Influence of genetics on cannabis dependence in adolescent females

Researchers have identified that a variant in a particular gene, that is found in about one-third of people, increases vulnerability to THC in females. It also has a large-scale impact on brain regions and pathways responsible for processing reward.

The brain's endocannabinoid system regulates the activity of cannabinoids that are normally produced by the body to influence brain development and regulate mood as well as those from external sources, such as the psychoactive ingredient THC, also known as D9-tetrahydrocannabinol, which is found in cannabis.

An enzyme called fatty acid amide hydrolase (FAAH) breaks down a cannabinoid called anandamide that is naturally found in the brain and is most closely related to THC, helping to remove it from circulation.

In the study which was published in 'Science Advances,' the researchers examined mice harbouring a human gene variant that causes FAAH to degrade more easily, increasing overall anandamide levels in the brain.

From the preclinical research by Weill Cornell Medicine investigators, they discovered that the variant resulted in an overactive reward circuit in female--but not male adolescent mice--that resulted in a higher preference for THC in females.

Dr. Caitlin Burgdorf, recent doctoral graduate from the Weill Cornell Graduate School of Medical Sciences, and the lead author said "Our study shows that a variant in the FAAH gene, which is found in about one-third of people, increases vulnerability to THC in females and has large-scale impact on brain regions and pathways responsible for processing reward."

"Our findings suggest that genetics can be a contributing factor for increased susceptibility to cannabis dependence in select populations," Caitlin added.

The result showcased that female mouse with the FAAH variant showed an increased preference for the environment in which they'd been exposed to THC over a neutral environment when they were exposed to the substance during adolescence, and the effect persisted into adulthood. 

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DRD2 May Protect Brain Regions from Alcohol-Induced Brain Damage

Brain scans of two strains of mice imbibing significant quantities of alcohol reveal serious shrinkage in some brain regions — but only in mice lacking a particular type of receptor for dopamine, the brain’s “reward” chemical. The study, conducted at the U.S. Department of Energy’s Brookhaven National Laboratory and published in the May 2012 issue of Alcoholism: Clinical and Experimental Research, now online, provides new evidence that these dopamine receptors, known as DRD2, may play a protective role against alcohol-induced brain damage.

“This study clearly demonstrates the interplay of genetic and environmental factors in determining the damaging effects of alcohol on the brain, and builds upon our previous findings suggesting a protective role of dopamine D2 receptors against alcohol’s addictive effects,” said study author Foteini Delis, a neuroanatomist with the Behavioral Neuropharmacology and Neuroimaging Lab at Brookhaven, which is funded through the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Coauthor and Brookhaven/NIAA neuroscientist Peter Thanos stated that, “These studies should help us better understand the role of genetic variability in alcoholism and alcohol-induced brain damage in people, and point the way to more effective prevention and treatment strategies.”

The current study specifically explored how alcohol consumption affects brain volume — overall and region-by-region — in normal mice and a strain of mice that lack the gene for dopamine D2 receptors. Half of each group drank plain water while the other half drank a 20 percent ethanol solution for six months. Then scientists performed magnetic resonance imaging (MRI) scans on all the mice and compared the scans of those drinking alcohol with those from the water drinkers in each group.

The scans showed that chronic alcohol drinking induced significant overall brain atrophy and specific shrinkage of the cerebral cortex and thalamus in the mice that lacked dopamine D2 receptors, but not in mice with normal receptor levels. Mice in both groups drank the same amount of alcohol.
“This pattern of brain damage mimics a unique aspect of brain pathology observed in human alcoholics, so this research extends the validity of using these mice as a model for studying human alcoholism,” Thanos said.

In humans, these brain regions are critically important for processing speech, sensory information, and motor signals, and for forming long-term memories. So this research helps explain why alcohol damage can be so widespread and detrimental.

“The fact that only mice that lacked dopamine D2 receptors experienced brain damage in this study suggests that DRD2 may be protective against brain atrophy from chronic alcohol exposure,” Thanos said. “Conversely, the findings imply that lower-than-normal levels of DRD2 may make individuals more vulnerable to the damaging effects of alcohol.”

That would in effect deal people with low DRD2 levels a double whammy of alcohol vulnerability: Previous studies conducted by Thanos and collaborators suggest that individuals with low DRD2 levels may be more susceptible to alcohol’s addictive effects.

“The increased addictive liability and the potentially devastating increased susceptibility to alcohol toxicity resulting from low DRD2 levels make it clear that the dopamine system is an important target for further research in the search for better understanding and treatment of alcoholism,” Thanos said.




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Anti-depressants can alter sensory processing in babies if consumed during pregnancy

A new study has revealed that exposure to anti-depressants during pregnancy and the first weeks of life can alter sensory processing well into adulthood.

