During this time, about 50 percent of the extra synapses are eliminated. In the visual cortex, pruning continues until about 6 years of age. Synaptic pruning continues through adolescence, but not as fast as before. The total number of synapses begins to stabilize. While researchers once thought the brain only pruned synapses until early adolescence, recent advancements have discovered a second pruning period during late adolescence. According to newer research, synaptic pruning actually continues into early adulthood and stops sometime in the late 20s.
Research that looks at the relationship between synaptic pruning and schizophrenia is still in the early stages. For example, when researchers looked at images of the brains of people with mental disorders, such as schizophrenia, they found that people with mental disorders had fewer synapses in the prefrontal region compared to the brains of people without mental disorders. Then, a large study analyzed post-mortem brain tissue and DNA from more than , people and found that people with schizophrenia have a specific gene variant that may be associated with an acceleration of the process of synaptic pruning.
More research is needed to confirm the hypothesis that abnormal synaptic pruning contributes to schizophrenia. While this is still a long way off, synaptic pruning may represent an interesting target for treatments for people with mental disorders.
To test this hypothesis, researchers looked at brain tissue of 13 children and adolescents with and without autism who passed away between ages 2 and The scientists found that the brains of the adolescents with autism had a lot more synapses than the brains of neurotypical adolescents. Young children in both groups had roughly the same number of synapses. This suggests that the condition may occur during the pruning process. This research only shows a difference in synapses, but not whether this difference might be a cause or an effect of autism, or just an association.
This under-pruning theory may help explain some of the common symptoms of autism, like oversensitivity to noise, lights, and social experiences, as well as epileptic seizures. If there are too many synapses firing at once, a person with autism will likely experience an overload of noise rather than a fine-tuned brain response.
Additionally, past research has linked autism with mutations in genes that act on a protein known as mTOR kinase. Large amounts of overactive mTOR have been found in the brains of autism patients.
Over-activity in the mTOR pathway has also been shown to be associated with an excess production of synapses. One study found that mice with overactive mTOR had defects in their synaptic pruning and exhibited ASD-like social behaviors. Synaptic pruning is an essential part of brain development. By getting rid of the synapses that are no longer used, the brain becomes more efficient as you age.
Today, most ideas about human brain development draw on this idea of brain plasticity. Researchers are now looking into ways to control pruning with medications or targeted therapy. Researchers are also studying how the shape of the synapses might play a role in mental disabilities. The process of synaptic pruning may be a promising target for treatments for people with conditions like schizophrenia and autism. However, research is still in the early stages. You can improve your brain health with the right diet.
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Also called an elevated toilet seat, a raised toilet…. Learn about end-of-life signs in older adults, and the timeline for experiencing them. The development of projections from cerebral cortex. Article Google Scholar. O'Leary, D. Development of connectional diversity and specificity in the mammalian brain by the pruning of collateral projections. An important review that complements this one, describing how the pruning of collateral projections first became recognized as a fundamental and widespread mechanism for the development of specific axonal connections.
Stanfield, B. The development of the corticospinal projection. Another important review describing early studies of exuberance in the rodent's developing corticospinal system, which became established as a powerful model in this field.
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Regressive events in the postnatal development of association projections in the visual cortex. Webster, M. Connections of inferior temporal areas TE and TEO with medial temporal-lobe structures in infant and adult monkeys.
This remains one of the most striking examples of exuberant cortical connections in the monkey. Assal, F. Transient intra-areal axons in developing cat visual cortex.
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Selective collateral elimination in early postnatal development restricts cortical distribution of rat pyramidal tract neurones. Curfs, M. Selective elimination of transient corticospinal projections in the rat cervical spinal cord gray matter.
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Neurons in the corpus callosum of the cat during postnatal development. Norris, C. Guidance of callosal axons by radial glia in the developing cerebral cortex. Shatz, C. Anatomy of interhemispheric connections in the visual system of Boston Siamese and ordinary cats. Tremblay, F. Distribution of visual callosal projection neurons in the siamese cat: an HRP study.
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Zufferey, P. The role of pattern vision in the development of cortico-cortical connections. Maturation of visual callosal connections in visually deprived kittens: a challenging critical period. Manger, P. The representation of the visual field in three extrastriate areas of the ferret Mustela putorius and the relationship of retinotopy and field boundaries to callosal connectivity. Cortex 12 , — This work makes an important contribution to the concept that the topographic projections from the retina guide the establishment of callosal connections.
Restrepo, C. Immature cortex lesions alter retinotopic maps and interhemispheric connections. A recent paper that confirms and extends the concept that competition among cortico-cortical axons is involved in shaping cortico-cortical networks.
Lesions of inferior temporal area TE in infant monkeys alter cortico-amygdalar projections. Neuroreport 2 , — Nakajima, T. Google Scholar. Gravel, C. Maturation of the corpus callosum of the rat: II.
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Huffman, K.
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