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Genetics

BRIEF-Seattle Genetics Announces Positive Results From Exploratory Analyses Of Her2climb For Tukysa – Reuters

May 29 (Reuters) - Seattle Genetics Inc:

* SEATTLE GENETICS ANNOUNCES POSITIVE RESULTS FROM EXPLORATORY ANALYSES OF HER2CLIMB FOR TUKYSA (TUCATINIB) IN BRAIN METASTASES PATIENTS WITH HER2-POSITIVE BREAST CANCER

* SEATTLE GENETICS INC - TUKYSA COMBINATION REDUCED RISK OF CANCER PROGRESSION IN BRAIN OR DEATH BY TWO-THIRDS

* SEATTLE GENETICS -RESULTS DEMONSTRATED ADDITION OF TUKYSA TO TRASTUZUMAB,CAPECITABINE IN PATIENTS WITH BRAIN METASTASES DELAYED PROGRESSION IN BRAIN Source text for Eikon: Further company coverage:

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BRIEF-Seattle Genetics Announces Positive Results From Exploratory Analyses Of Her2climb For Tukysa - Reuters

Genetics

Seattle Genetics Announces Positive Results from Exploratory Analyses of HER2CLIMB for TUKYSA (tucatinib) in Brain Metastases Patients With…

BOTHELL, Wash.--(BUSINESS WIRE)--Seattle Genetics, Inc. today announced positive results from exploratory analyses of intracranial efficacy, including survival, in patients with HER2-positive metastatic breast cancer (MBC) who had stable or active brain metastases in the HER2CLIMB pivotal trial of TUKYSA (tucatinib). HER2CLIMB compared TUKYSA in combination with trastuzumab and capecitabine to trastuzumab and capecitabine alone in patients with unresectable, locally advanced or metastatic HER2-positive breast cancer with or without brain metastases. Of the patients enrolled in the trial, 48 percent had a presence or history of brain metastases. Results demonstrated that the addition of TUKYSA to trastuzumab and capecitabine in patients with brain metastases delayed progression in the brain, doubled the intracranial response rate (tumor shrinkage in the brain) and reduced the overall risk of death by nearly half. The data were consistent across patients who had either stable or active brain metastases. Results were presented in an oral presentation in the virtual scientific program of the 2020 American Society of Clinical Oncology (ASCO) Annual Meeting and simultaneously published in the Journal of Clinical Oncology.

TUKYSA in combination with trastuzumab and capecitabine was approved by the U.S. Food and Drug Administration (FDA) in April 2020 for adult patients with advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have received one or more prior anti-HER2-based regimens in the metastatic setting. Primary results from HER2CLIMB were first presented at the San Antonio Breast Cancer Symposium in December 2019 and published in the New England Journal of Medicine.

It is immensely gratifying to see for the first time, results for patients with stable or active brain metastases who are not typically included in clinical trials, especially when you consider that nearly half of patients with HER2-positive metastatic breast cancer experience disease progression to the brain, said Nancy U. Lin, M.D., director of the Metastatic Breast Cancer Program in the Susan F. Smith Center for Womens Cancers at Dana-Farber in Boston, MA. These additional analyses provide further evidence that TUKYSA improves survival and delays cancer progression in the brain for patients with HER2-positive metastatic breast cancer who have brain metastases.

These additional analyses, together with the primary analysis of HER2CLIMB, show TUKYSA is active for patients with and without disease that has spread to the brain, said Roger Dansey, M.D., Chief Medical Officer of Seattle Genetics. We continue to be encouraged by the remarkable clinical activity of TUKYSA in combination with trastuzumab and capecitabine and look forward to evaluating its potential in additional treatment settings and tumor types through our ongoing clinical program.

The new data that further examine TUKYSAs effect in the brain include exploratory analyses for central nervous system progression-free survival (CNS-PFS), overall survival (OS), intracranial objective response rate (ORR-IC) and duration of response in HER2-positive metastatic breast cancer patients whose disease had spread to the brain.