Physicians are increasingly prescribing a common anti-depressant to their pregnant patients, even though the effect on the fetus isn't fully known. A working theory of depression implicates the neurotransmitter serotonin because many depressed patients experience relief when prescribed selective serotonin reuptake inhibitors (SSRIs). Whatever role it plays in depression, serotonin is critical for healthy brain development and function.

While previous research has shown changes in behaviour and brain structure with prenatal and early life exposure to SSRIs, Rahn et al explored changes in brain activity. After exposing mice to the SSRI fluoxetine during gestation and the first two weeks after birth, the team deployed optical imaging to examine the mouse brains exposed to fluoxetine and compare them to control mice.

In the resting state, the brains of both sets of mice were nearly identical. When their front paws were stimulated, the fluoxetine-exposed mice displayed abnormal brain activity in sensory areas. The effect was observed during adulthood in mice, suggesting this developmental exposure to SSRIs causes long-term changes to sensory processing.

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Reaction to traumatic events can lead to post-traumatic stress disorder

While trauma in itself can pose risk to a child's healthy development, over thinking on such events makes the kid more prone to suffering from post-traumatic stress disorder (PTSD), says a recent study.

If they think their reaction to traumatic events is not normal, they become more likely to develop PTSD, the study published in a Journal  has found. Children begin down this route when they have trouble processing their trauma and perceive their symptoms as being a sign that something is seriously wrong.

While most children recover well after a traumatic event, some go on to develop PTSD that may stay with them for months, years, or even into adulthood. Lead researcher  said: "Symptoms of PTSD can be a common reaction to trauma in children and teenagers. These can include distressing symptoms like intrusive memories, nightmares, and flashbacks."

"Many children who experience a severe traumatic stress response initially can go on to make a natural recovery without any professional support. But a minority go on to have persistent PTSD, which can carry on for much longer," he said.

Researchers worked with over 200 children aged between eight and 17 who had attended a hospital emergency department following a one-off traumatic incident. These included events such as car crashes, assaults, dog attacks, and other medical emergencies. These young people were interviewed and assessed for PTSD between two and four weeks following their trauma, and again after two months.

The team split the children's reactions into three groups - a 'resilient' group who did not develop clinically significant traumatic stress symptoms at either time point, a 'recovery' group who initially displayed symptoms but none at the two months follow up, and a 'persistent' group who had significant symptoms at both time points.

They also examined whether social support and talking about the trauma with friends or family may be protective against persistent problems after two months. They also took into account factors including other life stressors and whether the child was experiencing on-going pain.

"We found that PTSD symptoms are fairly common early on, for example between two and four weeks following a trauma. These initial reactions are driven by high levels of fear and confusion during the trauma," said the researcher.

"But the majority of children and young people recovered naturally without any intervention. Interestingly, the severity of physical injuries did not predict PTSD, nor did other life stressors, the amount of social support they could rely on, or self-blame," he added.

"The young people who didn't recover well, and who were heading down a chronic PTSD track two months after their trauma, were much more likely to be thinking negatively about their trauma and their reactions - they were ruminating about what happened to them," he explained.

According to him, kids perceived their symptoms as being a sign that something was seriously and permanently wrong with them, they didn't trust other people as much, and they thought they couldn't cope.

In many cases, more deliberate attempts to process the trauma, for example, trying to think it through or talk it through with friends and family, were actually associated with worse PTSD. The children who didn't recover well were those that reported spending a lot of time trying to make sense of their trauma. While some efforts to make sense of trauma might make sense, it seems that it is also possible for children to get 'stuck' and spend too long focusing on what happened and why.

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Low glucose in brain may trigger Alzheimer's disease

Glucose deprivation in the brain may trigger the onset of cognitive decline, especially memory impairment - the earliest signs of Alzheimer's disease, say scientists who have also found a protein that may be targeted to treat the disorder.

The hippocampus plays a key role in processing and storing memories. However, it relies exclusively on glucose for fuel-without glucose, neurons starve and eventually die.

The new study is the first to directly link memory impairment to glucose deprivation in the brain specifically through a mechanism involving the accumulation of a protein known as phosphorylated tau.

"Phosphorylated tau precipitates and aggregates in the brain, forming tangles and inducing neuronal death," said Domenico Pratico, Professor at Temple University in the US.

In general, a greater abundance of neurofibrillary tau tangles is associated with more severe dementia.

The study also is the first to identify a protein known as p38 as a potential alternate drug target in the treatment of Alzheimer's disease.

Neurons activate p38 protein in response to glucose deprivation, possibly as a defensive mechanism. In the long run, however, its activation increases tau phosphorylation, making the problem worse.

To investigate the impact of glucose deprivation on the brain, Pratico's team used a mouse model that recapitulates memory impairments and tau pathology in Alzheimer's disease.

