Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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Jon Hamilton Antidepressant drugs that work in hours instead of weeks could be on the market within three years, researchers say. "We're getting closer and closer to having really, truly next-generation treatments that are better and quicker than existing ones," says Dr. Carlos Zarate, a researcher at the National Institute of Mental Health. The new drugs are based on the anesthetic ketamine, which is also a popular club drug known as Special K. Unlike current antidepressants, which can take weeks to work, ketamine-like drugs have an immediate effect. They also have helped people with depression who didn't respond to other medications. The drug that is furthest along is esketamine, a chemical variant of ketamine that has been designated a potential breakthrough by the Food and Drug Administration. Esketamine is poised to begin Phase 3 trials, and the drug's maker, Johnson & Johnson, plans to seek FDA approval in 2018. Ketamine, used as a tranquilizer for animals and as an anesthetic in humans, is also being tested as a treatment for depression. Another ketamine-like drug on the horizon is rapastinel. It has completed Phase 2 studies, which showed "rapid, substantial, and sustained reductions in depressive symptoms," according to the drug's maker, Naurex. "I think it's highly probable that we'll see some version of one of these treatments being approved in the relatively near future," says Dr. Gerard Sanacora, director of the Yale Depression Research Program. "In my mind it is the most exciting development in mood disorder treatment in the last 50 years." © 2015 NPR
Link ID: 20999 - Posted: 05.30.2015
Stacey Vanek Smith I'm in a booth with a computer program called Ellie. She's on a screen in front of me. Ellie was designed to diagnose post-traumatic stress disorder and depression, and when I get into the booth she starts asking me questions — about my family, my feelings, my biggest regrets. Emotions seem really messy and hard for a machine to understand. But Skip Rizzo, a psychologist who helped design Ellie, thought otherwise. When I answer Ellie's questions, she listens. But she doesn't process the words I'm saying. She analyzes my tone. A camera tracks every detail of my facial expressions. The doctor may see you now "Contrary to popular belief, depressed people smile as many times as non-depressed people," Rizzo says. "But their smiles are less robust and of less duration. It's almost like polite smiles rather than real, robust, coming from your inner-soul type of a smile." Ellie compares my smile to a database of soldiers who have returned from combat. Is my smile genuine? Is it forced? Ellie also listens for pauses. She watches to see whether I look off to the side or down. If I lean forward, she notices. All this analysis seems to work: In studies, Ellie could detect signs of PTSD and depression about as well as a large pool of psychologists. Jody Mitic served with the Canadian forces in Afghanistan. He lost both of his feet to a bomb. And Mitic remembers that Ellie's robot-ness helped him open up. "Ellie seemed to just be listening," Mitic says. "A lot of therapists, you can see it in their eyes, when you start talking about some of the grislier details of stuff that you might have seen or done, they are having a reaction." © 2015 NPR
Dan Sung A 10-year study has revealed a startling link between high levels of anxiety and an increased risk of death from liver disease. The research, carried out by scientists at the University of Edinburgh, took account for obvious sociological and physiological factors such as alcohol consumption, obesity, diabetes and class, but still the data pointed to a clear relationship between the psychological conditions of stress and depression and the physical health of the hepatic system. There were over 165,000 participants surveyed for mental distress. They were each tracked for over a decade during which time the causes of death for those who passed on were recorded and categorised. What was found was that those who’d scored highly for signs of depression and stress were far more likely to suffer fatal liver disease. “This study provides further evidence for the important links between mind and body, and of the damaging effects psychological distress can have on physical wellbeing,” said Dr Tom Russ of the Centre for Clinical Brain Sciences. The work did not uncover any reasons for direct cause and effect but is the first to identify such a link between mental states and liver damage. Previous research has described how psychological conditions can lead to increased risk of cardiovascular disease which, in turn, may develop into obesity, raised blood pressure and then eventually to liver failure but, with this methodology controlling for such factors, it appears that the link is more direct than was previously thought.