The exploratory analyses demonstrated that patients with brain metastases who received the TUKYSA combination versus trastuzumab and capecitabine alone had:

Endpoint

TUKYSA Arm (TUKYSA + trastuzumab + capecitabine)

Control Arm (Placebo + trastuzumab + capecitabine)

OS Benefit in All Patients with Brain Metastases

N=198

N=93

Risk Reduction

42% (Hazard Ratio [HR]=0.58 [95% Confidence Interval (CI): 0.40, 0.85]; p=0.005)

One-Year OS

70.1% (95% CI: 62.1, 76.7)

46.7% (95% CI: 33.9, 58.4)

Median OS

18.1 months (95% CI: 15.5, not estimable)

12 months (95% CI: 11.2, 15.2)

CNS-PFS Benefit in All Patients with Brain Metastases

N=198

N=93

Risk Reduction

68% (HR=0.32 [95% CI: 0.22, 0.48]; p<0.0001)

One-year CNS-PFS

40.2% (95% CI: 29.5, 50.6)

0%

Median CNS-PFS

9.9 months (95% CI: 8.0, 13.9)

4.2 months (95% CI: 3.6, 5.7)

Intracranial Objective Response Rate (ORR-IC) in Patients with Active Brain Metastases and Measurable Intracranial Lesions at Baseline

N=55

N=20

Complete Response (CR)

3 (5.5%)

1 (5.0%)

Partial Response (PR)

23 (41.8%)

3 (15.0%)

Stable Disease

24 (43.6%)

16 (80.0%)

Progressive Disease

2 (3.6%)

0

Not Available

3 (5.5%)

0

ORR-IC (CR+PR)

26 (47%) (95% CI: 34, 61)

4 (20%) (95% CI: 6, 44)

Duration of Response-IC

6.8 months (95% CI: 5.5, 16.4)

3 months (95% CI: 3.0, 10.3)

About HER2CLIMB

HER2CLIMB is a multinational randomized (2:1), double-blind, placebo-controlled, active comparator, pivotal clinical trial comparing TUKYSA in combination with trastuzumab and capecitabine compared with trastuzumab and capecitabine alone in patients with locally advanced unresectable or metastatic HER2-positive breast cancer who were previously treated with trastuzumab, pertuzumab and T-DM1. The primary endpoint of the trial was PFS per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 as determined by blinded independent central review (BICR) in the first 480 patients enrolled in the trial. HER2CLIMB enrolled a total of 612 patients to support the analyses of key secondary endpoints, including OS, PFS per BICR in patients with brain metastases at baseline and confirmed ORR.1

Results of Primary Analysis of HER2CLIMB

Control Arm (Placebo + trastuzumab + capecitabine)

PFS by BICR in the first 480 patients

46% reduction in risk of progression or death (HR=0.54 [95% CI: 0.42, 0.71]; p<0.00001; N=480)

OS

34% reduction in risk of death (HR=0.66 [95% CI: 0.50, 0.87]; p=0.0048; N=612)

PFS* by BICR in patients with brain metastases

52% reduction in risk of progression or death (HR=0.48 [95% CI: 0.34, 0.69]; p<.0.00001; N=291)

One-Year PFS

25% (95% CI: 17, 34)

0%

Median PFS

7.6 months (95% CI: 6.2, 9.5)

5.4 months (95% CI: 4.1, 5.7)

*standard RECIST, includes brain and body

In HER2CLIMB, serious adverse reactions occurred in 26 percent of patients who received TUKYSA. Serious adverse reactions occurring in 2 percent or more of patients who received TUKYSA were diarrhea (4%), vomiting (2.5%), nausea, abdominal pain, and seizure (2% each). The most common adverse reactions occurring in 20 percent or more of patients who received TUKYSA were diarrhea, palmar-plantar erythrodysesthesia, nausea, fatigue, hepatotoxicity, vomiting, stomatitis, decreased appetite, abdominal pain, headache, anemia, and rash. Adverse reactions leading to treatment discontinuation occurred in 6 percent of patients who received TUKYSA; adverse reactions leading to treatment discontinuation of TUKYSA (in 1 percent or more of patients) were hepatotoxicity (1.5%) and diarrhea (1%).1

