Emerging evidence of insulin-like growth factor 2 as a memory enhancer: a unique animal model of cognitive dysfunction with impaired adult neurogenesis.

[22q11.2 deletion syndrome]

Abstract In the current aging society , cognitive dysfunction is one of the most serious issues that should be urgently resolved . It also affects a wide range of age groups harboring neurological and psychiatric disorders , such as Alzheimer 's disease and schizophrenia . Although the molecular mechanism of memory impairment still remains to be determined , neuronal loss and dysfunction has been revealed to mainly attribute to its pathology . The discovery of neural stem cells in the adult brain that are proliferating and able to generate functional neurons has given rise to the idea that neuronal loss could be rescued by manipulating endogenous neural progenitor and stem cells . To this end , we must characterize them in detail and their developmental programming must be better understood . A growing body of evidence has indicated that insulin -like peptides are involved in learning and memory and maintenance of neural progenitor and stem cells , and clinical trials of insulin as a memory enhancer have begun . In contrast to the expectation of insulin and IGF 1 , the roles of IGF 2 in cognitive ability have been poorly understood . However , recent evidence demonstrated in rodents suggests that IGF 2 may play a pivotal role in adult neurogenesis and cognitive function . Here , we would like to review the rapidly growing world of IGF 2 in cognitive neuroscience and introduce the evidence that its deficit is indeed involved in the impairment of the hippocampal neurogenesis and cognitive dysfunction in the model mouse of 22 q 11 .2 deletion syndrome , which deletes Dgcr 8 , a critical gene for microRNA processing .

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Diseases presenting "cognitive neuroscience" symptom

22q11.2 deletion syndrome

locked-in syndrome

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