By Will Lippincott In January 2012, two weeks after my discharge from a psychiatric hospital in Connecticut, I made a plan to die. My week in an acute care unit that had me on a suicide watch had not diminished my pain. Back in New York, I stormed out of my therapist’s office and declared I wouldn’t return to the treatment I’d dutifully followed for three decades. Nothing was working, so what was the point? I fit the demographic profile of the American suicide — white, male and entering middle age with a history of depression. Suicide runs in families, research tells us, and it ran in mine. My father killed himself at age 49 in April 1990. A generation before, an aunt of his took her life; before her, there were others. Shame runs in families, too, and no one in mine talked much about mental illness. The first time I was hospitalized for wanting to kill myself, as a teenager, my dad visited me a few days in. I made an effort to greet him with a firm handshake; he shared a few jokes with me. Dad was visibly concerned and told me he loved me. Only after his suicide a few years later did I learn that he, too, had been hospitalized, for depression, when he was in his early 20s. Setting out to start my own life after college, I felt that suicide was a clear and present opportunity, one that glowed more brightly during my depressive episodes. But I had an ambitious plan to beat it. I’d be a performer: work hard, keep my goals in the line of sight at all times, and make as much money as I could. Professional success would be my first line of defense to keep hopelessness at bay. In parallel, I’d find excellent doctors and be a compliant patient, take my meds and show up for talk therapy. And for a long time, through my 20s and 30s, that plan worked. © 2015 The New York Times Company
Link ID: 20949 - Posted: 05.19.2015
Nick Davis Mood disorders such as depression are devastating to sufferers, and hugely costly to treat. The most severe form of depression, often called clinical depression or major depressive disorder (MDD), increases the person’s likelihood of suicide and contributes significantly to a person’s disability-adjusted life years (DALYs), a measure of quality of life taking into account periods of incapacity. The healthcare burden of MDD is large in most countries, especially when the person requires a stay in hospital. Putting these factors together, it’s clear we need to develop effective treatments to combat depression. The mechanisms of depressive disorders are not well understood, and it seems likely that there is no single cause. Most modern therapies use drugs that target neurotransmitters – the chemicals that carry signals between neurons. For example, the class of drugs known as SSRIs, or selective serotonin reuptake inhibitors, prevent the neurotransmitter serotonin from being reabsorbed by a neuron; this means that more serotonin is available to wash around between the nerve cells, and is more likely to activate cells in the brain networks that area affected in MDD. But SSRIs and other drugs are not a pharmacological ‘free lunch’. Drug treatments for depression are ineffective for many people, cause side-effects, and may lose their therapeutic effect over time. For these reasons, many researchers are searching for alternative treatments for MDD that overcome these problems, and are more effective or less unpleasant. One potential treatment involves the use of pulses of magnetic energy over the head to target the brain’s mood circuits. This technique, called transcranial magnetic stimulation (TMS), may potentially address some of the problems of pharmaceutical treatments, but we still don’t know exactly how it works, or how effective it will be in treating MDD. © 2015 Guardian News and Media Limited
Link ID: 20946 - Posted: 05.18.2015
John Crace After over a year working in Westminster as this paper’s parliamentary sketchwriter, I thought I had learned a thing or two about bearpits. That was before I agreed to second Prof Allan Young in speaking against the motion that “This House believes that the long-term use of psychiatric medications is causing more harm than good”. It turned out that politicians are almost models of decency compared to psychiatrists fighting their own corner. I had wondered why I had been invited. I have no scientific knowledge of the subject under discussion; all I had to offer was my own personal experience of living with episodes of depression and acute anxiety for more than 20 years. For me, a combination of medication and therapy has proved effective; not so effective as to prevent recurrences of these mental health problems all together, but effective