About HER2-Positive Breast Cancer

Patients with HER2-positive breast cancer have tumors with high levels of a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells. An estimated 279,100 new cases of breast cancer will be diagnosed in the U.S. in 2020.2 Between 15 and 20 percent of breast cancer cases are HER2-positive.3 Historically, HER2-positive breast cancer tends to be more aggressive and more likely to recur than HER2-negative breast cancer.3,4,5 Up to 50 percent of metastatic HER2-positive breast cancer patients develop brain metastases over time. 6,7,8

About TUKYSA (tucatinib)

TUKYSA is an oral, small molecule tyrosine kinase inhibitor (TKI) of HER2, a protein that contributes to cancer cell growth.1,9 In vitro (in lab studies), TUKYSA inhibited phosphorylation of HER2 and HER3, resulting in inhibition of downstream MAPK and AKT signaling and cell growth (proliferation), and showed anti-tumor activity in HER2-expressing tumor cells. In vivo (in living organisms), TUKYSA inhibited the growth of HER2-expressing tumors. The combination of TUKYSA and the anti-HER2 antibody trastuzumab showed increased anti-tumor activity in vitro and in vivo compared to either medicine alone.1

Important Safety Information

Warnings and Precautions

If diarrhea occurs, administer antidiarrheal treatment as clinically indicated. Perform diagnostic tests as clinically indicated to exclude other causes of diarrhea. Based on the severity of the diarrhea, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Monitor ALT, AST, and bilirubin prior to starting TUKYSA, every 3 weeks during treatment, and as clinically indicated. Based on the severity of hepatoxicity, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Adverse Reactions

Serious adverse reactions occurred in 26% of patients who received TUKYSA. Serious adverse reactions in 2% of patients who received TUKYSA were diarrhea (4%), vomiting (2.5%), nausea (2%), abdominal pain (2%), and seizure (2%). Fatal adverse reactions occurred in 2% of patients who received TUKYSA including sudden death, sepsis, dehydration, and cardiogenic shock.

Adverse reactions led to treatment discontinuation in 6% of patients who received TUKYSA; those occurring in 1% of patients were hepatotoxicity (1.5%) and diarrhea (1%). Adverse reactions led to dose reduction in 21% of patients who received TUKYSA; those occurring in 2% of patients were hepatotoxicity (8%) and diarrhea (6%).

The most common adverse reactions in patients who received TUKYSA (20%) were diarrhea, palmar-plantar erythrodysesthesia, nausea, fatigue, hepatotoxicity, vomiting, stomatitis, decreased appetite, abdominal pain, headache, anemia, and rash.

Lab Abnormalities

In HER2CLIMB, Grade 3 laboratory abnormalities reported in 5% of patients who received TUKYSA were: decreased phosphate, increased ALT, decreased potassium, and increased AST. The mean increase in serum creatinine was 32% within the first 21 days of treatment with TUKYSA. The serum creatinine increases persisted throughout treatment and were reversible upon treatment completion. Consider alternative markers of renal function if persistent elevations in serum creatinine are observed.

Drug Interactions

Use in Specific Populations

For more information, please see the full Prescribing Information for TUKYSA here.

About Seattle Genetics

Seattle Genetics, Inc. is a global biotechnology company that discovers, develops and commercializes transformative medicines targeting cancer to make a meaningful difference in peoples lives. The company is headquartered in the Seattle, Washington area, and has offices in California, Switzerland and the European Union. For more information on our robust pipeline, visit http://www.seattlegenetics.com and follow @SeattleGenetics on Twitter.

Forward Looking Statements

Certain statements made in this press release are forward looking, such as those, among others, relating to the therapeutic potential of TUKYSA including its efficacy, safety and therapeutic uses, including its use in combination with trastuzumab and capecitabine to treat patients with HER2-positive metastatic breast cancer with brain metastases who have received one or more previous anti-HER2 therapies, and its potential use in additional treatment settings and tumor types. Actual results or developments may differ materially from those projected or implied in these forward-looking statements. Factors that may cause such a difference include the difficulty and uncertainty of pharmaceutical product development; the possibility that adverse events or safety signals may occur; that utilization and adoption of TUKYSA by prescribing physicians may be limited due to impacts related to the COVID-19 pandemic, availability and extent of reimbursement or other factors; and that adverse regulatory actions may occur. More information about the risks and uncertainties faced by Seattle Genetics is contained under the caption Risk Factors included in the companys Quarterly Report on Form 10-Q for the quarter ended March 31, 2020 filed with the Securities and Exchange Commission. Seattle Genetics disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law.

