Learning, memory, and transcription factors

Michael V. Johnston, Lily Alemi, Karen H. Harum

Research output: Contribution to journalReview article

Abstract

Cognitive disorders in children have traditionally been described in terms of clinical phenotypes or syndromes, chromosomal lesions, metabolic disorders, or neuropathology. Relatively little is known about how these disorders affect the chemical reactions involved in learning and memory. Experiments in fruit flies, snails, and mice have revealed some highly conserved pathways that are involved in learning, memory, and synaptic plasticity, which is the primary substrate for memory storage. These can be divided into short-term memory storage through local changes in synapses, and long-term storage mediated by activation of transcription to translate new proteins that modify synaptic function. This review summarizes evidence that disruptions in these pathways are involved in human cognitive disorders, including neurofibromatosis type I, Coffin-Lowry syndrome, Rubinstein-Taybi syndrome, Rett syndrome, tuberous sclerosis-2, Down syndrome, X-linked α-thalassemia/mental retardation, cretinism, Huntington disease, and lead poisoning.

Original languageEnglish (US)
Pages (from-to)369-374
Number of pages6
JournalPediatric research
Volume53
Issue number3
DOIs
StatePublished - Mar 1 2003

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

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