Chimp Intelligence “Runs In Families,” Environment Less Important

A chimpanzee’s intelligence is largely determined by its genes, while environmental factors may be less important than scientists previously thought, according to a Georgia State University research study.

The study found that some, but not all, cognitive, or mental, abilities, in chimpanzees depend significantly on the genes they inherit. The findings are reported in the latest issue of Current Biology.

“Intelligence runs in families,” said Dr. William Hopkins, professor in the Center for Behavioral Neuroscience at Georgia State and research scientist in the Yerkes National Primate Research Center at Emory University. “The suggestion here is that genes play a really important role in their performance on tasks while non-genetic factors didn’t seem to explain a lot. So that’s new.”

The role of genes in human intelligence or IQ has been studied for years, but Hopkins’ study is among the first to address heritability in cognitive abilities in nonhuman primates. Studies have shown that human intelligence is inherited through genes, but social and environmental factors, such as formal education and socioeconomic status, also play a role and are somewhat confounded with genetic factors. Chimpanzees, which are highly intelligent and genetically similar to humans, do not have these additional socio-cultural influences.

“Chimps offer a really simple way of thinking about how genes might influence intelligence without, in essence, the baggage of these other mechanisms that are confounded with genes in research on human intelligence,” Hopkins said.

The study involved 99 chimpanzees, ranging in age from 9 to 54, who completed 13 cognitive tasks designed to test a variety of abilities. Hopkins used quantitative genetics analysis to link the degree of relatedness between the chimpanzees to their similarities or differences in performance on the various cognitive measures to determine whether cognitive performance is inherited in chimpanzees.

Genes were found to play a role in overall cognitive abilities, as well as the performance on tasks in several categories.

Traditionally, researchers studying animal intelligence or animal learning have shared the view that environment and how previous behavior is reinforced affect how animals perform on a particular task.

“In our case, at least, it suggests that purely environmental explanations don’t really seem to tell the whole story,” Hopkins said. “Genes matter as well.”

Hopkins also studied the structure of chimpanzee intelligence to determine whether there were any similarities to the structure of human intelligence.

“We wanted to see if we gave a sample of chimpanzees a large array of tasks,” he said, “would we find essentially some organization in their abilities that made sense. The bottom line is that chimp intelligence looks somewhat like the structure of human intelligence.”

In the future, Hopkins wants to continue the study with an expanded sample size. He would also like to pursue studies to determine which genes are involved in intelligence and various cognitive abilities as well as how genes are linked to variation in the organization of the brain.

Hopkins also would like to determine which genes changed in human evolution that allowed humans to have such advanced intelligence.

(Image: Anup Shah / Nature Picture Library)

Cinnamon May Be Used to Halt the Progression of Parkinson’s disease

Neurological scientists at Rush University Medical Center have found that using cinnamon, a common food spice and flavoring material, can reverse the biomechanical, cellular and anatomical changes that occur in the brains of mice with Parkinson’s disease (PD). The results of the study were recently published in the June 20 issue of the Journal of Neuroimmune Pharmacology.

“Cinnamon has been used widely as a spice throughout the world for centuries,” said Kalipada Pahan, PhD, study lead researcher and the Floyd A. Davis professor of neurology at Rush. “This could potentially be one of the safest approaches to halt disease progression in Parkinson’s patients.”

“Cinnamon is metabolized in the liver to sodium benzoate, which is an FDA-approved drug used in the treatment for hepatic metabolic defects associated with hyperammonemia,” said Pahan. It is also widely used as a food preservative due to its microbiocidal effect.

Chinese cinnamon (Cinnamonum cassia) and original Ceylon cinnamon (Cinnamonum verum) are two major types of cinnamon that are available in the US.

“Although both types of cinnamon are metabolized into sodium benzoate, by mass spectrometric analysis, we have seen that Ceylon cinnamon is much more pure than Chinese cinnamon as the latter contains coumarin, a hepatotoxic molecule,” said Pahan.

“Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of PD,” said Pahan. “It is known that some important proteins like Parkin and DJ-1 decrease in the brain of PD patients.”

The study found that after oral feeding, ground cinnamon is metabolized into sodium benzoate, which then enters into the brain, stops the loss of Parkin and DJ-1, protects neurons, normalizes neurotransmitter levels, and improves motor functions in mice with PD.