1 TUKYSA [package insert]. Bothell, WA: Seattle Genetics, Inc.2 Cancer Facts & Figures 2020. American Cancer Society website. https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2020/cancer-facts-and-figures-2020.pdf. Accessed May 28, 2020.3 Loibli S, Gianni L. HER2-positive breast cancer. Lancet. 2017; 389(10087): 2415-29.4 Slamon D, Clark G, Wong S, et al. Human breast cancer: correlation of relapse and survival with amplification of the HER-2/neu oncogene. Science. 1987; 235(4785): 177-82.5 Breast Cancer HER2 Status. American Cancer Society website. http://www.cancer.org/cancer/breast-cancer/understanding-a-breast-cancer-diagnosis/breast-cancer-her2-status.html. Accessed May 28, 2020.6 Freedman RA, Gelman RS, Anders CK, et al. TBCRC 022: a phase II trial of neratinib and capecitabine for patients with human epidermal growth factor receptor 2-positive breast cancer and brain metastases. J Clin Oncol. 2019;37:1081-1089.7 Olson EM, Najita JS, Sohl J, et al. Clinical outcomes and treatment practice patterns of patients with HER2-positive metastatic breast cancer in the post-trastuzumab era. Breast. 2013;22:525-531.8 Bendell JC, Domchek SM, Burstein HJ, et al. Central nervous system metastases in women who receive trastuzumab-based therapy for metastatic breast carcinoma. Cancer. 2003;97:2972-2977.9 Anita Kulukian, Patrice Lee, Janelle Taylor, et al. Preclinical Activity of HER2-Selective Tyrosine Kinase Inhibitor Tucatinib as a Single Agent or in Combination with Trastuzumab or Docetaxel in Solid Tumor Models. Mol Cancer Ther 2020;19:976-987.

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Seattle Genetics Announces Positive Results from Exploratory Analyses of HER2CLIMB for TUKYSA (tucatinib) in Brain Metastases Patients With...

Genetics

How to know your risk factors for hypertension and whether high blood pressure is genetic – Insider – INSIDER

Hypertension is the medical term for high blood pressure. It can cause serious health problems, like heart disease or stroke, if left untreated.

There are many risk factors that make it more likely for someone to develop hypertension. These include genetic factors, age, race, medical conditions, and unhealthy lifestyle choices.

Here's what you need to know about what increases the risk of high blood pressure.

Overall, one or more of these factors are most likely to cause high blood pressure:

One of the biggest culprits is smoking, which can double or triple the risk of developing hypertension. That's because smoking damages blood vessels and can reduce blood flow to the heart.

But these factors won't always cause hypertension alone genetics and medical conditions can also increase your risk.

"I would say the simplest answer to this is, yes, there is a genetic component," says Joshua Shatzkes, MD, a cardiologist at Mt. Sinai Hospital.

If your parents have hypertension, you are at an increased risk for high blood pressure.

A 2018 study involving over a million people identified 500 genes that influence blood pressure. Some of these genes influence the cells lining blood vessels, causing them to be abnormally constricted and raise blood pressure.

Other genes can cause high cholesterol, especially in a condition known as hypercholesterolemia, which can also increase blood pressure.

In addition, genetic factors often combine with other adverse lifestyle choices, which can further increase the risk of hypertension.

For example, when you're growing up, if your family eats an unhealthy diet high in sodium, creates a high stress environment, smokes too many cigarettes, and doesn't exercise often, then you're more likely to inherit those behaviors and more likely to develop hypertension.

While there's no universal way to describe obesity, it's often considered a condition where someone has a high body mass index (BMI). A BMI over 40 can double or triple your likelihood of developing obesity-related illnesses.

"When someone is obese, it simply takes more work for the heart to pump blood throughout the whole body," says Christopher Granger, MD, a cardiologist at Duke Health. "And when it has to pump blood throughout the whole body, it has to generate a higher kind of pressure to do so."

