A single base change makes a difference

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SUMMARY

A recent study published in Science reveals that a single SNP (single nucleotide polymorphism) significantly influences memory performance, with individuals possessing the Thymine base at a specific locus demonstrating superior short-term memory capabilities compared to those with the Cystine base. This genetic variation affects the KIBRA protein, which is crucial for learning and memory processes. Further research by Ji et al. (2019) elucidates the molecular mechanisms by which KIBRA interacts with Dendrin, a postsynaptic density protein, thereby modulating synaptic transmission and memory functions.

PREREQUISITES
  • Understanding of SNP (single nucleotide polymorphism) and its implications in genetics.
  • Familiarity with the KIBRA protein and its role in learning and memory.
  • Knowledge of synaptic transmission and its relevance to cognitive functions.
  • Basic comprehension of molecular biology techniques used in protein interaction studies.
NEXT STEPS
  • Research the role of KIBRA in Alzheimer's disease and Tourette syndrome.
  • Explore the mechanisms of synaptic transmission and long-term potentiation.
  • Investigate the development and application of peptide inhibitors in neuroscience.
  • Learn about the implications of genetic variations on cognitive abilities.
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Neuroscientists, geneticists, and researchers focused on cognitive function, as well as healthcare professionals interested in the genetic basis of neurological disorders.

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There's a new paper in Science that investigates the effect of a single SNP (single nucleotide polymorphism) on memory usage effectiveness. People with the Thymine base in a certain locus do markedly better in task involving short-term memory than those with the Cystine base at that location. The location affects the protein KIBRA.

See this discussion by John Hawks, which has links to the original paper and some other references.

http://johnhawks.net/weblog/reviews/genetics/brain/kibra_memory_association_2006.html
 
Biology news on Phys.org
Here's a more recent paper proposing some molecular mechanisms for how the Kibra protein might contribute to learning and memory:

Ji et al. Kibra Modulates Learning and Memory via Binding to Dendrin. Cell Rep 26: 2064 (2019) https://www.sciencedirect.com/science/article/pii/S2211124719301342?via=ihub
Abstract:
Kibra is a synaptic scaffold protein regulating learning and memory. Alterations of Kibra-encoding gene WWC1 cause various neuronal disorders, including Alzheimer’s disease and Tourette syndrome. However, the molecular mechanism underlying Kibra’s function in neurons is poorly understood. Here we discover that Kibra, via its N-terminal WW12 tandem domains, binds to a postsynaptic density enriched protein, Dendrin, with a nanomolar dissociation constant. On the basis of the structure of Kibra WW12 in complex with Dendrin PY motifs, we developed a potent peptide inhibitor capable of specifically blocking the binding between Kibra and Dendrin in neurons. Systematic administration of the inhibitory peptide attenuated excitatory synaptic transmission, completely blocked long-term potentiation induction, and impaired spatial learning and memory. A Kibra mutation found in Tourette syndrome patients causes defects in binding to Dendrin. Thus, Kibra can modulate spatial learning and memory via binding to Dendrin.
 

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