Jan. 16, 1923, in Vienna. His father, Julius, was a doctor in general practice who was trained in radiology. His mother, Bronislava (Lowenthal) Fink, known as Bronia, left medical school at the University of Vienna after three years; later, in the mid-1950s, she became a social worker. Max and his mother immigrated to the United States in 1924, joining his father there. (His brother, Sidney, who was born in 1927, also became a doctor, specializing in gastroenterology.) Advertisement As a boy, Max developed X-ray film in his father's office. He started college at 16, at New York University's University Heights campus in the Bronx, and graduated in three years, with a bachelor's degree in biology, in 1942. After earning his medical degree at the NYU College of Medicine (now the Grossman School of Medicine) three years later and interning at Morrisania Hospital in the Bronx, he served in the Army from 1946-47, attending the School of Military Neuropsychiatry. After his discharge from the Army, he worked as a surgeon on three passenger ships. From 1948-53, Dr. Fink served as a resident at Montefiore, Bellevue, Hillside and Mount Sinai hospitals. From 1954-62, he ran the division of experimental psychiatry at Hillside. He later served as director of the Missouri Institute of Psychiatry and as a professor of psychiatry at New York Medical College. From 1972-97, he was a professor of psychiatry and neurology at Stony Brook University, where he later became a professor emeritus. Dr. Fink's research had unusual breadth. He showed early in his research career that penicillin, still an experimental drug, was better than sulfa for patients with pleural cavity infections. He studied the pharmacology of LSD, marijuana and opioids; used electroencephalograms, or EEG tests, to measure the changes caused by electroshock, insulin coma and psychoactive drugs; and wrote about the effects of changing the placements of electrodes in ECT. He was also among the scholars who successfully argued for the recognition of catatonia — a syndrome characterized by irregular movements and immobility — by the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, or DSM, as separate from schizophrenia. Advertisement Dr. Fink's other books include 'Convulsive Therapy: Theory and Practice' (1979), 'Electroshock: Restoring the Mind' (1999), 'Ethics in Electroconvulsive Therapy' (2004, with Jan-Otto Ottosson) and 'The Madness of Fear: A History of Catatonia' (2018, with Edward Shorter). He wrote or collaborated on about 800 scientific papers, including one on catatonia that was accepted for publication by Journal of the Academy of Consultation-Liaison Psychiatry shortly before his death. In addition to his son, Dr. Fink is survived by two daughters, Rachel and Linda, and four grandchildren. His wife, Martha (Gross) Fink, died in 2016. In a 2018 interview for Stony Brook, Dr. Fink reflected on his career and its influence. 'I think I was very lucky,' he said. 'However I worked it out, I was always able to find projects and kept busy.' He later added: 'We've saved lives knowingly. It's been a very interesting life.' This article originally appeared in
CBC
21-06-2025
- Entertainment
- CBC
How music fuelled, and was fuelled by, the No Kings protests
If you were online last week, you probably saw footage from the No Kings protests. The gigantic demonstration against U.S. President Donald Trump took place across the United States and portions of Canada — but was connected by one prevailing aspect: music. There was Les Miserables 's rousing Do You Hear the People Sing?, sung by a crowd in Auburn, Calif. There was Bella Ciao — a lesser-known piece strongly linked to the Italian anti-fascist movement of the 1940s — performed by a brass band to drown out counter-protesters in Atlanta. And there was a raft of other music, new and old, by musicians looking to tie themselves to the No Kings demonstrations. "There's a fascinating mixture of new music as well as old songs being brought back into the mix," said Benjamin Tausig, an associate professor of critical music studies at New York's Stony Brook University. It's "inspiring people in the context of protest at this moment." That's because of music's inextricable connection to — and ability to inspire — political action, he says. When used in a specific way, some songs can become almost irresistible calls to action. And the beginning of protest movements often fundamentally alter both what music we are exposed to, and what music artists choose to release, says Tausig. But when it comes to protest