enough for me to have managed them without having to return as an in-patient at the psychiatric hospital I wound up in 20 years earlier. I could perhaps have done more to look after myself, I suppose. I could have given up my Spurs season ticket. But apart from that … Having raised concerns about my credentials, I was assured that it was important to have a patient’s voice heard. I thought so, too. So I agreed. But on the way home from the debate last night, I did wonder if the reason I had been asked was because everyone else had turned them down. Things didn’t get off to a great start, when there was a pre-debate vote in the packed theatre at King’s College’s Institute of Psychiatry, Psychology and Neuroscience, which had apparently sold out within hours of the tickets being made available in March. 126 people – a mixture of mental health practitioners, students and members of the public – believed the motion to be correct; 28 abstained, and only 64 were on my side. © 2015 Guardian News and Media Limited
Link ID: 20936 - Posted: 05.16.2015
Haroon Siddique Long-term depression in people over 50 could more than double their risk of suffering a stroke, with the risk remaining significantly higher even after the depression allays, research suggests. The US study of more than 16,000 people, which documented 1,192 strokes, found that onset of recent depression was not associated with higher stroke risk, suggesting the damage is done by depressive symptoms accumulating over time. The study’s lead author, Paola Gilsanz, from Harvard University’s TH Chan School of Public Health, said: “Our findings suggest that depression may increase stroke risk over the long term. Looking at how changes in depressive symptoms over time may be associated with strokes allowed us to see if the risk of stroke increases after elevated depressive symptoms start or if risk goes away when depressive symptoms do. We were surprised that changes in depressive symptoms seem to take more than two years to protect against or elevate stroke risk.” The research, published on Wednesday in the Journal of the American Heart Association, used data from between 1998 and 2010 from the Health and Retirement Study, which interviews a panel of representative Americans aged over 50 every two years, on their depressive symptoms, history of stroke, and stroke risk factors. Gilsanz, with colleagues from universities in Washington, California and Minnesota, and Bronx Partners for Healthy Communities, found that people with high depressive symptoms at two consecutive interviews had a 114% higher risk of suffering a first stroke, compared with people without depression at either interview. Those who had depressive symptoms at one interview but not at the next had a 66% higher risk. © 2015 Guardian News and Media Limited
By Melissa Mancini, Many veterans are turning to marijuana to ease symptoms of post traumatic stress disorder, despite concerns from the medical community about how effective pot is at treating the condition. There are a "tremendous" number of testimonials from patients with post traumatic stress disorder who say dried cannabis helps them, but there is a lack of randomized, controlled trials, said Dr. Stewart Cameron, a family physician and professor at Dalhousie University's faculty of medicine. In September 2014, the College of Family Physicians of Canada released a document to help doctors decide how to use cannabis in their practices. "They strongly recommended that it not be used for PTSD," said Cameron. "They suggested it should be reserved as a third or fourth line agent in people who suffer certain types of pain." Veterans Affairs paid out $5.2 million for medical marijuana to veterans across Canada last year. Of that, $3.4 million went to veterans in Atlantic Canada. The department could not say which ailments the veterans are treating with marijuana, because Veterans Affairs doesn't track cannabis reimbursement by condition. Medical marijuana advocate Fabian Henry says most of the 500 veterans who visited his company last year were looking for authorization to use marijuana to help with post traumatic stress disorder. Henry's company, Marijuana for Trauma, connects veterans with physicians willing to authorize medical cannabis. The organization has helped hundreds of veterans fill out forms for medical pot reimbursement from Veterans Affairs Canada. Marijuana for Trauma calls cannabis "a natural choice medicine" and says it's "proven to be effective in 85 per cent of those who suffer with PTSD." But Canadian medical authorities are far from assigning such a high efficacy rate to the drug. ©2015 CBC/Radio-Canada.
