Groups of People to Brain Scan

As neuroscience gains more predictive power, the field opens up greater opportunities for identifying violent and impulsive people before they commit crimes. Right now it’s too expensive and time-consuming to scan the huge number of people in these populations. Miniature MRI machines and improved algorithms to reduce scanning time may make this a possibility. The Department of Defense’s DARPA agency currently explores opportunities for understanding the brain. Just as criminal suspects are fingerprinted, they should be brainprinted too. These are some potential groups of people to brain scan:

Violent Crime Suspects:

Scanning suspects of violent crimes may identify abnormalities in their brains that predict the potential for committing even deadlier crimes in the future. Think of the Navy Yard shooter who was arrested multiple times prior to his mass killings. Those arrests stemmed from shooting out the tires of a vehicle and discharging a gun in his apartment building. Analyzing the brains of people like that could identify when treatment or institutionalization is necessary to prevent even worse crimes. Scans of the Colorado theater shooter’s brain showed that he had decreased brain volume in regions related to emotion processing and decision making. New information reveals that the recent shooter in Virginia killed his pet cats in a fit of rage after losing his job. While the police weren’t aware of that, animal cruelty could also necessitate a brain scan.

Illegal Gun Owners:

People caught with illegal guns, especially felons, should be brain scanned for the same reasons as those apprehended for violent crimes. Having a gun illegally may indicate a greater propensity for violence and a brain scan could provide additional information.

Prisoners:

Brain scans of prisoners could identify which ones have higher probabilities of recidivism and which prisoners have better chances for rehabilitation.

Undocumented Immigrants:

Instead of being subjected to immediate deportation, scanning the brains of undocumented immigrants may identify those who could enhance their new country by possessing neural correlates of compassion and intelligence. Brain scans could also identify undocumented immigrants with neural correlates of psychopathy so they can be returned to their country of origin to be tracked by that country’s government.

Law Enforcement:

Sadism and impulsivity are personality traits that have a basis in the brain just like other personality traits. Brain scans could identify which police officer candidates are likely to become future liabilities to their departments and communities.

Military Personnel:

The Armed Forces has a separate legal system that allows for noninvasive scanning of military personnel. All military branches share great interest in gathering and tracking information on people in the military. I’m sure they would be interested in scanning recruits to identify which individuals have the most leadership potential.

I Have a Humanities Degree and Think the Arts and Humanities are Worthless

I recently thought about starting a side project as someone politicians turn to when they seek voter support for defunding humanities education and arts programs. I graduated with a humanities degree but was fortunate enough to graduate in 2006 when the unemployment rate was at a low point. I experienced even greater luck when I graduated without debt as a result of scholarships from great high school grades and standardized test performance before my brain started degrading from the chronic social stress of the college environment. I simply lucked out by graduating before the recession and spending much of my spare time reading about business and technology to gain marketable skills. Most students in the arts and humanities don’t experience the same good fortune.

STEM (Science / Technology / Engineering / Mathematics) students often think humanities students live lives of nonstop partying. I spent most of my time in college living with anxiety and depression with few social connections. With that mental load, I couldn’t study anything challenging or useful. I didn’t drink alcohol because I worried about losing control under the influence and harming myself or others. Since I limited myself to an undergraduate degree, my thoughts might differ from graduate students in the arts and humanities who invest much more of their self-image in their course of study due to sunk costs of time and money.

These thoughts bubbled up when reading the new book Faith Versus Fact by biology professor Jerry Coyne. I agree with Dr. Coyne regarding free will skepticism and many other topics, but in one passage in the book I think he doesn’t go far enough. At first I thought he included this passage as a defense against critics charging him with “scientism” but he talks about his interest in the arts on his website so there’s no reason to doubt his sincerity. The passage in question:

In arguing that science is the only way we can really learn things about our universe, I am not calling for a society completely dominated by science, which most people see as a robotic world lacking emotion, empty of art and literature, and devoid of the human need to feel part of something larger than oneself – a need that draws many to religion. Such a world would indeed be sterile and joyless… I am at least as emotional, and enamored of the arts, as the next person, am easily brought to tears by a good movie or book, and do my best to help the less fortunate. All I lack is faith.

I’d gladly give up all works the arts and humanities ever produced in exchange for better psychopharmacological treatments. All literature, music, films, and other classic works of art hold little meaning when compared with the possibility of experiencing pharmaceutically-induced bliss inside my brain. The arts and humanities represent flawed and imprecise attempts to increase meaning in life. Those indirect paths should give way to direct ways of stimulating emotion in the brain. Drugs are the new art.

I don’t think Harvard professor Steven Pinker shares my fanatical take on this topic, but he did an admirable job defending the sciences in the face of onslaughts from humanities enthusiast Leon Wieseltier. I think Pinker remains too conciliatory and forgiving towards the humanities. My attitude towards the arts and humanities is much harsher. Those fields outlived their usefulness and never mattered in the first place. The humanities promote obsolete knowledge that maintains a disproportionate hold on global thought and legislation. Supporters of the humanities often argue that they give students critical thinking skills. You know what’s even better than amorphous ideas about critical thinking? The scientific method.

Defenders of the humanities claim that those programs help students develop meaningful philosophies of life. What if philanthropists and colleges who supported the humanities chose to invest their funds in developing better antidepressants instead? Maybe the suicide rate in the USA wouldn’t outpace deaths from even the colossal number of car accidents like it does now. The arts and humanities also held back mental health treatment from developing better biologically-based treatment options. Cognitive therapy rests on a fundamentally victim-blaming foundation. Psychotherapists expect victims of genes and stressful environments to put hard work into changing their thoughts. People who suffer through psychotherapy pay for the privilege of reopening old wounds and doing therapy homework while the people who victimized them live carefree lives. Popularizers of cognitive therapy like psychiatrist David Burns abandoned his pioneering early-career research in neuroscience and psychopharmacology to go back to a regressive interest in philosophy and its influences on psychotherapy. In fact, newer studies show that the effectiveness of CBT is declining.