This research was supported by grants from National Institutes of Health.

“Now we need to translate this finding to the clinic and test ground cinnamon in patients with PD. If these results are replicated in PD patients, it would be a remarkable advance in the treatment of this devastating neurodegenerative disease,” said Dr. Pahan.

Parkinson’s disease is a slowly progressive disease that affects a small area of cells within the mid-brain known as the substantia nigra. Gradual degeneration of these cells causes a reduction in a vital chemical neurotransmitter, dopamine. The decrease in dopamine results in one or more of the classic signs of Parkinson’s disease that includes: resting tremor on one side of the body; generalized slowness of movement; stiffness of limbs; and gait or balance problems. The cause of the disease is unknown. Both environmental and genetic causes of the disease have been postulated.

Parkinson’s disease affects about 1.2 million patients in the United States and Canada. Although 15 percent of patients are diagnosed before age 50, it is generally considered a disease that targets older adults, affecting one of every 100 persons over the age of 60. This disease appears to be slightly more common in men than women.

Study cracks how the brain processes emotions

Although feelings are personal and subjective, the human brain turns them into a standard code that objectively represents emotions across different senses, situations and even people, reports a new study by Cornell University neuroscientist Adam Anderson.

“We discovered that fine-grained patterns of neural activity within the orbitofrontal cortex, an area of the brain associated with emotional processing, act as a neural code which captures an individual’s subjective feeling,” says Anderson, associate professor of human development in Cornell’s College of Human Ecology and senior author of the study. “Population coding of affect across stimuli, modalities and individuals,” published online in Nature Neuroscience.

Their findings provide insight into how the brain represents our innermost feelings – what Anderson calls the last frontier of neuroscience – and upend the long-held view that emotion is represented in the brain simply by activation in specialized regions for positive or negative feelings, he says.

“If you and I derive similar pleasure from sipping a fine wine or watching the sun set, our results suggest it is because we share similar fine-grained patterns of activity in the orbitofrontal cortex,” Anderson says.

“It appears that the human brain generates a special code for the entire valence spectrum of pleasant-to-unpleasant, good-to-bad feelings, which can be read like a ‘neural valence meter’ in which the leaning of a population of neurons in one direction equals positive feeling and the leaning in the other direction equals negative feeling,” Anderson explains.

For the study, the researchers presented participants with a series of pictures and tastes during functional neuroimaging, then analyzed participants’ ratings of their subjective experiences along with their brain activation patterns.

Anderson’s team found that valence was represented as sensory-specific patterns or codes in areas of the brain associated with vision and taste, as well as sensory-independent codes in the orbitofrontal cortices (OFC), suggesting, the authors say, that representation of our internal subjective experience is not confined to specialized emotional centers, but may be central to perception of sensory experience.

They also discovered that similar subjective feelings – whether evoked from the eye or tongue – resulted in a similar pattern of activity in the OFC, suggesting the brain contains an emotion code common across distinct experiences of pleasure (or displeasure), they say. Furthermore, these OFC activity patterns of positive and negative experiences were partly shared across people.

“Despite how personal our feelings feel, the evidence suggests our brains use a standard code to speak the same emotional language,” Anderson concludes.

Discovery of New Drug Targets for Memory Impairment in Alzheimer’s Disease

We are now a step closer to having a drug that can cure dementia and memory loss. Research team in Korea has discovered that reactive astrocytes, which have been commonly observed in Alzheimer’s patients, aberrantly and abundantly produce the chief inhibitory neurotransmitter GABA and release it through the Best1 channel. The released GABA strongly inhibits neighboring neurons to cause impairment in synaptic transmission, plasticity and memory. This discovery will open a new chapter in the development of new drugs for treating such diseases.

Alzheimer’s disease, which is the most common cause of dementia, is fatal and currently, there is no cure. In Alzheimer’s disease, brain cells are damaged and destroyed, leading to devastating memory loss. It is reported that 1 in 8 Americans aged 65 or over have Alzheimer’s disease. In 2011, 7,600 elderly people with dementia lost their way back home and became homeless in Korea. However, to date, there has been no clear understanding of the mechanisms underlying dementia in Alzheimer’s disease. So far, neuronal death is the only proposed mechanism available in scientific literature.