Sarah Boseley Health editor Psychiatric drugs do more harm than good and the use of most antidepressants and dementia drugs could be virtually stopped without causing harm, an expert on clinical trials argues in a leading medical journal. The views expressed in a British Medical Journal debate by Peter Gøtzsche, professor and director of the Nordic Cochrane Centre in Denmark, are strongly opposed by many experts in mental health. However, others say the debate around the use of psychiatric drugs is important and acknowledge that there has been overuse of antipsychotics to quieten aggressive patients with dementia. Gøtzsche says more than half a million people over the age of 65 die as a result of the use of psychiatric drugs every year in the western world. “Their benefits would need to be colossal to justify this, but they are minimal,” he writes. He claims that trials carried out with funding from drug companies into the efficacy of psychiatric drugs have almost all been biased, because the patients involved have usually been on other medication first. They stop their drugs and often experience a withdrawal phase prior to starting the trial drug, which then appears to have a big benefit. He also claims that deaths from suicide in clinical trials are under-reported. In trials of the modern antidepressants fluoxetine and venlafaxine, says Gøtzsche, it takes only a few extra days for depression in the placebo group – given dummy pills – to lift as much as in the group given the drugs. He argues that there is spontaneous remission of the disease over time. © 2015 Guardian News and Media Limited
By Melissa Healy contact the reporter Schizophrenia is one of psychiatry's most puzzling afflictions, with a complex of symptoms that goes far beyond its hallmark hallucinations and delusional thinking. But new research has found connections among several of schizophrenia's peculiar collection of symptoms -- including agitation and memory problems -- and linked them to a single genetic variant among the hundreds thought to heighten risk of the disorder. The findings offer new insights into the molecular basis for schizophrenia and could lead to treatments for the disease that are more targeted and more comprehensive. Published Monday in the journal Nature Neuroscience, the study looks at how a gene variant called Arp2/3 contributes to psychosis, agitation and problems of short- and long-term memory. Mice that were genetically modified to lack the Arp2/3 gene variant showed all three symptoms (although to measure psychosis in mice, scientists looked instead for an abnormal startle response that is also seen in humans in the grips of psychosis). The study's authors, led by Duke University neurobiologist Scott Soderling, then dug below those behaviors to see whether brain abnormalities linked to such behaviors had anything in common. Mice that lacked the Arp2/3 gene variant, they discovered, had not only symptoms of schizophrenia, but also several of the underlying brain abnormalities most closely linked to psychosis, agitation and memory problems seen in those with schizophrenia.
Link ID: 20895 - Posted: 05.06.2015
|By Michele Solis An individual with obsessive-compulsive disorder (OCD) is overcome with an urge to engage in unproductive habits, such as excessive hand washing or lock checking. Though recognizing these behaviors as irrational, the person remains trapped in a cycle of life-disrupting compulsions. Previous studies found that OCD patients have abnormalities in two different brain systems—one that creates habits and one that plays a supervisory role. Yet whether the anomalies drive habit formation or are instead a consequence of doing an action over and over remained unclear. To resolve this question, a team at the University of Cambridge monitored brain activity while people were actually forming new habits. Lapses in supervision are to blame, the researchers reported in a study published online in December 2014 in the American Journal of Psychiatry. They scanned 37 people with OCD and 33 healthy control subjects while they learned to avoid a mild shock by pressing on a foot pedal. Pressing the pedal became a habit for everyone, but people with OCD continued to press even when the threat of shock was over. Those with OCD showed abnormal activity in the supervisory regions important for goal-directed behavior but not in those responsible for habit formation. The finding suggests that shoring up the goal-directed systems through cognitive training might help people with OCD. The growing understanding of OCD's roots in the brain may also help convince individuals to engage in standard habit-breaking treatments, which expose a person to a trigger but prevent his or her typical response. “It's hard for people to not perform an action that their whole body is telling them to do,” says first author Claire Gillan, now at New York University. “So if you have an awareness that the habit is just a biological slip, then it makes OCD a lot less scary and something you can eventually control.” © 2015 Scientific American
By Tina Hesman Saey People with depression have more mitochondrial DNA and shorter telomeres than nondepressed people do, an international team of researchers reports online April 23 in Current Biology. Mitochondria are organelles that produce energy for cells. Mitochondria seem to become inefficient under stress, the team found, so more mitochondria may be needed to produce enough energy. Telomeres are the DNA endcaps on chromosomes that prevent the genetic material from unraveling. Short telomeres are associated with shorter life spans. The altered DNA may reflect metabolic changes associated with depression, the researchers say. Experiments with mice showed that these DNA changes are brought on by stress or by stress hormones. Four weeks after scientists stopped stressing the mice, their mitochondrial and telomere DNA had returned to normal. Those results indicate that the molecular changes are reversible. Researchers also studied DNA from more than 11,000 people to learn whether past stress was responsible for the molecular changes seen in people with depression. Depression was associated with the DNA changes, but having a stressful life was not. For instance, people who had experienced childhood sexual abuse but were not depressed did not have statistically meaningful changes to their DNA compared with people who had no history of abuse. The findings suggest that stress can change DNA but many people can bounce back. Depressed people may have a harder time recovering from the molecular damage. © Society for Science & the Public 2000 - 2015.