Feelings of meaning in life develop from a neurobiological basis in the brain. Ketamine reduces intense suicidal ideation in depressed people in less than an hour and the positive effects last for weeks until the next infusion. The action of ketamine and its analogs stem from a defined biological basis instead of nebulous psychotherapeutic approaches. Companies are working on forms of ketamine with more specificity of action and greater ease of use. A cheap anesthetic that existed since the early 1960’s could give people more meaning in life than psychotherapy (which in many cases shares more in common with the humanities than the social sciences) or philosophy ever did.

Humanities students are victims but not in the way that that conservatives say programs like gender studies create professional victims. Humanities students often have brain disorders or come to college unprepared. They arrive in college from family backgrounds disrupted by alcoholism or family histories of mood disorders. Many people who gravitate towards the arts and humanities would benefit from mental health care. The average non-institutionalized child in the 1980s reported more anxiety than the average child psychiatric patient of the 1950s. The generation of young people in 2002 scored a standard deviation higher for depression and paranoia than young people who lived through the Great Depression. People in the humanities often possess genes predisposing them to mental illness. Engineers tend to be more tough-minded and emotionally resilient, which has a basis in the brain resulting from genes and environment. The end of this post features a list of studies on mental illnesses in creative professions and personality differences between humanities and engineering students. You can look them up in the academic search engine of your choice.

Colleges allow students to study humanities programs that don’t lead to jobs. Those students accumulate student debt that the government prevents them from discharging in bankruptcy. Studying the arts and humanities involves a valuable cost in time that gets squandered – time that could have been invested in something more useful. Humanities students need programs that help them integrate into more useful majors. The Abe administration in Japan announced a plan to incentivize universities to shift funding away from humanities departments and towards more practical subjects. Politicians in the USA should pursue a similar strategy, possibly as part of a student loan reform plan that makes it more difficult for students to get loans for pursuing humanities degrees. Most criticism of the humanities comes from conservatives and libertarians while I tend to lean more towards the political left in terms of compassion for the poor and support for science. Even some conservatives support “Great Books” programs and rehabilitating the humanities by focusing on courses that study Western civilization, but I think they’re misguided in their approach. Classical education lacks value when compared to medical research.

In some cases biology and neuroscience majors make even less money than humanities graduates but I think their programs of study offer immense value to the world and the future. Biology provides a basis for future medical treatments that relieve suffering. That alone is a good reason for all humanities and arts funding to go towards biomedical research funding instead. Funding additional research into the foundations of quantum physics could add trillions of dollars in future economic value in addition to a better understanding of the universe. Most college students currently major in business. As with other popular majors like law and education, many business programs are based on unscientific and outdated folklore instead of evidence-based research and current data. Economics and psychology programs have the same flaws, and some studies in psychology research fail tests of reproducibility.

Even programs where fresh graduates command large starting salaries like petroleum engineering or computer science are still vulnerable to market forces that drive oil below $40 a barrel or cause companies to transfer software development jobs offshore. The fields of regenerative medicine and biogerontology are more important than any other course of study. Someone with a computer science or chemical engineering or finance degree may make lots of money for a while, but their life’s work is ultimately pointless if they eventually just grow old and die someday. Even the smartest engineering graduates will just experience brain degeneration towards the end of their lives unless medical research develops better treatments for age-related conditions.

References:

• A comparison of personality characteristics of male and female engineering students

• Ability tilt on the SAT and ACT predicts specific abilities and college majors

• An Analysis of Computing Major Students’ Myers-Briggs Type Indicator Distribution

• Brain activity measurement during program comprehension with NIRS

• Brain structures in the sciences and humanities

• Can educational streaming be linked to personality? A possible link between extraversion, neuroticism, psychoticism and choice of subjects

• Comparison of three theoretically derived variables in predicting career and academic behavior: Self-efficacy, interest congruence, and consequence thinking

• Convergence of personality and interests: Meta-analysis of the Multidimensional Personality Questionnaire and the Strong Interest Inventory

• Creativity and mental disorder: family study of 300 000 people with severe mental disorder

• Creativity and mental illness: prevalence rates in writers and their first-degree relatives

• Familial Linkage between Neuropsychiatric Disorders and Intellectual Interests

• Key personality traits of engineers for innovation and technology development

• Non-ability correlates of the science-math trait complex: searching for personality characteristics and revisiting vocational interests

• Perceptions of engineering, nursing, and psychology students’ personalities

• Personality characteristics of engineers

• Predicting Engineering Major Status From Mathematics Achievement and Interest Congruence

• The Development and Personality of Engineers

• The Myers-Briggs Personality Type and Its Relationship to Computer Programming

• Understanding understanding source code with functional magnetic resonance imaging

• Women’s career development: Can theoretically derived variables predict persistence in engineering majors?

Immigrants and Brain Scans

Politicians in the USA and Europe spend greater amounts of time discussing undocumented people and migrants. This brings up difficult questions. How can you save the lives of people from dangerous places while at the same time protecting a country’s existing voters? Will economic uncertainty lead to greater xenophobia and hostility towards immigrants? Neuroscience offers a way to solve this problem.

The human brain provides the answer. A country benefits from bringing in compassionate immigrants while keeping violent individuals out. Brain scans predict future violent behavior. These scans lack perfect precision, but they provide useful information that immigration officials currently lack. Researchers like Dr. Adrian Raine and Dr. Kent Kiehl published many studies on how the brains of psychopaths differ from the brains of nonviolent people. Dr. Richard Davidson investigated Buddhist monks’ brain waves and identified patterns of brain activity associated with compassion.

Compassionate immigrants build and protect their new communities. Psychopathic immigrants commit crimes and strain social services. I place an importance on compassion because it transcends ethnic boundaries, while the emotion of empathy may limit itself to one’s own ethnic group.