In fact, a study from 2015 suggests that excess body fat accounts for 65% to 75% of hypertension cases. Moreover, a 2017 study found that childhood obesity increased the rate of developing adult hypertension by 65%.

Diabetes is a condition where your body doesn't react to high blood sugar properly, which may cause it to be too high or too low longer than normal. Insulin is the hormone designed to take glucose (sugar) from the blood to the cells, but if there's not enough insulin, glucose stays in the blood, elevating blood sugar levels.

Over time, high blood sugar can cause plaque to build up in your blood vessels, which narrows the vessel and increases blood pressure.

Granger explains that high blood sugar can cause the arteries to stiffen because it can increase the production of free radicals tiny particles that damage cells and reduce nitrous oxide, a chemical that dilates blood vessels.

As a result, 30% of people with type 1 diabetes develop hypertension. Those with type 2 diabetes are 2.5 times more likely to develop hypertension and 50% to 80% will develop hypertension. However, diabetics who carefully control their blood sugar levels can effectively decrease the risk of developing hypertension.

The American Heart Association has found that over 40% of non-Hispanic African-Americans have high blood pressure, and that it can develop earlier in their lives and become more severe.

Overall, black Americans are twice as likely to develop hypertension by the age of 55 compared to white Americans. Systemic issues could explain this increase in blood pressure.

There's an association between racism and higher blood pressure in African-American men, according to the CDC. Black Americans are also exposed to more factors that can increase chronic stress such as discrimination and lower socioeconomic status which may contribute to high blood pressure.

Older people are more likely to develop hypertension because the arteries stiffen as we age. This process is called atherosclerosis, and it describes plaque build-up in blood vessels.

According to Granger, young people's arteries are able to expand and more effectively accommodate the pulse of blood flow.

Overall, your lifetime risk for developing hypertension is 90%, according to Johns Hopkins Medicine. Even if you have heart-healthy habits, you'll still most likely develop hypertension, according to the National Institute on Aging.

However, certain lifestyle changes, such as exercising every day, sleeping adequately, and avoiding smoking, can lower the risk of developing high blood pressure.

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How to know your risk factors for hypertension and whether high blood pressure is genetic - Insider - INSIDER

Neuroscience

Researchers deliver care packages to refugee children at the end of Ramadan – The South End

Celine Bazzi places a handwritten card inside a care package for Syrian refugee children and their families for Eid al-Fitr, the festival of breaking the fast at the end of Ramadan.

When COVID-19 hit Southeast Michigan, Dr. Arash Javanbakht and his crew of student researchers were forced to halt their studys data collection. It was a setback, certainly.

For nearly four years, Javanbakht and his team have been exploring the mental health impact and biological correlation of war trauma on Syrian refugees, many of them children, now living in the United States. But all Javanbakht could think about was the outbreaks impact on the families who have become so much more than research participants.

Given it was Ramadan, and especially during this stressful time of the pandemic, I thought of a way to bring a smile to the kids, said Javanbakht, associate professor of Psychiatry and Behavioral Neurosciences and director of the Stress, Trauma and Anxiety Research Clinic. We brainstormed and decided to make gift packages for the children and their families, and deliver them to their doors for Eid al-Fitr [the festival of breaking the fast at the end of Ramadan].

With the parents permission, Javanbakht and the team of undergraduate, graduate and postdoctoral students most of whom have Arabic backgrounds, and some who are also refugees created care packages of snacks and school supplies for the children and delivered it to their doors on May 22. In addition, Wayne State Marketing and Communications donated backpacks, pens and T-shirts.

While Javanbakht covered all the costs, he said the team did the hard work of choosing, purchasing, packaging and delivering the age-appropriate gifts.

Tailoring the box with respect to each specific family and their children provided such a valuable experience, said Celine Bazzi, 22, who graduated in spring 2020 with a bachelors in biological sciences and minors in philosophy and health care ethics. Being able to tend to each child individually, as well as brainstorm ideas of what they might enjoy, made the process that much more special.

While Bazzis last semester at Wayne State didnt end according to plan, she said she will take with her the memory of being sprawled out on her living room floor, surrounded by immense amounts of goodies, anticipating iftar [the time in which fast is broken], while handwriting the beautifully crafted cards.