music, not all songs are created equal, says Noriko Manabe, chair of Indiana University's department of music theory and co-editor of the upcoming Oxford Handbook of Protest Music. And the way that we engage with that music, she says, speaks to why some of the most widespread songs used at recent protests have been older, less traditionally popular tunes. Songs like Bella Ciao, Do You Hear the People Sing? or even The Star-Spangled Banner — which had moments of its own at the protests — tend to be of a specific type, she says. They are "participatory" versus "presentational." While presentational music is meant for one skilled performer, participatory music, like other iconic protest songs such as We Shall Overcome, is not. It's "more repetitive so that people can more easily join in," she said. "Whether or not they're virtuosic is actually not the point. The point is to get as many people involved as possible." And with participation, she says, comes ideology. "The idea of moving vocal cords and muscles together, where you have to listen to other people and feel their movements — " Manabe said. "Just the act of voicing it itself makes you feel that this is part of your belief system." Co-opted music Tausig says that participatory aspect can even eclipse what the song is actually about. Historically, he says, the most popular protest songs tend to be co-opted, with no direct or apparent connection to any political movement. That's because the cultural iconography associated with them tends to hold more weight. Kendrick Lamar and Beyonce became very important in the Black Lives Matter movement, for example. "Their songs didn't even specifically have to address Black Lives Matter to still become really effective at mobilizing people," he said. Some songs are even adopted by movements they seem to be explicitly against. For example, Tausig notes, Bruce Springsteen's Born in the U.S.A., about a disillusioned Vietnam War veteran, was famously referenced in a 1984 campaign speech by U.S. President Ronald Reagan. More recently, Creedence Clearwater Revival's draft-dodging ditty Fortunate Son was played at a military parade, prompting speculation over whether it was either a form of protest or due to a common misinterpretation of the song's meaning. In both cases, he says, what the song appeared to represent was more important than what it actually said. A long history But even still, songs being used by both sides of a political debate have a long history in protest music, Manabe says. Going back to Britain in the 1600s, warring factions of Royalists and Parliamentarians would disseminate "broadsheets": large pieces of paper with often-rhyming lyrics in support of their side. But to make sure they were easy to remember, they would be set to well-known tunes. That resulted in "contrafacta": each side singing the same "song," though with completely different words supporting completely different ideals. That phenomenon continues to today. Manabe points to protests in Hong Kong in 2014, when both defenders and critics of the democracy movement used Do You Hear the People Sing? Meanwhile, rock, country, EDM and hip-hop artists seemingly jumped on the bandwagon to release or re-release their political music, creating musical touchstones and viral moments in the protests themselves. Arkansas folk musician Jesse Welles, who crafted social media fame by releasing songs tied to the news, debuted a new track No Kings which has already racked up over 150,000 views on YouTube. In Salt Lake City, EDM musician Subtronics added a "No Kings" section to his performance, gaining over two million views on TikTok. Meanwhile, the Dropkick Murphys, Soundgarden and Pavement have all made posts connecting their music, old and new, to the protests — along with Canadian Grammy-winner Allison Russell, lesser known blues, country and bluegrass musicians and even an AI hip-hop track simply titled No Kings that's amassed over 750,000 views on YouTube. "Expressing dissent or resistance to authority through nonviolence is one of the most potent weapons that we can wield," said Canadian musician Jordan Benjamin (known artistically as Grandson) who also released new music directly tied to the No Kings protests. From an artist's standpoint, the sudden swell makes sense: given the cyclical nature of pop culture, music that may have seemed old-fashioned or out of step has suddenly become more in demand. And at the beginning of such changes in direction, Tausig says, which songs will define that movement becomes an important question.