If I immigrated to a country like Switzerland (notorious for its difficult-to-obtain citizenship) or Norway (at the top of the Human Development Index), I’d graciously accept offers to scan my brain to verify that it didn’t have abnormalities representing the neural correlates of psychopathy. This still doesn’t solve the problem of people in America with broken orbitofrontal cortices buying guns and going on shooting sprees, but that’s a problem for another day.

Probiotics and the Glow of Health

Body image issues that primarily used to affect women and girls are now affecting increasing numbers of men and boys. Media directed at gay men has leaked into mainstream media in ways that negatively impact body image for all males. Gay men have growing prominence in news and entertainment leadership roles and they broadcast their intense critical scrutiny of male bodies. The body dysmorphia and eating disorders that damaged the lives of many gay males now spreads to straight males. Most gay guys are good people, but the catty body-shaming ones ruin it for everyone:

Media directed at straight males also includes actors with optimal bodies and perfect skin. I’m not immune from the impact of this. I have creases on my cheeks that are something like tear troughs or malar festoons. You can read more about these at RealSelf, which is a website designed to give people new body image problems and to encourage unnecessary surgery. These don’t bother me too much and I felt even better after I watched the movie Drive and saw that Ryan Gosling seemed to have them too.

What does this have to do with probiotics? I took a picture of myself for a work ID about a month ago while I was experiencing a variety of gastrointestinal problems. The lighting was bad, but I still thought I looked haggard and decaying. To deal with the nervous stomach and digestive pain, I started taking up to 100 billion CFU (colony forming units) of probiotics a day in supplements and fermented soymilk and probiotic yogurt. I noticed that I started developing smoother skin and even the cheek creases started to become less noticeable.

I had read and forgotten about the gut-skin axis. Probiotics gained attention in dermatology for their ability to treat conditions like atopic dermatitis or eczema. Now researchers and companies are moving beyond the treatment of dermatological diseases to explore the cosmetic potential of probiotics. A study with the wonderful title Probiotic Bacteria Induce a ‘Glow of Health’ found that mice eating probiotic yogurt developed lustrous coats and healthy skin. A company called AOBiome is developing probiotic cosmetics applied by spraying beneficial bacteria on the skin.

Packaging and delivering probiotics requires more care than developing other supplements. Different strains of probiotics can have different effects. Companies also need to ensure the survival of probiotic bacteria through correct packaging and transportation and storage. Since collagen and hyaluronic acid also enhance skin appearance, it would be interesting to research ways of combining them with probiotics for either topical or oral use.

I think of probiotics in this way, as listed from greatest to least importance:

1: preventing mortality with probiotics that treat infectious diseases in developing countries and prevent infant mortality and prevent colon cancer (videos from the Human Microbiome Science: Vision for the Future conference describe interesting areas of microbiome research)

2: using probiotics to treat painful and inflammatory skin conditions

3: using probiotics for cosmetic purposes

Sadly the profitability of these will probably end up reversed, with probiotic cosmetics making the biggest profits. Meanwhile, saving infant lives with probiotics will remain the duty of low-paid international health workers. There’s still plenty of room for “doing well by doing good” where social enterprises could make money selling probiotic cosmetics while using a percentage of their profits to fund programs that use probiotics to cure deadly diseases.

Predicting the Future is a Matter of Life and Death

Predicting the future could be the most important pursuit available to a person. A single mistake can lead to a ruined reputation, serious injuries, or even death. The pain of dying is bad enough, but most people have a misplaced attitude of acceptance or resignation towards death. This often comes from what biogerontologist Aubrey de Grey calls the pro-aging trance. Most people accept that death comes eventually from illness or aging or accidents and resign themselves towards their fate. They use religion or distraction to deal with their existential anxiety regarding death. There’s a big problem with this approach.

Religious people and atheists claim to know for sure what happens after death. Religious groups maintain that either a person ends up in an afterlife (almost always a positive one) or reincarnated. Atheists think human consciousness just disappears after the brain irreversibly degrades. Each side finds evidence to support their viewpoint, but no one can say with 100% certainty what happens after death. That leaves it open for anxious people like me to interpret death as a worst-case scenario. What if there’s a tiny chance that the universe is not just uncaring but infinitely cruel? What if whatever happens to human consciousness after death is even worse than the worst fate anyone can imagine? What if trickster gods or extraterrestrials extract human consciousness at the point of death to torture it forever? I guess you could call this the Hellraiser Hypothesis, derived from the series of movies featuring extradimensional beings devoted to pain. This may be a remote possibility, but absence of evidence is not evidence of absence.

This is why it’s so important to identify and prevent every potential threat to life. This is a huge goal that can rapidly overwhelm the human brain, and I’ll return to it at the end of this post. One of the many cognitive biases the average human being has is the belief in a just world. This mistaken belief that people deserve whatever happens to them often occurs alongside the fundamental attribution error, where outcomes are viewed as resulting from stable personality traits instead of situational factors. If someone makes a mistake, these cognitive biases lead others to blame the victim and say someone should always anticipate anything that happens to him or her. Identifying areas of economic growth and profit is vastly less important than prolonging healthy human life but still holds the interest of many people.

Predicting the economy and the stock market and their effects on human life represent one of the largest areas of prediction. Most economists and people in finance have had a less than desirable track record in predicting the economy and stock market. This may be improving with quantitative finance techniques drawn from physics and analyzing big data like Google Trends, but these prediction methods still lack precision. When choosing a major, students are expected to predict the state of the global economy four years later. Students can pick petroleum engineering as a major one year when they see newly graduated petroleum engineers have the highest salaries of any graduates. When they earn their degree four (or five) years later then oil companies are cutting back hiring because oil dropped below $40 a barrel. I learned the importance of prediction when I got a worthless humanities degree because I thought nothing I could study would matter in the end anyway. Scrupulosity gave me religious obsessions about judgment and the end of the world. I also thought nearly everyone on earth would be dead before I graduated. If the end of days didn’t happen, I thought humanity would be wiped out by nuclear war or bioterrorism or from any number of causes. Terror management theory suggests that large parts of human psychology are devoted to dealing with the existential threat of death. Most people try not to think too much about death because worrying about death every day like I do can bring a person to the brink of madness.