The research team discovered that reactive astrocytes in the brains of Alzheimer’s disease model mice produce the inhibitory transmitter GABA by the enzyme Monoamine oxidase B(MAO-B) and release GABA through the Bestrophin-1 channel to suppress normal information flow during synaptic transmission. Based on this discovery, the team was able to reduce the production and release of GABA by inhibiting MAO-B or Bestrophin-1, and successfully ameliorate impairments in neuronal firing, synaptic transmission and memory in Alzheimer’s disease model mice.

In the behavioral test, the team used the fact that mice tend to prefer dark places. If a mouse experiences an electric shock in a dark place, it will remember this event and avoid dark places from then on. However, a mouse with modeled Alzheimer’s disease cannot remember if such shock is related to dark places and keeps going back to dark places. The team demonstrated that treating these mice with a MAO-B inhibitor fully recovered the mice’s memory. The selegiline is currently used in Parkinson’s disease as an adjunct therapy and considered as a one of best promising medicine for MAO-B inhibitor. But it has been previously shown to be less effective in Alzheimer’s disease.

The team proved that selegiline is effective for a short time, but when it is used in long term, it loses its efficacy in Alzheimer’s disease model mice. When treated for 1 week, selegiline brought the neuronal firing to a normal level. But when it was treated for 2 and 4 weeks, neuronal firing came back to the levels of untreated mice. From these results, the team proposed that there is a pressing need for a new drug that has long lasting effects.

Dr. C. Justin Lee said, “From this study, we reveal the novel mechanism of how Alzheimer’s patients might lose their memory. We also propose new therapeutic targets, which include GABA production and release mechanisms in reactive astrocytes for treatment of Alzheimer’s disease. Furthermore, we provide a stepping stone for the development of MAO-B inhibitors with long lasting efficacy.”

Discovery of new means to erase pain

A study published in the scientific journal Nature Neuroscience by Yves De Koninck and Robert Bonin, two researchers at Université Laval, reveals that it is possible to relieve pain hypersensitivity using a new method that involves rekindling pain so that it can subsequently be erased. This discovery could lead to novel means to alleviate chronic pain.

The researchers from the Faculty of Medicine at Université Laval and Institut universitaire en santé mentale de Québec (IUSMQ) were inspired by previous work on memory conducted some fifteen years ago. These studies had revealed that when a memory is reactivated during recall, its neurochemical encoding is temporarily unlocked. Simultaneous administration of a drug that blocks neurochemical reconsolidation of the memory results in its erasure.

The investigators wanted to see whether a similar mechanism was at play during neurochemical encoding of pain sensitization. To this end, they injected capsaicin in the foot of mice. Capsaicin, the pungent chemical in chili pepper, triggers a burning sensation. The procedure, which causes no physical damage, triggers pain hypersensitivity through a process of protein synthesis in the spinal cord. After capsaicin injections, the mechanical pressure at which mice would flinch was about a third of that in the normal situation.

Three hours later, the researchers administered a second dose of capsaicin and, at the same time, a drug that blocks protein synthesis. The hypersensitivity then vanished rapidly. Within less than 2 hours, the pressure tolerated by the mice was back to 70% of normal.

Yves De Koninck explains that “when the protein synthesis inhibitor is administered alone, the hypersensitivity remains. The second injection of capsaicin is necessary to render the sensitivity to pain unstable and be able to interfere with its neurochemical reconsolidation. The challenge now will be to find protein synthesis inhibitors that are nontoxic and cause minimal side effects in humans”.

Restoring Active Memory Program Poised to Launch

Teams will develop and test implantable therapeutic devices for memory restoration in patients with memory deficits caused by disease or trauma

DARPA has selected two universities to initially lead the agency’s Restoring Active Memory (RAM) program, which aims to develop and test wireless, implantable “neuroprosthetics” that can help servicemembers, veterans, and others overcome memory deficits incurred as a result of traumatic brain injury (TBI) or disease.