Yahoo
19-06-2025
- Science
- Yahoo
Scientists make revolutionary breakthrough that could transform energy storage: 'Truly a game-changer'
Tech Xplore recently shared how a group of scientists used AI to crack part of the code for cheaper, safer energy storage. Plus, they did it with a water-based battery that could one day cut pollution and lower energy bills. "AI is an important tool that can facilitate the advancement of science," Esther Takeuchi, chair of the Interdisciplinary Science Department at Brookhaven Lab and William and Jane Knapp Chair in Energy and the Environment at Stony Brook University, told Tech Xplore. "The research done by this team provides an example of the insights that can be gained by combining experiment and theory enhanced by the use of AI." In their study, published in PRX Energy, researchers were trying to understand why zinc-ion batteries run better when filled with a super-salty solution. To find out, they trained an AI model to simulate what happens inside the battery at an atomic level—something a standard computer would've needed years to do. "This work demonstrates the great impact artificial intelligence and machine learning can have for understanding the chemistry of materials and provides guidelines for optimizing battery electrolytes," lead researcher Deyu Lu told Tech Xplore. Turns out, the salt (zinc chloride) keeps water molecules from splitting apart into hydrogen gas, a common problem that usually wrecks performance. In this setup, the water molecules stop clinging to each other. That stabilizes the battery and keeps it running as intended. The high salt concentration also helps zinc ions move more easily between battery parts. That cuts down on energy waste and delays. Zinc-ion batteries are cheaper and less toxic to make than lithium ones. They're nonflammable, run on widely available materials, and could be a better option for storing energy from solar panels or other affordable sources, especially during outages or times of high demand. Solar installation companies such as EnergySage may soon offer such products. While this tech won't replace lithium overnight, it could soon show up in grid storage and emergency systems. This means there will be less need for pollutant sources like gas and coal, and cleaner air for the people breathing it. AI helped speed things up, but it's not all upside. Models like this require a ton of computing power. Some of them burn through electricity and water faster than you'd think. Training just one large model can produce as much pollution as five gas-powered cars do over their lifetimes. Still, used carefully, tools like this could help solve real problems. If zinc batteries become easier to make and store, clean energy becomes easier to use. That's a win worth paying attention to. "AI/ML is truly a game-changer in the study of complex materials," Lu told Tech Xplore. Should the U.S. invest more in battery innovations? Absolutely Depends on the project We're investing enough We should invest less Click your choice to see results and speak your mind. Join our free newsletter for weekly updates on the latest innovations improving our lives and shaping our future, and don't miss this cool list of easy ways to help yourself while helping the planet.
Yahoo
18-06-2025
- Health
- Yahoo
How rogue jumping genes can spur Alzheimer's, ALS
Back in 2008, neurovirologist Renée Douville observed something weird in the brains of people who'd died of the movement disorder ALS: virus proteins. But these people hadn't caught any known virus. Instead, ancient genes originally from viruses, and still lurking within these patients' chromosomes, had awakened and started churning out viral proteins. Our genomes are littered with scraps of long-lost viruses, the descendants of viral infections often from millions of years ago. Most of these once-foreign DNA bits are a type called retrotransposons; they make up more than 40 percent of the human genome. Many retrotransposons seem to be harmless, most of the time. But Douville and others are pursuing the possibility that some reawakened retrotransposons may do serious damage: They can degrade nerve cells and fire up inflammation and may underlie some instances of Alzheimer's disease and ALS (amyotrophic lateral sclerosis, or Lou Gehrig's disease). The theory linking retrotransposons to neurodegenerative diseases — conditions in which nerve cells decline or die — is still developing; even its proponents, while optimistic, are cautious. 'It's not yet the consensus view,' says Josh Dubnau, a neurobiologist at the Renaissance School of Medicine at Stony Brook University in New York. And retrotransposons can't explain all cases of neurodegeneration. Yet evidence is building that they may underlie some cases. Now, after more than a decade of studying this possibility in human brain tissue, fruit flies and mice, researchers are putting their ideas to the ultimate test: clinical trials in people with ALS, Alzheimer's and related conditions. These trials, which borrow antiretroviral medications from the HIV pharmacopeia, have yielded preliminary but promising results. Meanwhile, scientists are still exploring how a viral reawakening becomes full-blown disease, a process that may be marked by what Dubnau and others call a 'retrotransposon storm.' A retrotransposon is a kind of 'jumping gene.' These pieces of DNA can (or once could) move around in the genome by either copying or removing themselves from one spot and then pasting themselves into a new spot. Retrotransposons are copy-and-pasters. Many retrotransposons are old companions: Some predate the evolution of Homo sapiens or even