It’s important to predict the future at individual, local, national, and global levels. The growing fields of predictive analytics and futures studies attempt this. Predicting the future involves quantifying just how much importance to put in history, along with mapping relationships between existing local and global entities that can shape the future. Futurist and engineer Ray Kurzweil has a separate approach. Kurzweil’s strategy is to combine the idea of exponential change with tracking advancements in all fields of science and engineering. He also describes that importance of identifying the optimal point where people become accepting of new inventions. As an inventor, he had to time the adoption of inventions because being too early or too late to market can doom an invention. His report How My Predictions Are Faring takes a look at his earlier predictions and evaluates their accuracy. Kurzweil’s upcoming book The Singularity is Nearer is rumored to describe the progress of the predictions from his earlier book The Singularity is Near. Philip Tetlock, who studies forecasts made by experts, is publishing a book titled Superforecasting about identifying strategies of experts who can actually make accurate predictions.

In my view, using prediction to prevent all causes of death is the most important aspect of predicting the future. This involves predicting and preventing leading causes of mortality, predicting and preventing crimes, and predicting and preventing future epidemics. This involves spotting new trends in pools of data and rapidly responding to them. It also includes using statistical models and quantitative prediction. This involves using mathematical models in public health and crime prevention (Statistical physics of crime: A review). Journals like Technological Forecasting and Social Change publish research on forecasting various areas.

An important aspect of prediction is thinking in probabilistic ways. It’s extremely difficult to predict the future with perfect precision, so most decision analysis involves probability. The problem is that the human brain isn’t very good at calculating probabilities, especially in rapidly changing situations or situations that involve extremely large amounts of information. A computer can calculate probabilities faster and more accurately than humans. IBM’s Watson computer can already understand and extract information from medical research. The next step is a computer like Watson that can read and understand all scientific, engineering, statistical, and mathematical research and make predictions from that research.

Individual people could enhance their decision-making capabilities with heads-up displays like Google Glass. They could combine this with wearing an attachment in a big hat that monitors the environment, similar to the electronics on top of Google’s self-driving cars. Looking like a dweeb is a small price to pay for staying safe. However, I think there’s an alternative that allows people to improve their decisions while staying fashionable and inconspicuous without having to wear massive headgear. Security cameras in the environment integrated into a cloud network could use computer vision and deep learning to identify environmental threats. This system could identify if someone is acting agitated and has folds in their clothes indicating they have a gun. That information could be integrated into a display embedded in fashionable glasses indistinguishable from other sets of glasses. The network could also identify people coughing and warn people to avoid certain areas with diseases, or it could identify anomalous patterns in the environment to help people avoid potential accidents.

I feel guilty every time I eat something that isn’t a medicinal and functional food or which doesn’t enhance longevity. A heads-up display in glasses could use image recognition combined with communication to a medical computer like Watson. This system could integrate information from epidemiological studies and lab animal studies and personal genomics to show the effect any particular food has on long-term health. Each of those individual methods (dietary epidemiology, lab animal studies, personalized medicine) has imperfections but they might work well when combined together in a predictive framework.

The next stage is brain implants for instantaneous decision enhancement. A neuroprosthesis already improved decision-making in monkeys. Neuroprosthetics also improved memory in non-human primates. Future neural engineering and neuroprosthetics could restore brain function to people with Alzheimer’s disease or traumatic brain injuries. After brain implants prove their value and safety in people with brain diseases, the next step is to allow healthy people to improve their decisions with neuroprosthetics.

Advertising is Mind Rape

Advertising is non-consensual at its core. Advertising jumps right at you or sneaks up on you. Advertising penetrates your consciousness without asking for your permission first. Advertising presses its full weight on your mind and doesn’t let go until it pounds itself into your body image and self-image, damaging it for a lifetime. Advertising is mind rape and advertisers are rapists of the mind. Advertising may not be as emotionally distressing as sexual assault, but it’s still fundamentally non-consensual in nature. Advertising gets people to ruin their personal finances by convincing them to buy things they don’t need, negatively impacts body image, and will soon reshape the brain with even greater force through the use of neuromarketing. An annotated bibliography at the end of this post describes the impact of advertising on the brain and its negative effects on human psychology.

The company PageFair recently released its ad blocking report in partnership with Adobe. According to the report, 45 million users in the USA are now fighting back against intrusive advertising by using ad blockers. The number of people using ad blocking technology is growing by 41% globally year over year. The heroic and forward-thinking people who use ad blockers are denying nearly $22 billion in revenue to the mind-rapists (advertisers and their sycophants). There’s still plenty of room for ad blocking to grow on desktop browsers and especially on mobile browsers.

Apple is going to offer technology for mobile web ad blocking in iOS 9. Unfortunately, Apple will still have in-app ads through iAd unless someone finds a workaround. I’m glad Google is organizing itself into its new Alphabet form so now the new conglomerate can keep its dirty ad-driven businesses away from its more pure divisions that focus on life extension and energy efficiency.

One line of argument states that blocking ads hurts publishers, but most publishers and sources of news deserve to go away anyway. Many news sites just steal others’ work or spread rumors or post slightly rewritten press releases. As native advertising grows, those publishers will become even more useless when they start adding more and more sponsored content. Most of the sites are already useless since PR copy from corporations and interest groups started infiltrating lazy journalists’ stories a long time ago. People would be better off learning useful skills and gaining scientific knowledge from nonprofit sources instead of reading the average news site. I would gladly trade all advances in web and mobile technology over the past twenty years for twenty years of additional advancement in medicine instead.

