[Mimic#202_Scientific]Synapses and Human_Chelsea

Science 22 November 2013:
Vol. 342 no. 6161 pp. 944-945
DOI: 10.1126/science.1247515

PERSPECTIVENEUROSCIENCE

Synapses, Language, and Being Human

Philip Lieberman

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FOXP2 has become a “gene of interest” in the mystery that surrounds the evolution of the human brain. It first came to notice in a study of the behavioral deficits of the members of a large extended family who had only one copy of the gene. These individuals had profound difficulties in talking, comprehending, and forming sentences, and had depressed scores on intelligence tests (2). Anomalies in their basal ganglia, subcortical structures deep in the brain, were also noted (3). FOXP2 is one of the few human genes that differ from its chimpanzee version. A series of mutations in FOXP2 has occurred in the last 500,000 years; the most recent one took place about 200,000 years ago, when modern humans appeared in Africa (4). When a form of FOXP2 shared by humans, Neandertals, and Denisovans (another extinct hominin species) was introduced into mouse pups, synaptic plasticity and connections between basal ganglia neurons increased (5). But the mechanisms by which FOXP2 shapes the neural circuitry associated with language acquisition have not been clear. The CNTNAP2 gene, for example, also is targeted by FOXP2 and is linked to language disorders (6).

First draft:

FOXP2 has become the[a] "gene of interest" in the mystery that surrounds the evolution of human brain. It first came to notice in a study of [the] behavioral deficits of the members from[of] a large extended family who had only one copy of the gene. These individuals had profound difficulties in talking, comprehending, [and] forming sentences, and [had] depressed scores in[on] intelligence tests. Anomalies in the[their] basal ganglia, subcortical structure[s] deep in the brain, was [were also] noted. FOXP2 is one the few human genes that differ from its chimpanzee version. A series [of] mutations [in FOXP2] [has] occurred in the last 500,000 years; the most recent one took place [about] 200,000 years ago, when modern humans appeared in Africa. When a form of FOXP2 that shared by humans, Neandertals, and Denisovans (another extinct huminin[hominin] species) was introduced into mouse pops, synapse[synaptic] plasticity and connections between basal ganglia neurons increased. But the mechanisms by which FOXP2 shapes the neuron[neural] circuitry that relates[associated with] language acquisition remains to be unclear[have not been clear]. The CNTNAP2 gene, for example, is also [is] targeted by FOXp2, and is linked to language disorders.

Second draft:

FOXP2 has become one of the[a] "gene of interest" in the mystery that surrounds the evolution of human brain. It came to notice in a study of the behavioral deficits of the members of a large extended family who had only one copy of the gene. These individuals had profound difficulties in talking, comprehending and forming sentences, and had depressed scores on intelligence tests. Anomalies in the[ir] basal ganglia, subcortical structures deep in the brain, were [also] noted. FOXP2 is one the few human genes that differ from its chimpanzee version. A series of mutations of [in] FOXP2 had occurred in the last 500,000 years; the most recent one took place around  [about] 200,000 years ago,[.]  when the modern humans appeared in Africa. When a form of FOXP2 shared with humans, Neandertals, and Denisovans (another extinct hominin species) was introduced into mouse pops, synaptic plasticity and connections between the basic ganglia neurons increased. But the mechanisms in[by] which FOXP2 shapes the neural circuitry associated with language acquisition have not been clear. The CNTNAP2 gene, for example, also is targeted by FOXP2, and is linked to language disorders. 

FOXP2 has become a “gene of interest” in the mystery that surrounds the evolution of the human brain. It first came to notice in a study of the behavioral deficits of the members of a large extended family who had only one copy of the gene. These individuals had profound difficulties in talking, comprehending, and forming sentences, and had depressed scores on intelligence tests (2). Anomalies in their basal ganglia, subcortical structures deep in the brain, were also noted (3). FOXP2 is one of the few human genes that differ from its chimpanzee version. A series of mutations in FOXP2 has occurred in the last 500,000 years; the most recent one took place about 200,000 years ago, when modern humans appeared in Africa (4). When a form of FOXP2 shared by humans, Neandertals, and Denisovans (another extinct hominin species) was introduced into mouse pups, synaptic plasticity and connections between basal ganglia neurons increased (5). But the mechanisms by which FOXP2 shapes the neural circuitry associated with language acquisition have not been clear. The CNTNAP2 gene, for example, also is targeted by FOXP2 and is linked to language disorders (6).

P.S. Gosh I just memorized the whole thing... lol...