Irvine, Calif. -- Psychological stress during infancy has beenfound to cause early impaired memory and a decline in related cognitiveabilities, according to a UC Irvine School of Medicine study. The studysuggests that the emotional stress associated with parental loss, abuseor neglect may contribute to the type of memory loss during middle-ageyears that is normally seen in the elderly.
The study, conducted in rats, is believed to be the first to showthat early life emotional stress initiates a slow deterioration ofbrain-cell communication in adulthood. These cell-signaling deficitsoccur in the hippocampus, a brain region involved in learning, storageand recall of learned memories. Study results appear in the Oct. 12issue of the Journal of Neuroscience.
"The loss of cognitive function later in life is probably a result ofboth genetic and environmental factors," said study leader Dr. TallieZ. Baram, the Danette Shepard Chair in Neurological Sciences. "While itis not yet possible to change a person's genetic background, it may befeasible to block the environmental effects, particularly of early lifestress, on learning and memory later in life. These studies point tothe development of new, more effective ways to prevent cognitiveimpairment later in life."
In their study, Baram, post-graduate researcher Kristen Brunson andcolleagues found that limiting the nesting material in cages whereneonatal rats lived with their mothers led to emotional stress for bothmothers and pups. All evidence of this stress disappeared by the timethe pups reached adulthood.
However, starting in middle age, these "graduates" of early life stressbegan to exhibit deficits in their ability to remember the location ofobjects they had seen before, as well as to recognize objects that theyhad encountered on the previous day. Strikingly, these difficultiesworsened as the rats grew older, much more rapidly than in rats thatwere raised for their first week of life under typical nurturingenvironment.
The researchers teamed up with Gary Lynch, a UCI professor ofpsychiatry and human behavior and a world leader in the study of themechanisms of learning and memory, to understand the effects early lifestress had on the brain-cell activity in the rats. The normal increasein brain communication through synapses, considered to be the cellularbasis for learning and memory, was found to be faulty in themiddle-aged rats exposed to early life stress.
In testing these cellular abnormalities, the researchers recorded theelectrical activity of brain cells, which appeared normal in youngadult rats exposed to early life stress, but became very disturbed asthey reached middle age. These changes in brain-cell activity wereconsistent with the rats' behavioral changes.
More than 50 percent of the world's children are raised under stressfulconditions, as revealed by UNESCO last year. While it has beensuspected that early life stress can lead to later cognitiveimpairment, it is not yet possible to affirm this suspicion in humanstudies, because children's genetic background or other confoundersmake these analyses too complex.
The current study allows investigators to show that the early stressitself is responsible for the cognitive decline. In addition, now thatconcrete deficits in brain-cell communication have been found, the newunderstanding of the cellular basis for how this occurs will permit theresearchers to find the specific molecules involved and to designmedicines to prevent the deficits.
Eniko Kramar, Bin Lin, Yuncai Chen, Laura Lee Colgin and Theodore K.Yanagihara of UCI contributed to the study, which was supported by theNational Institutes of Health.
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