Advertisers and publishers claim to be victims of ad blockers but they don’t extend that privilege to their real victims. A common pro-advertising argument states that people can just choose to ignore advertising. Unfortunately, most advertising is too intrusive to ignore. Just like free will, personal responsibility (like the presumed responsibility of people to ignore advertising or the choice to not be influenced by ad culture) is an unscientific myth that stems from victim blaming and just-world biases. If people become obese or spend all their money it’s actually not their fault but instead the result of a brain shaped by gene-environment interactions and influenced by the advertising industry. Advertising spending in the USA alone is projected to reach $200 billion by 2017. Global ad spending is estimated at $540 billion in 2015. Why would all this money be spent on advertising if it had no effect on people?

Everyone is a victim of something in life even if they don’t realize it yet. Free will never existed in the first place since human beings are controlled by physical forces, but human actions are even more determined now by advertising strategies powered by user tracking and big data. The Citizens United v. FEC decision means that interest groups and super PACs can spend as much as they want on neuromarketing and the psychology of advertising to brainwash people and influence the political process. Neuromarketing is also being used to promote alcohol, which remains a major cause of death and crime when used in excess. Neuromarketing is a growing field, aptly demonstrated by this extensive list of neuromarketing companies. Even when people give legal consent to be marketed to, like when they watch a program on TV, do they realize the true extent of the manipulation they signed up for?

Instead of doing something useful for humanity like medical researchers do, advertisers don’t do anything valuable to extend human lifespan. In many cases, advertisers contribute to ending human life and harming public health by promoting unhealthy food and tobacco products. Advertisers will contribute to millions of deaths through tobacco advertising in developing countries just like they did in the United States. Advertisers’ lives have no value since they’ll either end up in hell or have their consciousness disappear into nothingness after adding no value to others’ lives. The lives of advertisers’ children are also worthless since those children are just being raised by ad-men and ad-women who are empty at best and evil at worst. Thanks to their genes and environment, those children will probably grow up only to ignore consent and bully others and live lives just as empty as those their parents lived.

People who work in advertising will eventually grow older and fatter and out of touch with youth culture. When that happens, they will find themselves increasingly marginalized by a lookist and ageist society shaped as a result of their own work. Will they realize that they brought it on themselves through their contributions to the world of advertising? Regular people already realize the negative influence advertisers have on society. Advertisers are disliked nearly as much as criminals are. Women who work in the advertising industry are especially faced with challenges because of advertising’s non-consensual and body-shaming foundation. Advertisers aren’t moral enough to do something that actually helps people and they aren’t intelligent enough to do something that solves real problems. Advertisers are just disgusting mind rapists.

Advertising and the Brain:

Brain Responses to Food Logos in Obese and Healthy Weight Children – Obese children have greater activation in reward regions of the brain when seeing food logos.

Branding and a child’s brain: an fMRI study of neural responses to logos – Children’s brains show greater activation to food logos in regions associated with motivation and attention than to non-food logos.

Evaluation of TV commercials using neurophysiological responses – A “happiness index” measured by brain waves can be used to develop more engrossing commercials.

Leptin Is Associated With Exaggerated Brain Reward and Emotion Responses to Food Images in Adolescent Obesity – Obese adolescents show exaggerated activity in reward and emotion regions of the brain in response to food images.

Mapping a multidimensional emotion in response to television commercials – Emotional changes in the brain involving the inferior frontal gyri and middle temporal gyri, and in the right superior temporal gyrus and right middle frontal gyrus, play a role in human response to advertising.

Neural predictors of purchases – Activation in regions of the nucleus accumbens, insula, and mesial prefrontal cortex influences purchasing decisions.

Neuromarketing and consumer neuroscience: contributions to neurology – Brand preference, celebrity endorsement, and trust involve certain regions and networks of the brain and could be used by neuromarketers.

Neuromarketing: the hope and hype of neuroimaging in business – Many neuromarketers rely on activation in the nucleus accumbens, which has a strong statistical relationship with reward-related processes. Research on brain responses to political candidates could also be used to select candidates that are superficially appealing.

Predicting Advertising Success Beyond Traditional Measures: New Insights from Neurophysiological Methods and Market Response Modeling – Activity in the ventral striatum is the best predictor of response to advertising.

Relation of obesity to neural activation in response to food commercials – Adolescents experience greater activation in attention and reward regions of the brain during food commercials.

Severity of dependence modulates smokers’ neuronal cue reactivity and cigarette craving elicited by tobacco advertisement –  Tobacco advertising elicits brain activity associated with craving in both smokers and nonsmokers.

Advertising and Body Image:

Depicting Women as Sex Objects in Television Advertising: Effects on Body Dissatisfaction – Sexist ads increase body dissatisfaction in both women and men.

Extending Social Comparison: An Examination of the Unintended Consequences of Idealized Advertising Imagery – Advertising that includes images of physical attractiveness and financial success has negative effects on males’ self-perceptions.

Idealized media images and adolescent body image: “comparing” boys and girls – TV commercials promoting certain body ideals increase body dissatisfaction and negative mood.

The Effect Of Television Commercials On Mood And Body Dissatisfaction: The Role Of Appearance-Schema Activation – Appearance-related commercials increase anger and body dissatisfaction in women.

The Effect of Thin Ideal Media Images on Women’s Self-Objectification, Mood, and Body Image – Magazine ads lead to greater appearance anxiety, negative mood, and body dissatisfaction in women.

The Impact of Media Exposure on Males’ Body Image – Males become more depressed when shown ads with images of ideal males.

Amyotrophic Lateral Sclerosis Treatments

Animal experiments indicate there are some promising potential treatments for amyotrophic lateral sclerosis. While there’s no true cure for ALS yet, some of these experiments show that new compounds and natural substances can treat symptoms and extend lifespan.

