PSY410 Columbia Southern University Unit V Schizophrenia Article Review

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Unit V Article Review

For this assignment, you will be learning more about schizophrenia, which was covered in this unit. Locate the article below.

In order to access the resource below, you must first log into the myCSU Student Portal and access the Academic OneFile database within the CSU Online Library.

Mukherjee, S. (2016). Runs in the family: New findings about schizophrenia rekindle old questions about genes and identity. The New Yorker, 92(7), 26.

Write a review of the article, and relate it back to information covered in

Unit V. Be sure that your review includes the following information:

Briefly introduce and summarize the article.

Identify the author’s main points.

Who is the author’s intended audience?

Describe how the brain has been implicated in schizophrenia.

Describe the clinical symptoms of schizophrenia, including positive, negative, and disorganized symptoms.

Discuss the role of stress and other psychosocial factors in the etiology and relapse of schizophrenia.

Distinguish the medication treatments and psychological treatments for schizophrenia.

Explain how genetic factors are involved in the etiology of schizophrenia.

How does the article apply to this course? Does it support the information in your textbook?

Your article review must be a minimum of two pages in length. You must reference the article and your textbook, but other sources may be used in addition to these.

Use APA style for all citations and for the formatting of your paper.


Text book:

Kring, A. M., Johnson, S. L., Davison, G. C., & Neale, J. M. (2016). Abnormal psychology: The science and treatment of psychological disorders (13th ed.). Hoboken, NJ: Wiley.

