Word: hippocampus
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Dates: during 2000-2009
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Consider, for a moment, how memory is supposed to operate. Consider, that is, the hippocampus. A cashew-shaped node of tissue, the hippocampus sits deep in the temporal lobe of the brain, near the amygdala, which is the seat of emotions. If the brain has a gatekeeper of sensory information, the hippocampus is it. The aroma and sizzle of bacon frying, the smooth finish of polished granite, a phone number you need to call--all must pass through the hippocampus. Only if information gets in can it be moved along to the prefrontal cortex, where it will be held briefly...
...hang on to the number 10 minutes or even 10 months later. Why? Because that bit of information has gone through a chemical process called long-term potentiation (LTP) that strengthens the synapses. You need LTP to form long-term memories. And LTP takes place in the hippocampus...
...hippocampus begins to malfunction early in Alzheimer's disease. Imaging studies have shown that people with Alzheimer's typically have smaller than average hippocampi. Meanwhile, as the hippocampus is shrinking, the pathway between it and the prefrontal cortex also begins to degrade. Signals peter out and fade away, and questions take their place: Do I know you? Who am I? But it's not just with Alzheimer's: the hippocampus also goes at least somewhat awry in normal memory loss. "It's relatively stable in volume till about 60," Harvard neuroscientist Randy Buckner explains, "and then begins to change. People...
Small and his colleagues have been trying to understand this difference. Small's hunch--now proven--was that a node of the hippocampus different from the one affected in Alzheimer's was breaking down in normal memory loss. "In humans, monkeys and rats," he says, "normal aging targets a node called the dentate gyrus, while a different node--the entorhinal cortex--is relatively spared. But in Alzheimer's disease, it's almost exactly reversed." Small has gone deeper, pinpointing a protein molecule known as RbAp48 that is lower in the brains of people suffering ordinary age-related memory loss...
...basic research scientists, Tonegawa and McHugh don't claim that their work will lead to a drug or therapy--not yet. And if it does, nobody is likely to focus on déjà vu, a mere side effect of memory. But a fuller understanding of how the hippocampus works could lead to the creation of a drug that strengthens the pattern-recognition circuit, which could help people overcome fearful memories that are triggered by associations with a familiar-seeming place (like a dentist's office). Of course, if you strengthen the circuitry too much, you might get the opposite illusion...