For postdoctoral researcher Bassem Saad, 30, seeing the families reactions hit him deeply. As a person coming from the Middle East, an immigrant, my cause has always been supporting people who had suffered a lot through civil war, he said. I was over the moon that they feel recognized, accepted and understood in the academic scene.

Lana Grasser, a 24-year-old Ph.D. candidate going into her fourth year of Wayne States translational neuroscience program, hoped the care packages would bring a little joy during a time of hardship.

We have worked with these families not only in the labs, but also in the home. It felt like seeing my own family, but it was hard to not give them all hugs, she said. Through our Eid gift-giving, we were able to make a small part of the world in our own personal circles a little bit better and brighter. We are so grateful for all the time they have given us and stories they have shared. This was the least we could do.

That feeling was shared among the entire team.

As a research assistant, I have visited the homes of the families involved in our study and they always welcome us with so much hospitality, said Rajaa Shoukfeh, 22, who graduated in December 2019 with a bachelors in nutrition and food science. When Dr. Javanbakht first brought up the idea at one of our weekly team meetings, it was so heartwarming. Its such a kind gesture to repay their kindness and show them how much we appreciate their participation.

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Researchers deliver care packages to refugee children at the end of Ramadan - The South End

Neuroscience

Book Review: Unlocking the Mysteries of the Human Brain – Undark Magazine

We know little about the life of Alcmaeon of Croton: We can be pretty sure he hailed from the coastal city of Croton (present day Crotone), in the far south of Italy, and had a father named Peirithous; he may have been a student of Pythagoras. We dont know when he was born or when he died; only that he was active in the 5th century B.C. But we know he was fascinated by the human body, and was willing to challenge some of the established dogmas of his day. In particular, he may have been the first to assert that the brain not the heart is the seat of the mind. At the very least, he seems to have recognized the importance of this astonishing organ.

BOOK REVIEW The Idea of the Brain: The Past and Future of Neuroscience, by Matthew Cobb (Basic Books, 496 pages).

In The Idea of the Brain: The Past and Future of Neuroscience, Matthew Cobb, a biologist at the University of Manchester, shows just how long and arduous the road to understanding the brain has been and, as he makes clear, the journey has only just begun. The brain, we are often told, is the most complex entity in the known universe. And though we surmise that the brain is what allows us to think and feel and perceive and know, it is far from clear how it accomplishes this.

A good metaphor might help, if only we could latch onto the right one: Is the brain like a complicated electrical circuit, or a telephone switchboard, or a digital computer, or a neural network? Or none of the above? As Cobb lays out the history, from the ancient Greeks to the present day, he offers a candid analysis of where these analogies have been helpful, and where theyve fallen short.

In his book Elements of Eletro-Biology, published in 1849, an English polymath and inventor named Alfred Smee argued that the brain was made up of hundreds of thousands of tiny batteries, each of them somehow connected to a different part of the body. Emotions such as desire, and even consciousness itself, were supposedly the result of these little batteries working in various combinations. He even drew up plans for what he believed would be a thinking machine, composed of metal plates and hinges and other paraphernalia.

As Cobb points out, as fuzzy as some of Smees ideas were, he was also occasionally prescient, as with his proposal for sending what we would now call video signals over long distances. There is no reason, Smee wrote, why a view of St. Pauls in London should not be carried to Edinburgh through tubes like the nerves which carry the impression to the brain.

Is the mind merely the result of marvelously complex machinery? A famous criticism of the brain-as-machine metaphor comes from the German mathematician and philosopher Gottfried Leibniz. Suppose, Leibniz argued in 1714, you had a thinking machine that duplicated the function of the human brain, and scaled it up so that one could enter it as one does a mill. You get to then walk about the interior of this device, observing parts which push upon each other and yet one would find nothing which would explain a perception.

Echoes of Leibnizs argument can still be heard today, especially by those who find it hard to imagine that the mind has a material explanation. (I was a little disappointed that Cobb doesnt explore the numerous counterarguments that have been leveled against Leibniz over the years. The philosopher Daniel Dennett, for example, asks: Might it be that somehow the organization of all the parts which work one upon another yields consciousness as an emergent product? And if so, why couldnt we hope to understand it, once we had developed the right concepts?)