the split between plants and animals, Dubnau says. Their predecessors may have alternated between riding along stitched into a host chromosome and existing outside of it, he suggests. Some retrotransposons, after all that time, retain their ability to hop around human DNA. To do so, they copy themselves with the enzyme reverse transcriptase, which is also used by some viruses like HIV to copy RNA sequences into DNA. Once they're copied, the remnant viruses can pop into new locations on chromosomes. If it's terrifying to think of a genome littered with retroviral genes, some capable of bouncing around the genome, don't fret, says Douville, now at the University of Manitoba in Winnipeg. Remarkably, some retrotransposons have taken on helpful jobs, assisting the body with tasks like maintaining stem cells and development of the embryo and nervous system. And many retrotransposons are dormant or broken, and the cell has means to keep them (mostly) quiet. One technique is to stash them in DNA regions that are wound up so tight that the molecular machines needed to copy genes can't get near them. In essence, the cell shoves them into a closet and slams the door shut. But evidence is building that as people age, that closet door can creak open, letting retrotransposons spill out. Exactly what they do then isn't certain. Some scientists think it's not so much that they are jumping around and mutating DNA, but that their viralesque RNAs and proteins can screw up normal cellular activities. 'I think what's actually driving toxicity when transposons are activated is they're making all these factors that look like a virus to the cell,' says Bess Frost, a neurobiologist at Brown University in Providence, Rhode Island. The cell reacts, quite reasonably, with defensive inflammation, which is commonly associated with neurodegeneration. Retrotransposons also seem to team up with rogue proteins classically linked to neurodegeneration, damaging or killing nerve cells, and perhaps even setting off the disease in the first place. Scientists long suspected a link between viruses and ALS, which causes degeneration of the motor neurons that control movement. But the connection, when it was finally found, wasn't quite what anyone predicted. In the early 2000s, scientists reported that some people with ALS had the viral enzyme reverse transcriptase in their blood and, more rarely, spinal fluid. Some had as much reverse transcriptase as a person with an HIV infection. But at the time, says Dubnau, 'Nobody could find a virus.' Finally, Douville and colleagues discovered evidence for one of those leftover viruses, a kind of retrotransposon called HERV-K, in the brains of some people who had died of ALS. From there, scientists began to build a case linking jumping genes to ALS in people, lab animals and cells in dishes. A team reported in 2017 that numerous jumping genes had been activated in the brains of certain people with ALS. Douville's colleagues also documented damage inflicted by HERV-K: When they put a gene from the retrotransposon into mice, the animals' nerve cell projections shriveled and they exhibited ALS-like symptoms. As the scientists zeroed in on what might be waking up HERV-K, a familiar protein turned up. Called TDP-43, it had already been linked to ALS. But even before that, it was found to be involved in cells' responses to the retrovirus HIV. Scientists discovered in the 1990s that TDP-43 works in the cell's nucleus, where it hinders activation of HIV genes. It also regulates human genes there. But in the neurons of people with ALS or a related condition, frontotemporal dementia (FTD), TDP-43 departs the nucleus and goes on to form abnormal clumps in the cytoplasm. The globs have been associated with a number of neurodegenerative conditions and can spread from cell to cell. And when TDP-43 vacates the nucleus, it also creates a gap in gene regulation, throwing off the activity levels of many genes. TDP-43 gone bad is sufficient to cause neurodegeneration, but studies indicate its desertion of its nuclear role can also wake up retrotransposons. When TDP-43 leaves the nucleus, tightly coiled DNA next to certain retrotransposons starts to loosen up and unravel, a study of cells from the brains of people who died of ALS or FTD revealed. And researchers saw that in cultured cells, this loss of TDP-43 freed certain retrotransposons from their restraints. The closet door was now ajar, in other words, allowing the retrotransposons to jump out and around. Meanwhile, Dubnau and collaborators, were looking at data on TDP-43 and the genes it controls in rats, mice and people. They found that TDP-43 can naturally stick to the RNAs of a variety of jumping genes, suggesting a way that normal TPD-43 might continue to corral them, even if they've managed to get copied into RNA. That interaction was altered in people with FTD and in rodents with abnormally high or low amounts of TDP-43 — very much as if TDP-43 was unable to control the jumping genes anymore. The Dubnau group also turned to fruit flies. Both old age and the human TDP-43 gene caused retrotransposons in the fly brain to sneak out of the chromosomal closet, inducing brain cells to kill their neighbors and prompting neurodegeneration, the group reported in a series of papers from 2013 to 2023. Moreover, activation of certain retrotransposons also caused TDP-43 to clump together outside of the nucleus, creating a vicious cycle whereby TDP-43 and the retrotransposons reinforce each other's abnormal behaviors. Past a certain point, says Dubnau, 'It just takes off.' Based on the sum of all these findings, Dubnau suggests a possible way that ALS