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Runs in the family: new findings about schizophrenia rekindle old questions about genes and identity Siddhartha Mukherjee The New Yorker. 92.7 (Mar. 28, 2016): p26. Copyright: COPYRIGHT 2016 Conde Nast Publications, Inc.. All rights reserved. Reproduced by permission of The Conde Nast Publications, Inc. http://www.newyorker.com/ Full Text: Byline: BY SIDDHARTHA MUKHERJEE RUNS IN THE FAMILY New findings about schizophrenia rekindle old questions about genes and identity. In the winter of 2012, I travelled from New Delhi, where I grew up, to Calcutta to visit my cousin Moni. My father accompanied me as a guide and companion, but he was a sullen and brooding presence, lost in a private anguish. He is the youngest of five brothers, and Moni is his firstborn nephew-the eldest brother's son. Since 2004, Moni, now fifty-two, has been confined to an institution for the mentally ill (a "lunatic home," as my father calls it), with a diagnosis of schizophrenia. He is kept awash in antipsychotics and sedatives, and an attendant watches, bathes, and feeds him through the day. My father has never accepted Moni's diagnosis. Over the years, he has waged a lonely campaign against the psychiatrists charged with his nephew's care, hoping to convince them that their diagnosis was a colossal error, or that Moni's broken psyche would somehow mend itself. He has visited the institution in Calcutta twice-once without warning, hoping to see a transformed Moni, living a secretly normal life behind the barred gates. But there was more than just avuncular love at stake for him in these visits. Moni is not the only member of the family with mental illness. Two of my father's four brothers suffered from various unravellings of the mind. Madness has been among the Mukherjees for generations, and at least part of my father's reluctance to accept Moni's diagnosis lies in a grim suspicion that something of the illness may be buried, like toxic waste, in himself. Rajesh, my father's third-born brother, had once been the most promising of the Mukherjee boysthe nimblest, the most charismatic, the most admired. But in the summer of 1946, at the age of twenty-two, he began to behave oddly, as if a wire had been tripped in his brain. The most obvious change in his personality was a volatility: good news triggered uncontained outbursts of joy; bad news plunged him into inconsolable desolation. By that winter, the sine curve of Rajesh's psyche had tightened in its frequency and gained in its amplitude. My father recalls an altered brother: fearful at times, reckless at others, descending and ascending steep slopes of mood, irritable one morning and overjoyed the next. When Rajesh received news of a successful performance on his college exams, he vanished, elated, on a two-night excursion, supposedly "exercising" at a wrestling camp. He was feverish and hallucinating when he returned, and died of pneumonia soon afterward. Only years later, in medical school, did I realize that Rajesh was likely in the throes of an acute manic phase. His mental breakdown was the result of a near-textbook case of bipolar disorder. Jagu, the fourth-born of my father's siblings, came to live with us in Delhi in 1975, when I was five years old and he was forty-five. His mind, too, was failing. Tall and rail thin, with a slightly feral look in his eyes and a shock of matted, overgrown hair, he resembled a Bengali Jim Morrison. Unlike Rajesh, whose illness had surfaced in his twenties, Jagu had been troubled from his adolescence. Socially awkward, withdrawn from everyone except my grandmother, he was unable to hold a job or live by himself. By 1975, he had visions, phantasms, and voices in his head that told him what to do. He was still capable of extraordinary bursts of tenderness-when I accidentally smashed a beloved Venetian vase at home, he hid me in his bedclothes and informed my mother that he had "mounds of cash" stashed away, enough to buy "a thousand" replacement vases. But this episode was symptomatic: even his love for me extended the fabric of his psychosis and confabulation. Unlike Rajesh, Jagu was formally diagnosed. In the late nineteen-seventies, a physician in Delhi examined him and determined that he had schizophrenia. But no medicines were prescribed. Instead, Jagu continued to live at home, half hidden away in my grandmother's room. (As in many families in India, my grandmother lived with us.) For nearly a decade, she and my father maintained a fragile truce, with Jagu living under her care, eating meals in her room and wearing clothes that she stitched for him. At night, when Jagu was consumed by his fears and fantasies, she put him to bed like a child, with her hand on his forehead. She was his nurse, his housekeeper, his only friend, and, more important, his public defender. When my grandmother died, in 1985, Jagu joined a religious sect in Delhi and disappeared, until his death, a dozen years later. We lost contact with Moni, too. He shuttled between schools and dropped out of college. The commanders in his head became stronger and more insistent. In 2004, he was beaten up by a group of goons, ostensibly for urinating in a public garden. (An internal voice had instructed him, "Piss here; piss here.") In the winter of that year, after yet another breakdown with hallucinations and hissing internal voices, he was institutionalized in Calcutta. When my father and I visited Moni in 2012, I had not seen him for nearly two decades. Even so, I expected to recognize him. But the person I met in the visiting room bore such little resemblance to my memory of my cousin that-had his attendant not confirmed the name-I could easily have been meeting a stranger. He had aged beyond his years. His speech, once effusive and rapid, was hesitant and fitful; the words emerged with a sudden, surprising force, as if he were spitting out pips of food that had been put into his mouth. The most memorable feature of his illness, though, was not the storm within his mind but the lull in his eyes. The word moni means "gem" in Bengali, but in common usage it also refers to something ineffably beautiful: the shining pinpricks of light in each eye. But this was precisely what was missing in Moni. The twin points of light in his eyes had dulled and nearly vanished, as if someone with a minute brush had painted them gray. That schizophrenia runs in families was evident even to the person who first defined the illness. In 1911, Eugen Bleuler, a Swiss-German psychiatrist, published a book describing a series of cases of men and women, typically in their teens and early twenties, whose thoughts had