They include:

3-4 diaminopyridine

5-Hydroxytryptophan

5D10

Acetyl-L-Carnitine

Activated Protein C

AEOL 10150

AGS-499

AM-1241

Ammonium tetrathiomolybdate

Angiogenin

Arimoclomol

Ascorbate

Bee Venom

Caffeic Acid Phenethyl Ester

Cannabinol

Caprylic Triglyceride

Celastrol

CK-2017357

Clenbuterol

Colivelin

Creatine

Cyclosporine

D-Penicillamine

Dasatinib

Davunetide

Delta(9)-tetrahydrocannabinol

Dexpramipexole

Diallyl Trisulfide

Dichloroacetate

Dihydrotestosterone

Dimebon

DL-3-n-butylphthalide

DP-109

DP-460

Edaravone

EGb761 (Gingko Biloba Extract)

ENKAD

Epigallocatechin-3-gallate (EGCG)

Exendin-4

Fasudil

Folic Acid

Galactooligosaccharide

Gemals

Ginseng Root

GPI-1046

Granulocyte Colony Stimulating Factor

GSK-3 inhibitor VIII

Heat Shock Protein 70

Hepatocyte Growth Factor

HLA20

Iron Porphyrin

Ivermectin

Jiawei Sijunzi (JWSJZ)

L-745,870

L-arginine

Lead

Lenalidomide

Lipoic Acid

M30

Manganese Porphyrin

Melatonin

Memantine

Methionine Sulfoximine

Milk Whey Proteins

N-acetyl-L-cysteine

Nortriptyline

Olesoxime

Oxidized Galectin-1

P7C3A20

Pegfilgrastim

Phenylbutyrate

Pioglitazone

Polyamine-Modified Catalase

PRE-084

Progesterone

Pyruvate

Rasagiline

Recombinant Human Erythropoietin

Recombinant Human Insulinlike Growth Factor-I (rhIGF-I)

Resveratrol

Riluzole

Ro 28-2653

RPR 119990

S-adenosyl Methionine

S[+]-Apomorphine

Scolopendra Subspinipes Mutilans

Semapimod

SK-PC-B70M

Sodium Phenylbutyrate

Suppressor Factor

Talampanel

TAT-modified Bcl-X(L)

Tempol

Tianeptine

Trichostatin A

Trientine

TRO19622

Uridine

Vascular Endothelial Growth Factor

Vincristine

Vitamin D3

Vitamin E

VK-28

Wen-Pi-Tang

ZK 187638

References:

A dopamine receptor antagonist L-745,870 suppresses microglia activation in spinal cord and mitigates the progression in ALS model mice. http://www.ncbi.nlm.nih.gov/pubmed/18423451

A double-blind study of the effectiveness of cyclosporine in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/3281637

A phase II trial of talampanel in subjects with amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19961264

A pilot trial of memantine and riluzole in ALS: correlation to CSF biomarkers. http://www.ncbi.nlm.nih.gov/pubmed/20839903

Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells. http://www.ncbi.nlm.nih.gov/pubmed/19841542

Additive neuroprotective effects of a histone deacetylase inhibitor and a catalytic antioxidant in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16289867

AM1241, a cannabinoid CB2 receptor selective compound, delays disease progression in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16781706

Ammonium tetrathiomolybdate delays onset, prolongs survival, and slows progression of disease in a mouse model for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18617166

Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. http://www.ncbi.nlm.nih.gov/pubmed/15204022

An ALS mouse model with a permeable blood-brain barrier benefits from systemic cyclosporine A treatment. http://www.ncbi.nlm.nih.gov/pubmed/14756802

An attempt to inhibit the course of amyotrophic lateral sclerosis (ALS) by suppressor factor. http://www.ncbi.nlm.nih.gov/pubmed/8993772

Autophagy activation and neuroprotection by progesterone in the G93A-SOD1 transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23891729

Bee venom attenuates neuroinflammatory events and extends survival in amyotrophic lateral sclerosis models. http://www.ncbi.nlm.nih.gov/pubmed/20950451

Beneficial effect of ginseng root in SOD-1 (G93A) transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/11090864

Benefit of a combined treatment with trientine and ascorbate in familial amyotrophic lateral sclerosis model mice. http://www.ncbi.nlm.nih.gov/pubmed/10327155

Benefit of tianeptine and morphine in a transgenic model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16546757

c-Abl inhibition delays motor neuron degeneration in the G93A mouse, an animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23049975

Caffeic acid phenethyl ester extends survival of a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22206942

Cannabinol delays symptom onset in SOD1 (G93A) transgenic mice without affecting survival. http://www.ncbi.nlm.nih.gov/pubmed/16183560

Caprylic triglyceride as a novel therapeutic approach to effectively improve the performance and attenuate the symptoms due to the motor neuron loss in ALS disease. http://www.ncbi.nlm.nih.gov/pubmed/23145119

Celastrol blocks neuronal cell death and extends life in transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16909005

Chemotherapy delays progression of motor neuron disease in the SOD1 G93A transgenic mouse. http://www.ncbi.nlm.nih.gov/pubmed/15282441

Colivelin prolongs survival of an ALS model mouse. http://www.ncbi.nlm.nih.gov/pubmed/16564029

Combined riluzole and sodium phenylbutyrate therapy in transgenic amyotrophic lateral sclerosis mice. http://www.ncbi.nlm.nih.gov/pubmed/18618304

Control of motoneuron survival by angiogenin. http://www.ncbi.nlm.nih.gov/pubmed/19109488

Death receptor 6 (DR6) antagonist antibody is neuroprotective in the mouse SOD1(G93A) model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/24113175

Dexpramipexole effects on functional decline and survival in subjects with amyotrophic lateral sclerosis in a Phase II study: subgroup analysis of demographic and clinical characteristics. http://www.ncbi.nlm.nih.gov/pubmed/22985432

Dietary supplementation with S-adenosyl methionine delays the onset of motor neuron pathology in a murine model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19757209