could develop: Normally, TDP-43 in the nucleus helps to repress retrotransposons. But if aging or some other disturbance causes TDP-43 to decamp, those once-silenced retrotransposons spring to life, producing virus-like RNAs and proteins. While the retrotransposons might induce disease on their own, by jumping into new DNA locations or spurring inflammation, they also act on TDP-43. They force more TDP-43 to leave the nucleus and clump in the cytoplasm, causing further neurodegeneration that spreads to neighboring cells. This isn't the cause of all kinds of ALS, which is a complex disorder with many possible triggers. But in a 2019 study of postmortem brain samples, Dubnau and colleagues found that about one in five people with ALS had high levels of retrotransposon activation and TDP-43 dysfunction. Stay in the KnowSign up for the Knowable Magazine newsletter today As that ALS story was developing, other scientists were pursuing a connection between retrotransposons and another toxic protein in neurodegeneration: the tau protein, which twists into unruly tangles in the brain cells of people with Alzheimer's disease. It affects retrotransposons because it, like TDP-43, plays a role in keeping retrotransposons quiet, says Frost. That maintenance is a downstream effect of tau's association with the cell's interior skeleton. That skeleton is physically linked to the nucleus's skeletal structure, which in turn anchors the tightly wound-up DNA that silences retrotransposons. When tau goes bad, it changes the structure of the cell's main skeleton, making it more rigid. Frost and colleagues found that this structural defect propagates all the way to the nuclear skeleton and the chromosomes, just like tightening the strands on one side of a net could change the shape of the other side. This structural effect can unlock the tightly wound bits of chromosome in fruit flies, which damages their neurons, Frost reported in 2014. By 2018, she'd shown that tau problems unleashed jumping genes in the flies. 'They were legitimately jumping,' she says, going from their original chromosomal locations to other ones in the fly's brain cells. And the jumping genes contributed to the death of nerve cells. Frost and colleagues also studied mammals — mice — and in 2022 they reported that retrotransposons were also activated in mice with dysfunctional tau. Meanwhile, Frost and others examined brain cells from people who'd died of tau-related diseases such as Alzheimer's, which also revealed activated retrotransposons. 'They were legitimately jumping.' — BESS FROST This awakening of retrotransposons appears to happen early in the disease, according to the work of another team published in 2022. In blood samples from people on their way to developing Alzheimer's disease, the copying of retrotransposon genes into RNAs spiked, creating a 'retrotransposon storm,' just before their symptoms got bad enough to be labeled Alzheimer's. This growing body of evidence suggests that reactivating once-quiet retrotransposons, whether via dysfunctional tau or TDP-43, can create havoc. A potential treatment quickly comes to mind: Since these retrotransposons are a lot like viruses, scientists reason that antiviral drugs could help. Handily, doctors already have medications that stymie retroviruses: Millions of people take antiretroviral drugs to keep HIV in check or prevent it from gaining a foothold in their cells. Indeed, multiple studies over several years have investigated drugs from the HIV treatment playbook that block the enzyme reverse transcriptase. And in cells, flies and mice the drugs have dialed down retrotransposon activity and neurodegeneration. These medications are well understood and generally safe, and are already in trials for neurodegenerative disease. For example, researchers have tested the safety of a 24-week antiretroviral course in 40 people with ALS. Not only did most people safely complete the trial, but the levels of HERV-K in their blood went down, and they seemed to have a delay in progression of their ALS symptoms, the researchers reported in 2019. Frost recently published results from a small trial in which 12 people with early Alzheimer's disease took a reverse transcriptase inhibitor for 24 weeks. Her main goal was to determine if the treatment was safe, and it was — but the researchers also observed a drop in signs of inflammation in the participants' spinal fluid. Both Dubnau and Frost serve on the scientific advisory board for Transposon Therapeutics, which tested its own reverse transcriptase inhibitor in 42 people with ALS and/or FTD. The company says the drug was tolerable and yielded signs of less neurodegeneration and inflammation, plus a delay in the inevitable worsening of symptoms. The company is planning a larger trial; it also plans to test its drug in people with ALS, Alzheimer's and a related tau-based disease, progressive supranuclear palsy. Neither Frost nor Dubnau, who together recently summarized the field for the Annual Review of Neuroscience, believes that antiretroviral drugs alone are the solution to transposon-fueled Alzheimer's or ALS. As Douville notes, the drugs were designed to act only on specific target enzymes — they won't do anything to other retrotransposon genes, RNAs or proteins, which could also spur nerve-damaging inflammation. Meanwhile, scientists are looking beyond ALS and Alzheimer's as evidence accumulates that retrotransposons may contribute to other neurodegenerative and inflammatory conditions, such as Parkinson's disease and multiple sclerosis. 'It's really picking up speed,' Frost says. This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.