The University of California, Los Angeles (UCLA), and the University of Pennsylvania (Penn) will each head a multidisciplinary team to develop and test electronic interfaces that can sense memory deficits caused by injury and attempt to restore normal function. Under the terms of separate cooperative agreements with DARPA, UCLA will receive up to $15 million and Penn will receive up to $22.5 million over four years, with full funding contingent on the performer teams successfully meeting a series of technical milestones. DARPA also has a cooperative agreement worth up to $2.5 million in place with Lawrence Livermore National Laboratory to develop an implantable neural device for the UCLA-led effort.

“The start of the Restoring Active Memory program marks an exciting opportunity to reveal many new aspects of human memory and learn about the brain in ways that were never before possible,” said DARPA Program Manager Justin Sanchez. “Anyone who has witnessed the effects of memory loss in another person knows its toll and how few options are available to treat it. We’re going to apply the knowledge and understanding gained in RAM to develop new options for treatment through technology.”

TBI is a serious cause of disability in the United States. Diagnosed in more than 270,000 military servicemembers since 2000 and affecting an estimated 1.7 million U.S. civilians each year, TBI frequently results in an impaired ability to retrieve memories formed prior to injury and a reduced capacity to form or retain new memories following injury. Despite the scale of the problem, no effective therapies currently exist to mitigate the long-term consequences of TBI on memory. Through the RAM program, DARPA seeks to accelerate the development of technology needed to address this public health challenge and help servicemembers and others overcome memory deficits by developing new neuroprosthetics to bridge gaps in the injured brain.

“We owe it to our service members to accelerate research that can minimize the long-term impacts of their injuries,” Sanchez said. “Despite increasingly aggressive prevention efforts, traumatic brain injury remains a serious problem in military and civilian sectors. Through the Restoring Active Memory program, DARPA aims to better understand the underlying neurological basis of memory loss and speed the development of innovative therapies.”

Specifically, RAM performers aim to develop and test wireless, fully implantable neural-interface medical devices that can serve as “neuroprosthetics”—technology that can effectively bridge the gaps that interfere with an individual’s ability to encode new memories or retrieve old ones.

To start, DARPA will support the development of multi-scale computational models with high spatial and temporal resolution that describe how neurons code declarative memories—those well-defined parcels of knowledge that can be consciously recalled and described in words, such as events, times, and places. Researchers will also explore new methods for analysis and decoding of neural signals to understand how targeted stimulation might be applied to help the brain reestablish an ability to encode new memories following brain injury. “Encoding” refers to the process by which newly learned information is attended to and processed by the brain when first encountered.

Building on this foundational work, researchers will attempt to integrate the computational models developed under RAM into new, implantable, closed-loop systems able to deliver targeted neural stimulation that may ultimately help restore memory function. These studies will involve volunteers living with deficits in the encoding and/or retrieval of declarative memories and/or volunteers undergoing neurosurgery for other neurological conditions.

Unique to the UCLA team’s approach is a focus on the portion of the brain known as the entorhinal area. UCLA researchers previously demonstrated that human memory could be facilitated by stimulating that region, which is known to be involved in learning and memory. Considered the entrance to the hippocampus—which helps form and store memories—the entorhinal area plays a crucial role in transforming daily experience into lasting memories. Data collected during the first year of the project from patients already implanted with brain electrodes as part of their treatment for epilepsy will be used to develop a computational model of the hippocampal-entorhinal system that can then be used to test memory restoration in patients.

After developing an advanced, new wireless neuromodulation device—featuring ten-times smaller size and much higher spatial resolution than existing devices—the UCLA team will implant such devices into the entorhinal area and hippocampus of patients with traumatic brain injury.

The Penn team’s approach is based on an understanding that memory is the result of complex interactions among widespread brain regions. Researchers will study neurosurgical patients who have electrodes implanted in multiple areas of their brains for the treatment of various neurological conditions. By recording neural activity from these electrodes as patients play computer-based memory games, the researchers will measure “biomarkers” of successful memory function—patterns of activity that accompany the successful formation of new memories and the successful retrieval of old ones. Researchers could then use those models and a novel neural stimulation and monitoring system—being developed in partnership with Medtronic—to restore brain memory function. The investigational system will simultaneously monitor and stimulate a number of brain sites, which may lead to better understandings of the brain and how brain stimulation therapy can potentially restore normal brain function following injury or the onset of neuropsychological illness.