Dietary vitamin D3 supplementation at 10× the adequate intake improves functional capacity in the G93A transgenic mouse model of ALS, a pilot study. http://www.ncbi.nlm.nih.gov/pubmed/22591278

Dihydrotestosterone ameliorates degeneration in muscle, axons and motoneurons and improves motor function in amyotrophic lateral sclerosis model mice. http://www.ncbi.nlm.nih.gov/pubmed/22606355

Dimebon slows progression of proteinopathy in γ-synuclein transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/22179976

DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22056419

Effect of nutritional supplementation with milk whey proteins in amyotrophic lateral sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/20464297

Effect of recombinant human insulin-like growth factor-I on progression of ALS. A placebo-controlled study. The North America ALS/IGF-I Study Group. http://www.ncbi.nlm.nih.gov/pubmed/9409357

Effect of sex on lifespan, disease progression, and the response to methionine sulfoximine in the SOD1 G93A mouse model for ALS. http://www.ncbi.nlm.nih.gov/pubmed/23217569

Effects of 3-4 diaminopyridine (DAP) in motor neuron diseases. http://www.ncbi.nlm.nih.gov/pubmed/21321491

Effects of an inhibitor of poly(ADP-ribose) polymerase, desmethylselegiline, trientine, and lipoic acid in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/11259130

Exendin-4 ameliorates motor neuron degeneration in cellular and animal models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22384126

Exogenous delivery of heat shock protein 70 increases lifespan in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18045911

Fasudil, a rho kinase inhibitor, limits motor neuron loss in experimental models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23763343

Folic acid protects motor neurons against the increased homocysteine, inflammation and apoptosis in SOD1 G93A transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/18436268

Galactooligosaccharide improves the animal survival and alleviates motor neuron death in SOD1G93A mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23673277

Gemals, a new drug candidate, extends lifespan and improves electromyographic parameters in a rat model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18428000

Glutamate AMPA receptors change in motor neurons of SOD1G93A transgenic mice and their inhibition by a noncompetitive antagonist ameliorates the progression of amytrophic lateral sclerosis-like disease. http://www.ncbi.nlm.nih.gov/pubmed/16323214

Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21711557

Granulocyte-colony stimulating factor improves outcome in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18835867

Identification and characterization of cholest-4-en-3-one, oxime (TRO19622), a novel drug candidate for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17496168

Inhibition of glycogen synthase kinase-3 suppresses the onset of symptoms and disease progression of G93A-SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17433298

Inhibition of p38 mitogen activated protein kinase activation and mutant SOD1(G93A)-induced motor neuron death. http://www.ncbi.nlm.nih.gov/pubmed/17346981

Intake of polyunsaturated fatty acids and vitamin E reduces the risk of developing amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16648143

Intracerebroventricular infusion of monoclonal antibody or its derived Fab fragment against misfolded forms of SOD1 mutant delays mortality in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/20345765

Intrathecal cyclosporin prolongs survival of late-stage ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/11251210

Intrathecal delivery of hepatocyte growth factor from amyotrophic lateral sclerosis onset suppresses disease progression in rat amyotrophic lateral sclerosis model. http://www.ncbi.nlm.nih.gov/pubmed/17984685

Investigation of the therapeutic effects of edaravone, a free radical scavenger, on amyotrophic lateral sclerosis (Phase II study). http://www.ncbi.nlm.nih.gov/pubmed/17127563

Iron porphyrin treatment extends survival in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/12641736

Ivermectin inhibits AMPA receptor-mediated excitotoxicity in cultured motor neurons and extends the life span of a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17045808

Late stage treatment with arimoclomol delays disease progression and prevents protein aggregation in the SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/18673445

Lead exposure stimulates VEGF expression in the spinal cord and extends survival in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/19914377

Lenalidomide (Revlimid) administration at symptom onset is neuroprotective in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19733563

Life span extension and reduced neuronal death after weekly intraventricular cyclosporin injections in the G93A transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15255263

Manganese porphyrin given at symptom onset markedly extends survival of ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/16049935

Mechano-growth factor, an IGF-I splice variant, rescues motoneurons and improves muscle function in SOD1(G93A) mice. http://www.ncbi.nlm.nih.gov/pubmed/19038252

Melatonin inhibits the caspase-1/cytochrome c/caspase-3 cell death pathway, inhibits MT1 receptor loss and delays disease progression in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23537713

Memantine prolongs survival in an amyotrophic lateral sclerosis mouse model. http://www.ncbi.nlm.nih.gov/pubmed/16262676

Methionine sulfoximine, an inhibitor of glutamine synthetase, lowers brain glutamine and glutamate in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/20060132

Modulation of astrocytic mitochondrial function by dichloroacetate improves survival and motor performance in inherited amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22509356

Motor neuronal protection by L-arginine prolongs survival of mutant SOD1 (G93A) ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/19427829

MRS study of the effects of minocycline on markers of neuronal and microglial integrity in ALS. http://www.ncbi.nlm.nih.gov/pubmed/20832222

Muscle-derived but not centrally derived transgene GDNF is neuroprotective in G93A-SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17034790

N-acetyl-L-cysteine improves survival and preserves motor performance in an animal model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/10943709

NAP (davunetide) modifies disease progression in a mouse model of severe neurodegeneration: protection against impairments in axonal transport. http://www.ncbi.nlm.nih.gov/pubmed/23631872

Neurochemical correlates of differential neuroprotection by long-term dietary creatine supplementation. http://www.ncbi.nlm.nih.gov/pubmed/16140286

Neuroprotective and neuritogenic activities of novel multimodal iron-chelating drugs in motor-neuron-like NSC-34 cells and transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19638399

Neuroprotective effect of oxidized galectin-1 in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15899257

Neuroprotective effects of (-)-epigallocatechin-3-gallate in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17021948

Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/10086395

Neuroprotective effects of diallyl trisulfide in SOD1-G93A transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21147075

