Neurofibromatosis type 1 (NF1) is the most common cause of learning disabilities, caused by a mutation in a gene that makes a protein called neurofibromin. Mouse research has now revealed that these mutations are associated with higher levels of the inhibitory neurotransmitter GABA in the medial prefrontal cortex. Brain imaging in humans with NF1 similarly showed reduced activity in the prefrontal cortex when performing a working memory task, with the levels of activity correlating with task performance.
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Two independent studies have found that students whose birthdays fell just before their school's age enrollment cutoff date—making them among the youngest in their class—had a substantially higher rate of ADHD diagnoses than students who were born later. One study, using data from the Early Childhood Longitudinal Study-Kindergarten cohort, found that ADHD diagnoses among children born just prior to their state’s kindergarten eligibility cutoff date are more than 60% more prevalent than among those born just afterward (who therefore waited an extra year to begin school).
I have often spoken of the mantra: What’s good for your heart is good for your brain. The links between cardiovascular risk factors and cognitive decline gets more confirmation in this latest finding that people whose hearts pumped less blood had smaller brains than those whose hearts pumped more blood. The study involved 1,504 participants of the decades-long Framingham Offspring Cohort who did not have a history of stroke, transient ischemic attack or dementia. Participants were 34 to 84 years old.
A pilot study involving six patients with mild Alzheimer’s has shown using Deep Brain Stimulation (DBS) is safe and may help improve memory, or at least slow decline. Patients received continuous stimulation for 12 months, between 2005 and 2008. Impaired glucose utilization in the temporal and parietal lobes was dramatically reversed early in the treatment, and maintained after the year of continuous stimulation. Performance on cognitive tests showed possible improvement and/or slowing in the rate of cognitive decline at 6 and 12 months in three of the six patients.
Commercial use is a long way off, but research with mice offers hope for a ‘smart drug’ that doesn’t have the sort of nasty side-effects that, for example, amphetamines have. The mice, genetically engineered to produce dramatically less (70%) kynurenic acid, had markedly better cognitive abilities. The acid, unusually, is produced not in neurons but in glia, and abnormally high levels are produced in the brains of people with disorders such as schizophrenia, Alzheimer's and Huntington's. More acid is also typically produced as we get older.
A small study comparing 18 obese adolescents with type 2 diabetes and equally obese adolescents without diabetes or pre-diabetes has found that those with diabetes had significantly impaired cognitive performance, as well as clear abnormalities in the integrity of their white matter (specifically, reduced white matter volume, especially in the frontal lobe, as well as impaired integrity in both white and grey matter).
Children’s ability to remember past events improves as they get older. This has been thought by many to be due to the slow development of the prefrontal cortex. But now brain scans from 60 children (8-year-olds, 10- to 11-year-olds, and 14-year-olds) and 20 young adults have revealed marked developmental differences in the activity of the mediotemporal lobe.
A study involving over 180,000 older veterans (average age 68.8 at study start), of whom 29% had PTSD, has revealed that those with PTSD had a significantly greater risk of developing dementia. Over the seven years of the study, 10.6% of the veterans with PTSD developed dementia compared to 6.6% of those without PTSD. When age was used as the time scale, the risk for those with PTSD was more than double. Results were similar when those with a history of head injury, substance abuse, or clinical depression, were excluded.
Data from a 35-year study of women from Gothenburg in Sweden has revealed that the risk of dementia was about 65% higher in women who reported repeated periods of stress in middle age than in those who did not. The risk increased with number of periods of stress, with women who reported stress on all three occasions they were asked (1968, 1974 and 1980) having more than double the risk of dementia. Stress was defined as a sense of irritation, tension, nervousness, anxiety, fear or sleeping problems lasting a month or more due to work, health, family or other problems.
A number of studies in recent years have revealed the amazing ability of the human brain to compensate for damage down to its part. In the latest of these, it’s been found that loss of the amygdala doesn’t have to mean that new memories will be void of emotion. Instead, it appears, a region called the bed nuclei can step in to take its place. The bed nuclei are slower to process information than the amygdala, and in normal circumstances are inhibited by the amygdala. The study looked specifically at fear conditioning, for which the amygdala has been considered crucial.