Brain frontal lobes not sole centre of human intelligence
Human intelligence cannot be explained by the size of the brain’s frontal lobes, say researchers.
Research into the comparative size of the frontal lobes in humans and other species has determined that they are not - as previously thought - disproportionately enlarged relative to other areas of the brain, according to the most accurate and conclusive study of this area of the brain.
It concludes that the size of our frontal lobes cannot solely account for humans’ superior cognitive abilities.
The study by Durham and Reading universities suggests that supposedly more ‘primitive’ areas, such as the cerebellum, were equally important in the expansion of the human brain. These areas may therefore play unexpectedly important roles in human cognition and its disorders, such as autism and dyslexia, say the researchers.
The study is published in the Proceedings of the National Academy of Sciences (PNAS) today.
The frontal lobes are an area in the brain of mammals located at the front of each cerebral hemisphere, and are thought to be critical for advanced intelligence.
Lead author Professor Robert Barton from the Department of Anthropology at Durham University, said: “Probably the most widespread assumption about how the human brain evolved is that size increase was concentrated in the frontal lobes.
“It has been thought that frontal lobe expansion was particularly crucial to the development of modern human behaviour, thought and language, and that it is our bulging frontal lobes that truly make us human. We show that this is untrue: human frontal lobes are exactly the size expected for a non-human brain scaled up to human size.
“This means that areas traditionally considered to be more primitive were just as important during our evolution. These other areas should now get more attention. In fact there is already some evidence that damage to the cerebellum, for example, is a factor in disorders such as autism and dyslexia.”
The scientists argue that many of our high-level abilities are carried out by more extensive brain networks linking many different areas of the brain. They suggest it may be the structure of these extended networks more than the size of any isolated brain region that is critical for cognitive functioning.
Previously, various studies have been conducted to try and establish whether humans’ frontal lobes are disproportionately enlarged compared to their size in other primates such as apes and monkeys. They have resulted in a confused picture with use of different methods and measurements leading to inconsistent findings.
The Durham and Reading researchers, funded by The Leverhulme Trust, analysed data sets from previous animal and human studies using phylogenetic, or ‘evolutionary family tree’, methods, and found consistent results across all their data. They used a new method to look at the speed with which evolutionary change occurred, concluding that the frontal lobes did not evolve especially fast along the human lineage after it split from the chimpanzee lineage.
New subtype of ataxia identified
The finding opens the door for presymptomatic diagnostics and genetic counselling for patients and it is the first step in identifying the cause and developing therapies
(Image: Antony Gormley)
Researchers from the Germans Trias i Pujol Health Sciences Research Institute Foundation (IGTP), the Bellvitge Biomedical Research Institute (IDIBELL), and the Sant Joan de Déu de Martorell Hospital, has identified a new subtype of ataxia, a rare disease without treatment that causes atrophy in the cerebellum and affects around 1.5 million people in the world. The results have been published online on April 29 in the journal JAMA Neurology.
The cause of ataxia is a diverse genetic alteration. For this reason it is classified in subtypes. The new subtype identified described by the researchers has been called SCA37. The study has found this subtype in members of the same family living in Barcelona, Huelva and Madrid and Salamanca (Spain). The finding will allow in the medium term that these families and all who suffer the genetic alteration identified will have personalized therapies and diagnostics prior to the development of the disease. The study was funded by La Marató de TV3 (the Catalan public TV) in 2009, dedicated to rare diseases.
The cerebellum is a part of the brain located behind the brain that, among other functions, coordinates the movements of the human body. When it is atrophied, movement disorders appear, and when the ataxia evolves, the patients suffer frequent falls and swallowing problems. Progressively, they end up needing a wheelchair. Until now, there have been identified more than 30 different subtypes of ataxia, the first of which was described in 1993 by Dr. Antoni Matill, head of the Neurogenetics Unit, IGTP, and Dr. Victor Volpini, head of the Center for Molecular Genetic Diagnosis at IDIBELL.
The publication of this paper has been possible thanks to the collaboration of the Hospital de Sant Pau, Universitat Pompeu Fabra and the Pitie-Salpêtrière Hospital in Paris.
Particular eye movements
The first symptoms of ataxia may develop during the childhood or adult stage, depending on the subtype. The SCA37 subtype, the first cases of which were identified by Carme Serrano, neurologist at the Sant Joan de Deu Hospital, Martorell (Barcelona), is expressed at 48 years on average. One of the features of SCA37 subtype is the difficulty for vertical eye movements. Besides the patients identified in Spain by Dr. Serrano and Germans Trias and IDIBELL researchers, there are evidence of the existence of more people affected with this subtype of ataxia in France, Holland and Britain, and for this reason it seems to be a quite prevalent subtype of ataxia in Europe.
All SCA37 patients have a common genetic alteration in the portion 32 of the short arm of chromosome 1, wherein there are a hundred genes. Currently, researchers are sequencing it with new generation technologies to find the specific mutation that causes ataxia. When it is found it will be possible to make an accurate diagnosis in family members who do not yet have developed symptoms. Also, it will be possible to investigate the biological mechanisms that cause ataxia in order to develop and implement personalized therapies, with drugs or stem cells therapy.