begun to tangle and degenerate. "In this malady, the associations lose their continuity," Bleuler wrote. "The threads between thoughts are torn." Psychotic visions and paranoid thoughts flashed out of nowhere. Some patients "feel themselves weak, their spirit escapes, they will never survive the day. There is a growth in their heads. Their bones have turned liquid; their hearts have turned into stone. . . . The patient's wife must not use eggs in cooking, otherwise he will grow feathers." His patients were often trapped between flickering emotional states, unable to choose between two radically opposed visions, Bleuler noted. "You devil, you angel, you devil, you angel," one woman said to her lover. Bleuler tried to find an explanation for the mysterious symptoms, but there was only one seemingly common element: schizophrenic patients tended to have first-degree relatives who were also schizophrenic. He had no tools to understand the mechanism behind the heredity. The word "gene" had been coined just two years before Bleuler published his book. The notion that a mental illness could be carried across generations by unitary, indivisible factors-corpuscles of information threading through families-would have struck most of Bleuler's contemporaries as mad in its own right. Still, Bleuler was astonishingly prescient about the complex nature of inheritance. "If one is looking for ' the heredity,' one can nearly always find it," he wrote. "We will not be able to do anything about it even later on, unless the single factor of heredity can be broken down into many hereditary factors along specific lines." In the nineteen-sixties, Bleuler's hunch was confirmed by twin studies. Psychiatrists determined that if an identical twin was schizophrenic the other twin had a forty-to-fifty-per-cent chance of developing the disease-fiftyfold higher than the risk in the general population. By the early twothousands, large population studies had revealed a strong genetic link between schizophrenia and bipolar disorder. Some of the families described in these studies had a crisscrossing history that was achingly similar to my own: one sibling affected with schizophrenia, another with bipolar disorder, and a nephew or niece also schizophrenic. "The twin studies clarified two important features of schizophrenia and bipolar disorder," Jeffrey Lieberman, a Columbia University psychiatrist who has studied schizophrenia for thirty years, told me. "First, it was clear that there wasn't a single gene, but dozens of genes involved in causing schizophrenia-each perhaps exerting a small effect. And, second, even if you inherited the entire set of risk genes, as identical twins do, you still might not develop the disease. Obviously, there were other triggers or instigators involved in releasing the illness." But while these studies established that schizophrenia had a genetic basis, they revealed nothing about the nature of the genes involved. "For doctors, patients, and families in the schizophrenia community, genetics became the ultimate mystery," Lieberman said. "If we knew the identity of the genes, we would find the causes, and if we found the causes we could find medicines." In 2006, an international consortium of psychiatric geneticists launched a genomic survey of schizophrenia, hoping to advance the search for the implicated genes. With 3,322 patients and 3,587 controls, this was one of the largest and most rigorous such studies in the history of the disease. Researchers scanned through the nearly seven thousand genomes to find variations in gene segments that were correlated with schizophrenia. This strategy, termed an "association study," does not pinpoint a gene, but it provides a general location where a disease-linked gene may be found, like a treasure map with a large "X" scratched in a corner of the genome. The results, reported in 2009 (and updated in 2014) in the journal Nature , were a dispiriting validation of Bleu-ler's hunch about multiple hereditary factors: more than a hundred independent segments of the genome were associated with schizophrenia. "There are lots of small, common genetic effects, scattered across the genome," one researcher said. "There are many different biological processes involved." Some of the putative culprits made biological sense-if dimly. There were genes linked to transmitters that relay messages between neurons, and genes for molecular channels that move electrical signals up and down nerve cells. But by far the most surprising association involved a gene segment on chromosome 6. This region of the genome-termed the MHC region-carries hundreds of genes typically associated with the immune system. "The MHC-segment finding was so strange and striking that you had to sit up and take notice," Lieberman told me. "Here was the most definitive evidence that something in the immune system might have something to do with schizophrenia. There had been hints about an immunological association before, but this was impossible to argue with. It raised an endlessly fascinating question: what was the link between immune-response genes and schizophrenia?" Lieberman pulled out a figure from the paper to illustrate the strength of the association. One method of plotting the results of a gene-association study is called a Manhattan plot, in which the height of a bar corresponds to the strength of the risk for the disease. In the schizophrenia plot, the segment on chromosome 6 loomed over all other contenders-about twice the height of most of the other risk-conferring gene segments. The MHC region, the central repository of most of our immune-system genes, was like a lone skyscraper towering over the skyline of a newly built metropolis. The Delhi of my childhood was a low-rise city. In the nineteen-sixties, my father, having clambered through the ranks of a Japanese multinational company (it was a folie e deux; he spoke incomprehensible English, and his managers didn't understand any), had built himself a sizable two-story house, a far step from the two-room flat in Calcutta that he had shared with his four brothers and his mother after Partition. The house, he believed, would be his ticket to firm middleclass respectability, but a dyslexic neighborhood sign painter, hired on the cheap to paint "MUKHERJEE" by the front door, had, to my father's endless chagrin, reversed the letter "J," so that its tail curled to the right, like the Greek . The incongruous letter remained there throughout much of my childhood-a discomfiting advertisement to the world that not everything inside the house was quite normally aligned. A memory: It is 1981 or 1982, and I am eleven or twelve. My father