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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Temporal Lobe

 
 
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Disease relevance of Temporal Lobe

 

Psychiatry related information on Temporal Lobe

 

High impact information on Temporal Lobe

 

Chemical compound and disease context of Temporal Lobe

 

Biological context of Temporal Lobe

 

Anatomical context of Temporal Lobe

  • The EphA4 receptor tyrosine kinase regulates the formation of the corticospinal tract (CST), a pathway controlling voluntary movements, and of the anterior commissure (AC), connecting the neocortical temporal lobes [26].
  • Fluphenazine, but not clozapine, increased metabolic rates in the subcortical and lateral temporal lobes, whereas clozapine, but not fluphenazine, decreased inferior prefrontal cortex activity [27].
  • Correlations of metabolic increases in the dorsolateral prefrontal cortex, medial temporal lobe (amygdala), and cerebellum with self-reports of craving suggest that a distributed neural network, which integrates emotional and cognitive aspects of memory, links environmental cues with cocaine craving [28].
  • Expression of human epileptic temporal lobe neurotransmitter receptors in Xenopus oocytes: An innovative approach to study epilepsy [29].
  • Similar results were observed in 13 specimens of anterolateral temporal neocortex obtained during temporal lobectomies in patients with intractable temporal lobe epilepsy, compared with postmortem human specimen or control brain tissues [30].
 

Associations of Temporal Lobe with chemical compounds

 

Gene context of Temporal Lobe

  • CONCLUSIONS: Specific alleles of the DISC1 and TRAX genes on 1q42 appear to contribute to genetic risk for schizophrenia through disruptive effects on the structure and function of the prefrontal cortex, medial temporal lobe, and other brain regions [35].
  • LGI1, one member of the LGI gene family, encodes a approximately 63 kDa protein, with strong regional expression in neurons within the temporal lobe [36].
  • We also show that changes in the expression of other ITFs (Fos, Jun-D and Krox-20) and the BDNF/trkB neurotrophin system may play a central role in the development of hippocampal kindling, an animal model of human temporal lobe epilepsy [37].
  • These findings indicate that chronic temporal lobe seizures are associated with differential changes in hippocampal NR1 and NR2A-D hybridization densities that vary by subfield and clinical-pathological category [38].
  • Death-associated protein kinase expression in human temporal lobe epilepsy [23].
 

Analytical, diagnostic and therapeutic context of Temporal Lobe

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