Neuroprotective effects of the Sigma-1 receptor (S1R) agonist PRE-084, in a mouse model of motor neuron disease not linked to SOD1 mutation. http://www.ncbi.nlm.nih.gov/pubmed/24141020

Neuroprotective efficacy of aminopropyl carbazoles in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23027932

Nortriptyline delays disease onset in models of chronic neurodegeneration. http://www.ncbi.nlm.nih.gov/pubmed/17686041

Novel telomerase-increasing compound in mouse brain delays the onset of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22351600

Olesoxime delays muscle denervation, astrogliosis, microglial activation and motoneuron death in an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/22369784

Open Randomized Clinical Trial on JWSJZ Decoction for the Treatment of ALS Patients. http://www.ncbi.nlm.nih.gov/pubmed/24093046

Peroxisome proliferator-activated receptor-gamma agonist extends survival in transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15649489

Preliminary investigation of effect of granulocyte colony stimulating factor on amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19922135

Prevention of motor neuron degeneration by novel iron chelators in SOD1(G93A) transgenic mice of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21346313

Pyruvate slows disease progression in a G93A SOD1 mutant transgenic mouse model. http://www.ncbi.nlm.nih.gov/pubmed/17174029

Randomized double-blind placebo-controlled trial of acetyl-L-carnitine for ALS. http://www.ncbi.nlm.nih.gov/pubmed/23421600

Rasagiline alone and in combination with riluzole prolongs survival in an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/15372249

Recombinant human erythropoietin suppresses symptom onset and progression of G93A-SOD1 mouse model of ALS by preventing motor neuron death and inflammation. http://www.ncbi.nlm.nih.gov/pubmed/17439481

Reduced oxidative damage in ALS by high-dose enteral melatonin treatment. http://www.ncbi.nlm.nih.gov/pubmed/17014688

Regenerative therapies for amyotrophic lateral sclerosis using hepatocyte growth factor. http://www.ncbi.nlm.nih.gov/pubmed/22277532

Resveratrol upregulated heat shock proteins and extended the survival of G93A-SOD1 mice. http://www.ncbi.nlm.nih.gov/pubmed/23000195

RPR 119990, a novel alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid antagonist: synthesis, pharmacological properties, and activity in an animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11561094

S[+] Apomorphine is a CNS penetrating activator of the Nrf2-ARE pathway with activity in mouse and patient fibroblast models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23608463

Safety, tolerability and pharmacodynamics of a skeletal muscle activator in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22591195

Scolopendra subspinipes mutilans attenuates neuroinflammation in symptomatic hSOD1G93A mice. http://www.ncbi.nlm.nih.gov/pubmed/24168240

Selective up-regulation of the glial Na+-dependent glutamate transporter GLT1 by a neuroimmunophilin ligand results in neuroprotection. http://www.ncbi.nlm.nih.gov/pubmed/16274998

Sigma-1R agonist improves motor function and motoneuron survival in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/22935988

SK-PC-B70M alleviates neurologic symptoms in G93A-SOD1 amyotrophic lateral sclerosis mice. http://www.ncbi.nlm.nih.gov/pubmed/20971081

Tempol moderately extends survival in a hSOD1(G93A) ALS rat model by inhibiting neuronal cell loss, oxidative damage and levels of non-native hSOD1(G93A) forms. http://www.ncbi.nlm.nih.gov/pubmed/23405225

The CB2 cannabinoid agonist AM-1241 prolongs survival in a transgenic mouse model of amyotrophic lateral sclerosis when initiated at symptom onset. http://www.ncbi.nlm.nih.gov/pubmed/17241118

The Chinese prescription Wen-Pi-Tang extract delays disease onset in amyotrophic lateral sclerosis model mice while attenuating the activation of glial cells in the spinal cord. http://www.ncbi.nlm.nih.gov/pubmed/19252282

The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/9240414

The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice. http://www.ncbi.nlm.nih.gov/pubmed/16356650

The lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17630988

The matrix metalloproteinases inhibitor Ro 28-2653 [correction of Ro 26-2853] extends survival in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/16516196

The oral antidiabetic pioglitazone protects from neurodegeneration and amyotrophic lateral sclerosis-like symptoms in superoxide dismutase-G93A transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/16120782

The serotonin precursor 5-hydroxytryptophan delays neuromuscular disease in murine familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/14527871

Therapeutic benefit of polyamine-modified catalase as a scavenger of hydrogen peroxide and nitric oxide in familial amyotrophic lateral sclerosis transgenics. http://www.ncbi.nlm.nih.gov/pubmed/11117554

Therapeutic benefits of intrathecal protein therapy in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18543336

Therapeutic effects of clenbuterol in a murine model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16388902

Therapeutic effects of dl-3-n-butylphthalide in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22800896

Therapeutic efficacy of EGb761 (Gingko biloba extract) in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11665866

Treatment of amyotrophic lateral sclerosis with ribonucleotides. http://www.ncbi.nlm.nih.gov/pubmed/1266475

Treatment with arimoclomol, a coinducer of heat shock proteins, delays disease progression in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/15034571

Treatment with edaravone, initiated at symptom onset, slows motor decline and decreases SOD1 deposition in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/18718468

Treatment with trichostatin A initiated after disease onset delays disease progression and increases survival in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21712032

Uridine ameliorates the pathological phenotype in transgenic G93A-ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/20565334

Vascular endothelial growth factor prolongs survival in a transgenic mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/15389897

VEGF delivery with retrogradely transported lentivector prolongs survival in a mouse ALS model. http://www.ncbi.nlm.nih.gov/pubmed/15164063

Vitamin D deficiency and its supplementation in patients with amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23815870

Vitamin E intake and risk of amyotrophic lateral sclerosis: a pooled analysis of data from 5 prospective cohort studies. http://www.ncbi.nlm.nih.gov/pubmed/21335424

Vitamin E intake and risk of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15529299

Vitamin E serum levels and controlled supplementation and risk of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23286756