Though we surmise that the brain is what allows us to think and feel and perceive and know, it is far from clear how it accomplishes this.

It wasnt until the middle of the 19th century that scientists came to understand that different brain regions accomplished different tasks. Often this knowledge came through observing victims of brain damage. A famous example involved an American railway worker named Phineas Gage. In 1848, Gage suffered a traumatic head injury when an explosion sent a 1.1-meter-long iron rod through his skull. Incredibly, Gage survived, living another 20 years but his personality was radically changed. A model employee before the accident, Gage became fitful, irreverent, indulging at times in the grossest profanity, according to a doctor who knew him. It was the front of Gages brain that received the most damage; as Cobb notes, the case suggested that various aspects of mental life linked to attention and behavior were somehow localized in the frontal parts of the brain.

Enter Darwin, whose theory of natural selection forced us to think of the brain as the product of countless eons of evolution. If humans and apes share a common ancestor, then our brains, and perhaps our minds, couldnt be all that different. Inspired by Darwin, Thomas Henry Huxley Darwins bulldog compared human and ape brains, concluding that there is no dispute as to the resemblance in fundamental characters, between the apes brain and mans, noting the wonderfully close similarity between our brains and those of chimpanzees and orangutans.

Neurons the brains cells were discovered in the 1830s, though the method by which they send signals to one another was only discerned in the 20th century, as the science behind synaptic transmission took shape, and the role of neurotransmitters became clearer. As telephones and telegraphs flourished in the 1800s, so did analogies between the brain and a telephone network, but, writes Cobb, discoveries in biology soon showed how limited this analogy was. Even if we talk of switches in the brain, these switches did not work in the same way as those in a piece of electrical equipment. Biological discovery was outstripping the dominant technological metaphor and revealing that the brain is not a telephone exchange.

The 20th century brought the digital computer, and the brain-as-computer metaphor persists to this day. Of the many fascinating historical details in the book, one of the most remarkable is the mid-20th-century collaboration between neurologist Warren McCullogh and a self-taught teenage prodigy named Walter Pitts. Working together, they developed the first computational theory of the mind: a fascinating mix of mathematical logic, computer science, and biology. Yet as promising as their work was, the sheer complexity of the human brain threatened to derail the whole effort. An early critique came from computer science pioneer John von Neumann. As Cobb puts it, von Neumann realized that real nervous systems were far more complicated than those described by McCullogh and Pitts and that neurons unfortunately did not always function in the all-or-nothing fashion of the electronic switches in a digital computer.

By the final decades of the 20th century, the discoveries were coming fast and furious. Functional magnetic resonance imaging (fMRI) offered tantalizing hints of what areas of the brain are most active, when we do or think about certain things. And the new science of neural networks, which is continuing to revolutionize computer science as we speak, offered new metaphors for the brains function.

And yet, the end goal a true understanding of the brains connections, and how they produce their mental counterparts still seems like a distant mirage. While acknowledging astonishing progress, Cobb writes that, in his view, it will probably take 50 years before we understand the maggot brain. Later, after a discussion of mental illness and the search for effective treatments, Cobb writes that unravelling the genetic architecture of the human brain and how it interacts with the environment will be the work of centuries.

And there remains what Cobb refers to as this question of questions the puzzle of consciousness.

The Idea of the Brain offers a compelling account of the twists and turns that our quest to understand this remarkable organ has taken over the centuries. How wonderful it would be to know how the story ends, but that will have to wait. The brain is so complex that it has not yet come to know itself.

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Book Review: Unlocking the Mysteries of the Human Brain - Undark Magazine

Neuroscience

Last Minute Deal: FitMind Neuroscience-Based Meditation App, Save 75% – Geeky Gadgets

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Last Minute Deal: FitMind Neuroscience-Based Meditation App, Save 75% - Geeky Gadgets

Neuroscience

Prothena to Present at the Jefferies Virtual Healthcare Conference on June 3 – GlobeNewswire

DUBLIN, Ireland, May 27, 2020 (GLOBE NEWSWIRE) -- Prothena Corporation plc (NASDAQ:PRTA), a clinical-stage neuroscience company with expertise in protein misfolding, today announced that members of its senior management team will present and participate in the Jefferies Virtual Healthcare Conference on Wednesday June 3 at 3:30 PM ET.