By Smitha Mundasad Health reporter, BBC News A mindfulness-based therapy could offer a "new choice for millions of people" with recurrent depression, a Lancet report suggests. Scientists tested it against anti-depressant pills for people at risk of relapse and found it worked just as well. The therapy trains people to focus their minds and understand that negative thoughts may come and go. In England and Wales doctors are already encouraged to offer it. Patients who have had recurrent clinical depression are often prescribed long-term anti-depressant drugs to help prevent further episodes. And experts stress that drug therapy is still essential for many. In this study, UK scientists enrolled 212 people who were at risk of further depression on a course of mindfulness-based cognitive therapy (MBCT) while carefully reducing their medication. Patients took part in group sessions where they learned guided meditation and mindfulness skills. The therapy aimed to help people focus on the present, recognise any early warning signs of depression and respond to them in ways that did not trigger further reoccurrences. Researchers compared these results to 212 people who continued to take a full course of medication over two years. By the end of the study, a similar proportion of people had relapsed in both groups. And many in the MBCT group had been tapered off their medication. Scientists say these findings suggest MBCT could provide a much-needed alternative for people who cannot or do not wish to take long-term drugs. In their report, they conclude it "may be a new choice for millions of people with recurrent depression on repeat prescriptions." © 2015 BBC
By KATIE THOMAS Last fall, an article in the American Journal of Psychiatry caught the attention of specialists who treat borderline personality disorder, an intractable condition for which no approved drug treatment exists. The article seemed to offer a glimmer of hope: The antipsychotic drug Seroquel XR reduced some of the disorder’s worst symptoms in a significant number of patients. “It was an exciting development,” recalled Mark F. Lenzenweger, a professor at Binghamton University and Weill Cornell Medical College and an expert in borderline personality disorder. In the realm of clinical trials, however, reality is sometimes far messier than the tidy summaries in medical journals. A closer look at the Seroquel XR study shows just how complicated things can get when a clinical trial involves psychiatric disorders and has its roots in intersecting and sometimes competing interests: a drug company looking to hold onto sales of a best-selling drug, a prominent academic with strong ties to the pharmaceutical industry and a university under fire for failing to protect human study subjects. The trial was paid for by AstraZeneca, the maker of Seroquel XR, and was conducted by Dr. S. Charles Schulz, the head of psychiatry at the University of Minnesota. Two of the study participants were living in a residential treatment facility for sex offenders and may have lied about their diagnosis to qualify for the trial. One of those men slipped the drugs to unwitting treatment center residents and staff, an alarming development that nevertheless did not seem to ruffle the university oversight board that is charged with looking into such episodes. The University of Minnesota’s clinical trial practices are now under intense scrutiny. In February, a panel of outside experts excoriated the university for failing to properly oversee clinical trials and for paying inadequate attention to the protection of vulnerable subjects. The review, commissioned by the university after years of criticism of its research practices, singled out Dr. Schulz and his department of psychiatry, describing “a culture of fear” that pervaded the department. © 2015 The New York Times Company
Link ID: 20814 - Posted: 04.18.2015
Michaeleen Doucleff It began with anxiety and depression. A few months later, hallucinations appeared. Then the Texas man, in his 40s, couldn't feel the left side of his face. He thought the symptoms were because of a recent car accident. But the psychiatric problems got worse. And some doctors thought the man might have bipolar disorder. Cattle feeding practices have been changed in an effort to halt the spread of mad cow disease. Eventually, he couldn't walk or speak. He was hospitalized. And about 18 months after symptoms began, the man died. An autopsy confirmed what doctors had finally suspected: the human version of mad cow disease, called variant Creutzfeldt-Jakob disease.* The case, published Wednesday in the journal Emerging Infectious Diseases, is only the fourth one diagnosed in the U.S. In those previous cases, people caught the disease in another country. Right away the man's diagnosis raised a new question: How did a rare disease linked to contaminated beef in the U.K. more than a decade ago get to a Texas man? Back in the early '80s, British ranchers noticed some of their cows were dying of a strange neurological disease. The cows became aggressive. They couldn't walk. Eventually, scientists figured out the culprit. A rogue protein formed large clumps in the brain and spinal cord. Over time, the clumps spread throughout the brain and damaged tissue. © 2015 NPR
Link ID: 20812 - Posted: 04.18.2015
