Scientists have found that blocking the ability to move the body causes changes in cognition and emotion, but there were always questions. (One of the test treatments caused widespread, if temporary, paralysis.) In contrast, Havas was studying people after a pinpoint treatment to paralyze a single pair of “corrugator” muscles, which cause brow-wrinkling frowns.

To test how blocking a frown might affect comprehension of language related to emotions, Havas asked the patients to read written statements, before and then two weeks after the Botox treatment. The statements were angry (“The pushy telemarketer won’t let you return to your dinner”); sad (“You open your email in-box on your birthday to find no new emails”); or happy (“The water park is refreshing on the hot summer day.”)

Havas gauged the ability to understand these sentences according to how quickly the subject pressed a button to indicate they had finished reading it. “We periodically checked that the readers were understanding the sentences, not just pressing the button,” says Havas.

The results showed no change in the time needed to understand the happy sentences. But after Botox treatment, the subjects took more time to read the angry and sad sentences. Although the time difference was small, it was significant, he adds. Moreover, the changes in reading time couldn’t be attributed to changes in participants’ mood.

The use of Botox to test how making facial expressions affect emotional centers in the brain was pioneered by, Andreas Hennenlotter of the Max Planck Institute in Leipzig, Germany.

“There is a long-standing idea in psychology, called the facial feedback hypothesis,” says Havas. “Essentially, it says, when you’re smiling, the whole world smiles with you. It’s an old song, but it’s right. Actually, this study suggests the opposite: When you’re not frowning, the world seems less angry and less sad.”

The Havas study broke new ground by linking the expression of emotion to the ability to understand language, says Havas’s advisor, UW-Madison professor emeritus of psychology Arthur Glenberg. “Normally, the brain would be sending signals to the periphery to frown, and the extent of the frown would be sent back to the brain. But here, that loop is disrupted, and the intensity of the emotion, and of our ability to understand it when embodied in language, is disrupted.”

Practically, the study “may have profound implications for the cosmetic-surgery,” says Glenberg. “Even though it’s a small effect, in conversation, people respond to fast, subtle cues about each other’s understanding, intention and empathy. If you are slightly slower reacting as I tell you about something made me really angry, that could signal to me that you did not pick up my message.”

To better understand its neurobiology, Feusner and colleagues examined 17 patients with BDD and matched them by sex, age and education level with 16 healthy people. Participants underwent functional magnetic resonance imaging (fMRI) while viewing photographs of two faces — their own and that of a familiar actor — first unaltered, and then altered in two ways to parse out different elements of visual processing.

One altered version included only high-spatial frequency information, which would allow detailed analysis of facial traits, including blemishes and hairs. The other showed only low-spatial frequency information, conveying the general shape of the face and the relationship between facial features.

Compared to the control participants, individuals with BDD demonstrated abnormal brain activity in visual processing systems when viewing the unaltered and low-spatial frequency versions of their own faces. They also had unusual activation patterns in their frontostriatal systems, which help control and guide behavior and maintain emotional flexibility in responding to situations.

Brain activity in both systems correlated with the severity of symptoms. In addition, differences in activity in the frontostriatal system varied based on participant reports of how disgusting or repulsive they found each image. Basically, how ugly the individuals viewed themselves appeared to explain abnormal brain activity in these systems.

The abnormal activation patterns, especially in response to low-frequency images, suggest that individuals with body dysmorphic disorder have difficulties perceiving or processing general information about faces.

“This may account for their inability to see the big picture — their face as a whole,” Feusner said. “They become obsessed with detail and think everybody will notice any slight imperfection on their face. They just don’t see their face holistically.”

Intel has invested large amounts of money on research and development of thought-controlled devices, otherwise known as brain-computer interfaces. Research is underway to determine the best way to harness the power of thought. The internal method requires a craniotomy to implant electrodes in or upon the brain, while the external method consists of applying electrodes to the scalp to monitor brainwaves.

The implications of the research could hold many benefits for spinal cord injury sufferers and traumatic brain injury survivors. Electrodes implanted directly into a patient’s brain may control prosthetic limbs of the near future. The devices might even include some kind of sensors to simulate the sensation of touch along the prosthetic skin.

Monitoring devices grow increasingly complex, as companies develop computers that can collect psychological data. Attention Control Systems Inc. is developing a bot that will, “collect psychological data, detect panic attacks and measure psychological symptoms,” according to the Wired article.

For veterans suffering with the symptoms of traumatic brain injury, the military has invested in high-tech schedulers to remind patients to complete various tasks, to help them stay focused throughout the day, and to monitor their movement and give them prompts when necessary.

With current advances in neurology, electronics, brain-computer interfaces, wireless technology, biotechnology, genetics, stem cells, and prosthetics, the future looks bright for spinal cord injury and traumatic brain injury survivors.

A scientific group led by the Translational Genomics Research Institute (TGen) have identified three kinases, or proteins, that dismantle connections within brain cells, which may lead to memory loss associated with Alzheimer’s disease.

These findings, the results of a multi-year TGen study, are published in this month’s edition of BMC Genomics in a paper titled: High-content siRNA screening of the kinome identifies kinases involved in Alzheimer’s disease-related tau hyperphosphorylation.

The three kinases were found to cause a malfunction in tau, a protein critical to the formation of the microtubule bridges within brain cells, or neurons. These bridges support the synaptic connections that, like computer circuits, allow neurons to communicate with each other.

“The ultimate result of tau dysfunction is that neurons lose their connections to other neurons, and when neurons are no longer communicating, that has profound effects on cognition – the ability to think and reason,” said Dr. Travis Dunckley, an Associate Investigator in TGen’s Neurodegenerative Research Unit and the scientific paper’s senior author.

Tau performs a critical role in the brain by helping bind together microtubules, which are sub-cellular structures that create scaffolding in the neurons, allowing them to stretch out along bridges called axons. The axons su

pport the synaptic, or chemical, connections with other neurons.

Under normal circumstances, kinases regulate tau by adding phosphates. This process, called tau phosphorylation, enables the microtubules to unbind and then bind again, allowing brain cells to connect and reconnect with other brain cells.

“That facilitates synaptic plasticity. It facilitates the ability of people to form new memories – to form new connections between different neurons – and maintain those memories. So, it’s an essential function,” Dr. Dunckley said.

However, sometimes the tau protein becomes hyperphosphorylated, a condition in which the tau creates neurofibrillary tangles, one of the signature indicators of Alzheimer’s.

“When tau protein is hyperphosphorylated, the microtubule comes apart – basically destroying that bridge – and the neurons can no longer communicate with each other,” Dr. Dunckley said.

TGen investigators created sophisticated tests to look at all 572 known and theoretical kinases within human cells. They identified 26 associated with the phosphorylation of tau. Of these 26, three of them – EIF2AK2, DYRK1A and AKAP13 – were found to cause hyperphosphorylation of tau, permanently dismantling the microtubule bridges.

“This paper shows, for the first time, these three kinases affect Alzheimer’s disease-relevant tau hyperphosphorylation, in which most of the tau protein is now driven into a permanently phosphorylated form,” Dr. Dunckley said.

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The next step will be to identify drug compounds that can negate the effects of the three kinases linked to tau hyperphosphorylation.

“The reason that we did this study was to identify therapeutic targets for Alzheimer’s disease, whereby we could modify the progression of tau pathology,” Dr. Dunckley said. “This was a screen to identify what the relevant targets are. Now, we want to match those targets to treatments.”