Belfast Telegraph
13-06-2025
- Belfast Telegraph
Man (60s) arrested on suspicion of murder of Annie McCarrick 24 years ago ‘was known to her'
Ms McCarrick, originally from New York, disappeared without a trace on that dayAt the site of this morning's search in Clondalkin, gardaí moved in early to place metal hoardings around the front garden of the house Robin Schiller, Conor Feehan and Denise Calnan A man who was known to US woman Annie McCarrick has been arrested in Dublin on suspicion of her murder 24 years ago. Sources said that the suspect has led 'a normal life' in the three decades since the young woman went missing on March 26, 1993. The suspect was arrested at his home yesterday morning and was questioned on suspicion of her murder. A separate home in Clondalkin previously linked to the suspect, where his parents had lived, is also being examined. The man, aged in his 60s, was detained under the provisions of Section 4 of the Criminal Justice Act 1984 at a garda station in Dublin. A spokesperson said 'elements of that house and garden' would be searched and subject to both technical and forensic examinations. They stress that the current residents of this home are not connected in any way with Annie McCarrick or her disappearance. Ms McCarrick disappeared without trace on March 26, 1993, with the last confirmed sighting of her in Sandymount in Dublin. She was 26 years old at the time of her disappearance. She was an only child and originally from New York in the US. Ms McCarrick completed her third-level studies at St Patrick's College, Drumcondra, and at St Patrick's College, Maynooth, before returning to New York in 1991, where she completed her studies at Stony Brook University. She moved to Ireland to live permanently in January 1993 and settled into rental accommodation at St Cathryn's Court in Sandymount with two other tenants. The young woman had spoken to both her flatmates before they left separately to travel home for the weekend. Ms McCarrick invited friends to her apartment for dinner the following day — Saturday, March 27. She was also making plans for her mother Nancy's visit to Ireland on March 30. On the Sunday of that weekend, friends of Annie became concerned for her welfare. She was not at home on the Saturday when they called for dinner as invited. She had not turned up for work on the Saturday or on Sunday morning. A friend called to her apartment on the evening of Sunday, March 28, and spoke to Annie's two flatmates. Groceries Annie had bought on the morning of Friday, March 26, in Quinnsworth on Sandymount Road had been left unpacked in shopping bags. A receipt in the bags confirmed the date and time of purchase as 26/03/1993 at 11.02am. This is the last confirmed activity of Annie McCarrick. Ms McCarrick was reported missing by a friend at Irishtown Garda Station on the evening of Sunday, March 28. This missing person report was confirmed by her mother Nancy when she arrived in Dublin on Tuesday, March 30. The search for Annie McCarrick has continued since. At the site of the search, on Monastery Walk in Clondalkin, gardaí moved in early to place metal hoardings around the front garden of a house and parked a mini digger in the front garden. Other equipment including a concrete saw were also brought to the house. Members of the Garda Technical Bureau arrived at the scene at 10am, and a number of detectives could be seen going into and out of the property. News Catch Up - Thursday 12th June Neighbours said they were surprised and curious to see if the search would yield anything of evidential value that could progress the case. Because Ms McCarrick disappeared more than 30 years ago, many of the current residents of Monastery Walk were not living in the estate at the time. 'I was walking the dog this morning and I could see the hoarding being put up at the house, and I thought maybe the owners were getting building work done, but then I could see a few guys in suits arriving and talking with the men putting up the hoarding, and then garda vans and vehicles started to arrive,' said one neighbour. 'We didn't know what was happening but then we started to see the news reports. I hope they find something that would bring some answers to her family,' he added.
