Your DNA and Memory
According to information on page 375, memory involves alteration of gene activity and synthesis of proteins that change synaptic strength. Now research indicates that this process includes selective methylation and demethylation of genes. (You learned in Ch 6 that attachment of methyl groups to genes turns the genes off.) In 2007 Courtney Miller and David Sweatt found that fear conditioning in rats involves methylation and silencing of the memory suppressor gene PP1 and demethylation and activation of the synaptic plasticity gene reelin in the hippocampus. Neuron, Vol 53, 857-869. However, a day later the methylation levels return to normal, so these changes apparently represent short-term memory. Now a follow-up study by the same researchers has shown that the 7 days following learning are characterized by demethylation of some genes and methylation of others in the cortex and the amygdala. (Reported at the 2008 meeting of the Society for Neuroscience; also see graphic). Note that this shift in the location of activity is consistent with information in the text (p 368, p 376) that memory progresses from a short-term record in the hippocampus to a more permanent form in the cortex.
New Memories in the Hippocampus, Old Ones in the Cortex
Forming new memories requires the hippocampus in mice and rats, but over time the memory is transferred to cortical areas. In rats the transfer appears to be essentially complete by the end of 3 weeks (see p 368). An fMRI study has confirmed this two-stage memory process in humans, though the time period apparently is longer. Volunteers were asked to remember events from their past. As they recalled progressively older memories (extending back over a 12-year period), activity decreased in the hippocampus and increased in frontal, temporal and parietal cortex. Journal of Neuroscience, Vol 29, 930-938.
Early Effect of Alzheimer's Gene
The text indicates that the ApoE4 gene is found in a high percentage of late-onset Alzheimer's patients (Table 12.1, p. 383); the gene is also associated with anatomical and functional changes in the brains of healthy middle-aged and elderly individuals. Now an fMRI study of healthy young adults (20-35 years) has found that carriers of the ApoE4 gene show increased activity in temporal and prefrontal brain areas during rest and increased activity in the hippocampus during a memory task. Possible interpretations are that this excessive activity "wears out" the brain, or that these brain areas are already functioning inefficiently early in life. How well these measure might predict later Alzheimer's can't be determined without following such individuals for decades. Proceedings of the National Academy of Sciences (published online prior to print)
New Form of Epilepsy Targets Memory
A recently identified form of amnesia impairs memory without producing other symptoms typical of epilepsy, such as unconsciousness or convulsions. Transient epileptic amnesia (TEA) seizures usually last about an hour, during which the person cannot remember the way to work or that a brother died two days before; the memory loss persists after the seizure has ended. People with TEA have a slightly smaller hippocampus, which is involved in both consolidation and retrieval of memories (pp 366-7). Annals of Neurology, Vol 61, 587-598; Brain, Vol 132, 357-368.
Why Oldsters Forget?
In Chapter 12 you learn that memory appears to be enhanced when sleeping rats' brains replay the neural activity that occurred during learning. But when researchers at the University of Arizona compared activity in rats of different ages they found that replay is reduced in old rats and that the degree of memory impairment is proportional to this decrease. This finding substantiates the conclusion that resting period replay is important for memory consolidation. Journal of Neuroscience, Vol 28, 7883-7890.
Could Eating Less Improve Your Memory?
Overweight elderly volunteers who reduced their calorie intake 30% showed a 20% increase in memory (measured by comparing the number of words they were able to remember after a delay of 30 minutes.) There was little or no improvement among subjects who either did not change their diet or who increased their consumption of unsaturated fatty acids (such as those found in salmon or olive oil), which has been linked with improved cognition in previous studies. Proceedings of the National Academy of Sciences, Vol 106, 1255-1260.
Patient HM Dies at 82
The world's most famous patient and research subject died of respiratory failure on December 2, 2008. Henry Molaison—known as Patient HM to protect his privacy—was studied for more than five decades after extensive surgery to control debilitating epileptic seizures left him unable to form most new memories. As Chapter 12 explains, he intrigued neuroscientists by becoming proficient on new tasks such as mirror tracing, though he was unable to remember from one session to the next that he had ever seen the task before. According to the Times writer, "He left a legacy that cannot be erased." New York Times, Dec 4, 2008.