A webcast of the company presentation can be accessed through the investor relations section of the Company's website at http://www.prothena.com. Following the presentation, a replay of the webcast will be available on the Company's website for at least 90 days following the presentation date.

About Prothena

Prothena Corporation plc is a clinical-stage neuroscience company with expertise in protein misfolding, focused on the discovery and development of novel therapies with the potential to fundamentally change the course of devastating diseases. Fueled by its deep scientific expertise built over decades of research, Prothena is advancing a pipeline of therapeutic candidates for a number of indications and novel targets for which its ability to integrate scientific insights around neurological dysfunction and the biology of misfolded proteins can be leveraged. Prothenas partnered programs include prasinezumab (PRX002/RG7935), in collaboration with Roche for the potential treatment of Parkinsons disease and other related synucleinopathies, and programs that target tau, TDP-43 and an undisclosed target in collaboration with Bristol-Myers Squibb for the potential treatment of Alzheimers disease, amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) or other neurodegenerative diseases. Prothenas proprietary programs include PRX004 for the potential treatment of ATTR amyloidosis, and programs that target A (Amyloid beta) for the potential treatment of Alzheimers disease. For more information, please visit the Companys website at http://www.prothena.com and follow the Company on Twitter @ProthenaCorp.

Media and Investor Contact:

Ellen Rose, Head of Communications650-922-2405, ellen.rose@prothena.com

Continued here:
Prothena to Present at the Jefferies Virtual Healthcare Conference on June 3 - GlobeNewswire

Human Behavior

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Home - Human Behavior Hacker School

Human Behavior

20 Great Human Behavior Research Topics for College Students

It does not matter whether it is psychology, sociology, biology, management, philosophy, anthropology, history, or human resource management that you study human behavior constitutes an integral part of every single one of these courses. Apart from teaching us to understand each other, studying human behavior also helps us figure out reasons for acting this or that way in some situations or prevent us from facing fatal consequences of a wrong action. It is not the most complicated process, but the student should know some crucial nuances of it.

Communication and human behavior are interconnected which is why you will derive nothing but benefit from studying both subjects. It is essential when it comes to starting a business, building relationships, proving your truth, and many other things. To help students come up with ways of surviving in the highly dynamic modern world, tutors often assign homework tasks related to human behavior.

In some cases, you will be provided with a topic, while in others, the tutor may leave it up to the student to choose the research paper topic, and we can assure you that coming up with one may not be as easy as some students may think.

Before providing you with a list of research topics on human behavior, we would like to recall some of the major principles of selecting a good idea.

Be sure to consult with your tutor before making the final choice, because they may recommend you some better options or provide you with hints on how to collect essential information and properly structure your essay. You can also seek their help with a preferred format if you are not sure which one to pick. Keep in mind that psychology or human behavior essays are mostly written in American Psychological Association (APA) citation format.

Regardless of whether you research human behavior or another subject, the structure of the final document should be as follows: a title page, abstract, introduction, methodology, findings, discussion and conclusion, bibliography, and appendices (optional). Doing this type of academic assignment requires more time than writing an essay, so its always a good idea to give yourself some leeway. We recommend developing an abstract & thesis statement at the end once you are done with the rest of the paragraphs. Start with methods where you describe the tools & equipment used during the research process. Move smoothly to the results of your experiment, stressing the most important findings and discussing them with the audience.

In conclusion, explain the importance of your study and suggest ways of implementing your study findings in real life situations. Also, make some future forecasts to provide an opportunity for other researchers interested in the same question to pick up from where you left off. The sources listed in the bibliography (references) section will help your audience be more tolerant about the problem under discussion, so make sure you cite each source properly. Now, lets explore some exciting human behavior research topics!

Now, you have a list of the best ideas you may use while studying subjects associated with human behavior. But what if you still feel that creating a properly written research on human behavior is a task you can never accomplish on your own? Well, that's what were here for! Our professional academic writers are available 24/7 and can solve any academic problems you face in the shortest possible time! It's time to stop worrying yourself to death and place your order now!

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20 Great Human Behavior Research Topics for College Students