In addition to human clinical efforts, RAM will support animal studies to advance the state-of-the-art of quantitative models that account for the encoding and retrieval of complex memories and memory attributes, including their hierarchical associations with one another. This work will also seek to identify any characteristic neural and behavioral correlates of memories facilitated by therapeutic devices.

Burst spinal artery aneurysm linked to Ecstasy use

Taking the street drug Ecstasy could lead to a potentially fatal weakening and rupture of the spinal cord artery, doctors have warned in the Journal of NeuroInterventional Surgery.

Posterior spinal artery aneurysms - a blood-filled swelling of the spinal cord artery, caused by a weakening and distension of the vessel wall - are rare, with only 12 cases reported to date. But all of them caused spinal bleeding which affected the function of the spinal cord.

Doctors discovered one of these aneurysms in a previously healthy teenager who had taken Ecstasy or MDMA.

The morning after the night before, he woke up with headache, neck pain and muscle spasms. After a week these symptoms suddenly took a turn for the worse, accompanied by nausea, prompting him to seek help at his local emergency department.

A week later the teen was transferred to a specialist neurosurgical unit for further investigations, which revealed an aneurysm, measuring 2 x 1 mm, on the left side of the spinal cord artery at the back of his neck.

The aneurysm was successfully removed, along with the weakened portion of the artery. The teen made a full recovery, with no lasting nerve damage.

But the authors reiterate that Ecstasy use has already been linked to severe systemic and neurological complications, including stroke, inflammation of the arteries in the brain (vasculitis) and internal brain bleeds.

And now, posterior spinal artery aneurysm can be added to the list, they say.

The drug acts on the sympathetic nervous system, sparking a sudden hike in blood pressure, as a result of the surge in serotonin it releases. And this could make any pre-existing aneurysms or other arterial abnormalities prone to rupture, they warn.

Contradictory findings on how the full moon affect our sleep

A Swiss research study conducted last year showed that the full moon affects sleep. The findings demonstrated that people average 20 minutes less sleep, take five minutes longer to fall asleep and experience 30 minutes more of REM sleep, during which most dreaming is believed to occur.

Different outcome

Numerous studies through the years have attempted to prove or disprove the hypothesis that lunar phases affect human sleep. But results have been hard to repeat. A group of researchers at the famed Max Planck Institute and elsewhere analyzed data from more than 1,000 people and 26,000 nights of sleep, only to find no correlation.

International researchers are being urged to publish their results in hopes of getting to the bottom of the question. Michael Smith and his co-researchers at Sahlgrenska Academy have analyzed data generated by a previous sleep study and compared them with the lunar cycle.

20 minutes less sleep

Based on a study of 47 healthy 18-30 year-olds and published in Current Biology, the results support the theory that a correlation exists.

“Our study generated findings similar to the Swiss project,” Michael Smith says. “Subjects slept an average of 20 minutes less and had more trouble falling asleep during the full moon phase. However, the greatest impact on REM sleep appeared to be during the new moon.”

More susceptible brain

The retrospective study by the Gothenburg researchers suggests that the brain is more susceptible to external disturbances when the moon is full.

“The purpose of our original study was to examine the way that noise disturbs sleep,” Mr. Smith continues. “Re-analysis of our data showed that sensitivity, measured as reactivity of the cerebral cortex, is greatest during the full moon.”

Greater cortical reactivity was found in both women and men, whereas only men had more trouble falling asleep and slept less when the moon was full. Skeptics warn that both age and gender differences may be a source of error, not to mention more subtle factors such as physical condition and exposure to light during the day.

Need for more studies

Though fully aware of the issues, Mr. Smith is not prepared to dismiss the results of the Gothenburg study.

“The rooms in our sleep laboratories do not have any windows,” he says. “So the effect we found cannot be attributable to increased nocturnal light during full moon. Thus, there may be a built-in biological clock that is affected by the moon, similar to the one that regulates the circadian rhythm. But all this is mere speculation – additionally, more highly controlled studies that target these mechanisms are needed before more definitive conclusions can be drawn.”

The article Human sleep and cortical reactivity are influenced by lunar phase is published in Current Biology.