has returned from a business trip. It is one of those blistering afternoons when the ceiling fans seem merely to slosh heat around the room. Two of our neighbors are waiting for him. The air seems tense with anxiety. My father enters the living room, and the men talk to him for a few minutes. Their voices rise, and their words sharpen. I can make out the jagged contours of most of the sentences, even through the walls of the adjacent room, where I am supposed to be doing homework. Jagu has borrowed money from both of these men-not large sums, but enough to bring them to our house, demanding repayment. He told one of the men that he needed the cash for medicine (he has never been prescribed any), and the other that he needed it to buy a train ticket to Calcutta to visit his other brothers (no such trip had been planned; it would be impossible for Jagu to travel alone). "You should learn to control him," one of the men says. My father listens silently, but I can feel a meniscus of rage rising in him, coating his throat with bile. He walks to the steel closet, where we keep the household cash, and brings it to the men, making a point of not bothering to count the notes. They should keep the change. By the time the men leave, I know that there will be a bruising altercation. With the instinctual certainty of animals that run uphill before a tsunami, our cook has left the kitchen to summon my grandmother. The tension between my father and Jagu has been building for a while: Jagu's behavior at home has been particularly disruptive in recent weeks-and this episode seems to have pushed my father over some edge. A fragile varnish of class and normalcy has cracked. He walks into Jagu's room and yanks him off the bed. Jagu wails desolately, like a child who is being punished for a transgression that he does not understand. My father is livid, glowing with anger, dangerous. He shoves Jagu across the room. It is an inconceivable act of violence for him; he has never raised a hand. My mother is in the kitchen, crying. I watch the scene rise to an ugly crescendo from behind the living-room curtains, as if watching a film in slow motion. And then my grandmother emerges from her room, glowering like a she-wolf. She is screaming at my father, doubling down on his violence. Her eyes are alight like coals. Don't you dare touch him . "Get out," she hisses to Jagu, who retreats quickly behind her. I have never seen her more formidable. Her Bengali furls backward toward its village origins. I can make out some words, thick with accent and idiom: womb, wash, taint . When I piece the sentence together, its poison is remarkable: If you hit him, I will wash my womb with water to clean your taint, she says . I will wash my womb . My father is frothing with tears now. His head hangs heavily. Wash it, he says under his breath, pleadingly. Wash it, clean it, wash it. When Beth Stevens began work as a postdoctoral fellow at Stanford University, in 2004, she was not interested in studying schizophrenia or bipolar disorder. She was fascinated by the pinpricks of light in eyes. The human eye is born restless. Neural connections between the eyes and the brain are formed long before a child is born, establishing the wiring and the circuitry that allow her to begin visualizing the world the minute she emerges from the womb. Long before the eyelids open, during the early development of the visual system, waves of spontaneous activity ripple from the retina to the brain, like dancers running through their motions before a performance. These waves reconfigure the wiring of the brain-rehearsing its future circuits, strengthening and loosening the connections between neurons. (The neurobiologist Carla Shatz, who discovered these waves of spontaneous activity, wrote, "Cells that fire together, wire together.") This fetal warmup act is crucial to the performance of the visual system: the world has to be dreamed before it is seen. During this rehearsal period, synapses between nerve cells are generated in great excess, to be pruned back during later development. The elimination of synaptic connections, which results in the constant refinement of neural circuits, like the soldering and resoldering of wires on a circuit board, is not a feature unique to the visual system. Throughout the brain-particularly in the parts involved in cognition, memory, and learning-synapse pruning continues into our first three decades, which suggests that it may be responsible, in part, for the starburst of adaptive learning that characterizes the first decades of human life. We are hardwired not to be hardwired, and this anatomical plasticity may be the key to the plasticity of our minds. In the winter of 2004, having joined the laboratory of Ben Barres, a neuroscientist at Stanford, Stevens began to study the pruning of synapses in the visual system. "When I began my work in Ben's lab, little was known about how specific synapses are eliminated," she told me. "The pruning phenomenon was thought to be quite general." There was evidence of synapse pruning in the cortex of the brain during learning, cognition, and the formation of memories. But Stevens and Barres focussed their attention on visual neurons, because they were the easiest to study: the eye would be the eye to the brain. In 2007, they announced a startling discovery. Stevens was trying to identify the proteins that recognized and eliminated neuronal synapses during visual development. "The strangest finding was that a protein that usually tags and removes pieces of dead cells, bacterial remnants, or cellular debris was also being reworked to tag and remove the synapses," she said. Mice designed to lack tagging proteins-called complement proteins-had problems both in clearing cellular debris and in tagging and pruning their synapses. The Stevens and Barres study, published in the journal Cell in 2007, documented one of the most arresting instances of repurposing in biology: a protein designed to ticket germs and junk for destruction had been co-opted by the nervous system to ticket synapses for destruction. "It reinforces an old intuition," my psychiatrist friend Hans, in Boston, told me. "The secret of learning is the systematic elimination of excess. We grow, mostly, by dying." The following year, Stevens moved to Boston Children's Hospital, to set up her own lab. When I visited her on a recent icy March morning, the lab was thrumming. Graduate students were folded over microscopes, like half-open books. One woman sat on her bench determinedly mashing a freshly biopsied fragment of a human brain into individual cells so th ...
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