By ERICA GOODE He was described, in the immediate aftermath of the Germanwings crash, as a cheerful and careful pilot, a young man who had dreamed of flying since boyhood. But in the days since, it has seemed increasingly clear that Andreas Lubitz, 27, the plane’s co-pilot, was something far more sinister: the perpetrator of one of the worst mass murder-suicides in history. If what researchers have learned about such crimes is any indication, this notoriety may have been just what Mr. Lubitz wanted. The actions now attributed to Mr. Lubitz — taking 149 unsuspecting people with him to a horrifying death — seem in some ways unfathomable, and his full motives may never be fully understood. But studies over the last decades have begun to piece together characteristics that many who carry out such violence seem to share, among them a towering narcissism, a strong sense of grievance and a desire for infamy. Adam Lankford, an associate professor of criminal justice at the University of Alabama, said that in his research on mass killers who also took their own lives, he has found “a significant number of cases where they mention a desire for fame, glory or attention as a motive.” Before Adam Lanza, 20, the Sandy Hook Elementary School shooter, killed 20 children, six adults and himself in 2012, he wrote in an online forum, “Just look at how many fans you can find for all different types of mass murderers.” Robert Hawkins, 19, who committed suicide after killing eight people at a shopping mall in Omaha in 2007, left a note saying “I’m gonna be famous,” punctuating the sentence with an expletive. And Dylan Klebold, 17, of Columbine High School fame, bragged that the goal was to cause “the most deaths in U.S. history…we’re hoping. We’re hoping.” “Directors will be fighting over this story,” Mr. Klebold said in a video made before the massacre. © 2015 The New York Times Company
Arran Frood A psychedelic drink used for centuries in healing ceremonies is now attracting the attention of biomedical scientists as a possible treatment for depression. Researchers from Brazil last month published results from the first clinical test of a potential therapeutic benefit for ayahuasca, a South American plant-based brew1. Although the study included just six volunteers and no placebo group, the scientists say that the drink began to reduce depression in patients within hours, and the effect was still present after three weeks. They are now conducting larger studies that they hope will shore up their findings. The work forms part of a renaissance in studying the potential therapeutic benefits of psychedelic or recreational drugs — research that was largely banned or restricted worldwide half a century ago. Ketamine, which is used medically as an anaesthetic, has shown promise as a fast-acting antidepressant; psilocybin, a hallucinogen found in ‘magic mushrooms’, can help to alleviate anxiety in patients with advanced-stage cancer2; MDMA (ecstasy) can alleviate post-traumatic stress disorder; and patients who experience debilitating cluster headaches have reported that LSD eases their symptoms. Ayahuasca, a sacramental drink traditionally brewed from the bark of a jungle vine (Banisteriopsis caapi) and the leaves of a shrub (Psychotria viridis), contains ingredients that are illegal in most countries. But a booming ayahuasca industry has developed in South America, where its religious use is allowed, and where thousands of people each year head to rainforest retreats to sample its intense psychedelic insights. © 2015 Nature Publishing Group,
By Anne Skomorowsky Because Germanwings pilot Andreas Lubitz killed himself when he purposefully drove a plane carrying 149 other people into a mountain in the Alps, there has been an assumption that he suffered from “depression”—an assumption strengthened by the discovery of antidepressants in his home and reports that he had been treated in psychiatry and neurology clinics. Many patients and other interested parties are rightly concerned that Lubitz’s murderous behavior will further stigmatize the mentally ill. It is certainly true that stigma may lead those in need to avoid treatment. When I was a psychiatrist at an HIV clinic, I was baffled by the shame associated with a visit to see me. Patients at the clinic had advanced AIDS, often contracted through IV drug use or sex work, and many had unprotected sex despite their high viral loads. Some were on parole. Many had lost custody of their children. Many lived in notorious single-room occupancy housing and used cocaine daily. But these issues, somehow, were less embarrassing than the suggestion that they be evaluated by a psychiatrist. Even doctors invoke “depression” to explain anything a reasonable adult wouldn’t do. For my clinic patients, it was shameful to be mentally ill. But to engage in antisocial behavior as a way of life? Not so bad. I think my patients were on to something. Bad behavior—even suicidal behavior—is not the same as depression. It is a truism in psychiatry that depression is underdiagnosed. But as a psychiatrist confronted daily with “problem” patients in the general hospital where I work, I find that depression is also overdiagnosed. Even doctors invoke “depression” to explain anything a reasonable adult wouldn’t do. © 2014 The Slate Group LLC.