At about four or five months of age, some of the animals were treated with 2-deoxyglucose (DG), a compound that stops glucose from entering and being utilised by cells.

The compound was administered to the mice in a chronic manner, over a period of several months. The animals were then evaluated for cognitive function.

In a series of maze tests to assess memory, glucose-deprived mice performed significantly worse than their untreated counterparts.

When examined microscopically, neurons in the brains of DG-treated mice exhibited abnormal synaptic function, suggesting that neural communication pathways had broken down.

Of particular consequence was a significant reduction in long-term potentiation - the mechanism that strengthens synaptic connections to ensure memory formation and storage.

Upon further examination, researchers discovered high levels of phosphorylated tau and dramatically increased amounts of cell death in the brains of glucose-deprived mice.

To find out why, Pratico turned to p38, which has been identified as a driver of tau phosphorylation.

In the new study, they found that memory impairment was directly associated with increased p38 activation.

"There is now a lot of evidence to suggest that p38 is involved in the development of Alzheimer's disease," Pratico said.

The findings also show that chronically occurring, small episodes of glucose deprivation are damaging for the brain.

"There is a high likelihood that those types of episodes are related to diabetes, which is a condition in which glucose cannot enter the cell," he said.

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Decoded: What causes stuttering.

Stuttering is caused by a reduced blood flow in speech processing areas of the brain, a study by researchers has showed. 

The findings showed that regional cerebral blood flow is reduced in the Broca’s area — the region in the frontal lobe of the brain linked to speech production. 

In addition, a greater abnormality of cerebral blood flow in the posterior language loop — associated with processing of words that we hear — correlates with more severe stuttering.

According to researchers, a common patho-physiology throughout the neural “language” loop that connects the frontal and posterior temporal lobe likely contributes to stuttering severity.

“When other portions of the brain circuit related to speech were also affected according to our blood flow measurements, we saw more severe stuttering in both children and adults,” said lead author Jay Desai, MD, clinical neurologist at Children’s Hospital Los Angeles (CHLA) in California. 

In the study,  the researchers were able to zero in on the Broca’s area as well as related brain circuitry specifically linked to speech, using regional cerebral blood flow as a measure of brain activity, since blood flow is typically coupled with neural activity.
“Blood flow was inversely correlated to the degree of stuttering — the more severe the stuttering, the less blood flow to this part of the brain,  said Desai, adding that the study results were “quite striking”. 

The study was published in the journal Human Brain Mapping.

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Brain hard-wired to link what we see with what we do

Scientists have found for the first time that our brain’s ability to instantly link what we see with what we do is down to a dedicated information ‘highway’.

Researchers from University College London and Cambridge University found a specialised mechanism for spatial self-awareness that combines visual cues with body motion.

Standard visual processing is prone to distractions, as it requires us to pay attention to objects of interest and filter out others.

The new study found that our brains have separate’hard-wired’ systems to visually track our own bodies, even if we are not paying attention to them.

In fact, the newly discovered network triggers reactions even before the conscious brain has time to process them.

The researchers tested 52 healthy adults in a series of three experiments. In all experiments, participants used robotic arms to control cursors on two-dimensional displays,where cursor motion was directly linked to hand movement.

Their eyes were kept fixed on a mark at the centre of the screen, confirmed with eye tracking.

In the first experiment, participants controlled two separate cursors with their left and right hands, both equally close to the centre.

Occasionally, the cursor or target on one side would jump left or right, requiring subjects to take corrective action.
Each jump was ‘cued’ with a flash on one side, this was random so did not always correspond to the side about to change.

People reacted faster to target jumps when their attention was drawn to the ‘correct’ side by the cue. However,reactions to cursor jumps were fast regardless of cuing,suggesting that a separate mechanism independent of attention is responsible for tracking our own movements.

“The first experiment showed us that we react very quickly to changes relating to objects directly under our own control, even when we are not paying attention to them,” said Dr Alexandra Reichenbach of the UCL Institute of Cognitive Neuroscience, lead author of the study.

“This provides strong evidence for a dedicated neural pathway linking motor control to visual information,independently of the standard visual systems that are dependent on attention,” Reichenbach said.

The second experiment was similar to the first, but also introduced changes in brightness to demonstrate the attention effect on the visual perception system.

In the third experiment, participants had to guide one cursor to its target in the presence of up to four dummy targets and cursors, ‘distractors’, alongside the real ones.

In this experiment, responses to cursor jumps were less affected by distractors than responses to target jumps.

“These results provide further evidence of a dedicated’visuomotor binding’ mechanism that is less prone to distractions than standard visual processing,” said Reichenbach.

The newly discovered system could explain why some schizophrenia patients feel like their actions are controlled by someone else, researchers said.

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