Link ID: 20736 - Posted: 03.31.2015
|By Roni Jacobson As intangible as they may seem, memories have a firm biological basis. According to textbook neuroscience, they form when neighboring brain cells send chemical communications across the synapses, or junctions, that connect them. Each time a memory is recalled, the connection is reactivated and strengthened. The idea that synapses store memories has dominated neuroscience for more than a century, but a new study by scientists at the University of California, Los Angeles, may fundamentally upend it: instead memories may reside inside brain cells. If supported, the work could have major implications for the treatment of post-traumatic stress disorder (PTSD), a condition marked by painfully vivid and intrusive memories. More than a decade ago scientists began investigating the drug propranolol for the treatment of PTSD. Propranolol was thought to prevent memories from forming by blocking production of proteins required for long-term storage. Unfortunately, the research quickly hit a snag. Unless administered immediately after the traumatic event, the treatment was ineffective. Lately researchers have been crafting a work-around: evidence suggests that when someone recalls a memory, the reactivated connection is not only strengthened but becomes temporarily susceptible to change, a process called memory reconsolidation. Administering propranolol (and perhaps also therapy, electrical stimulation and certain other drugs) during this window can enable scientists to block reconsolidation, wiping out the synapse on the spot. The possibility of purging recollections caught the eye of David Glanzman, a neurobiologist at U.C.L.A., who set out to study the process in Aplysia, a sluglike mollusk commonly used in neuroscience research. Glanzman and his team zapped Aplysia with mild electric shocks, creating a memory of the event expressed as new synapses in the brain. The scientists then transferred neurons from the mollusk into a petri dish and chemically triggered the memory of the shocks in them, quickly followed by a dose of propranolol. © 2015 Scientific American
By Gary Stix One of the most intriguing new areas of research in neuroscience has to do with the discovery that proteins involved with Alzheimer’s, Parkinson’s and other neurodegenerative illnesses can contort into the wrong shape. The misshapen molecules can spread throughout the brain in a manner akin to prion diseases—the most notorious of which is variant Creutzfeldt-Jakob disease, better known as Mad Cow. Misfolded proteins can lead to a buildup of cellular gunk that then causes damage inside or outside cells. If the process of misfolding observed in Alzheimer’s and Parkinson’s is similar to the one in Mad Cow, the next question is whether these misshapen proteins are transmissible from one organism to another. Last month, an article appeared in Acta Neuropathologica Communications from researchers at the Centre for Biological Threats and Special Pathogens at the Robert Koch-Institut in Berlin that raised questions about whether medical instruments need to be decontaminated if they come into contact with post-mortem brain tissue from Alzheimer’s or Parkinson’s patients. The case for putting in place such prophylaxis is rooted in lab studies that show that injecting deposits of these proteins into an animal brain can initiate a “seeding” process in which one protein causes another to misfold. “Whether those harmful effects can be also caused by transmitted protein particles in humans who express mutated or normal alpha-synuclein, A-beta or tau is still unknown,” the article says. But then it goes on: “…the ability to decontaminate medical instruments from aggregated A-beta, tau and alpha-synuclein may potentially add to patient safety.” © 2015 Scientific American